Updated on 2025/07/30

写真a

 
TAZAWA Hiroshi
 
Organization
Scheduled update Associate Professor
Position
Associate Professor
External link

Degree

  • 医学博士 ( 秋田大学 )

Research Interests

  • Gastroenterological Surgery

  • Gene therapy

Research Areas

  • Life Science / Digestive surgery

  • Life Science / Tumor diagnostics and therapeutics

Education

  • Akita University   大学院   医学研究科

    1996.4 - 2000.3

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  • Akita University   医学部   医学科

    1989.4 - 1995.3

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  • 富山県立高岡高等学校     普通科

    1986.4 - 1989.3

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Research History

  • Okayama University   新医療研究開発センター 探索的医薬品開発室   Associate Professor

    2016.7

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  • Okayama University   新医療研究開発センター 探索的医薬品開発室   Assistant Professor

    2011.10 - 2016.6

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  • Okayama University   遺伝子・細胞治療センター   Assistant Professor

    2010.4 - 2011.9

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  • Okayama University   Graduate School of Medicine , Dentistry and Pharmaceutical Sciences

    2007.12 - 2010.3

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  • 国立がんセンター研究所   研究員

    2005.2 - 2007.11

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  • WHO国際癌研究機関(IARC、フランス)   客員研究員

    2002.4 - 2005.1

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  • 山形県鶴岡協立病院   医員

    2000.4 - 2002.3

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  • Hokkaido University   School of Medicine

    1998.4 - 2000.3

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  • Akita University   University Hospital

    1997.4 - 1998.3

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  • 秋田県厚生連雄勝中央病院   研修医

    1995.4 - 1997.3

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Professional Memberships

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Committee Memberships

  • 日本バイオセラピィ学会   評議員  

    2022.6   

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  • 日本癌学会   評議員  

    2019.1   

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    Committee type:Academic society

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  • 日本遺伝子細胞治療学会   評議員  

    2017.7   

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Papers

  • ADAR1 as a prognostic marker for patients with colorectal cancer and synchronous liver metastasis and a predictor of chemotherapy efficacy. Reviewed International journal

    Kaori Nitta, Kunitoshi Shigeyasu, Yoshitaka Kondo, Hibiki Umeda, Toshiaki Takahashi, Kazuya Moriwake, Kazuhiro Yoshida, Sho Takeda, Yuki Matsumi, Hiroyuki Kishimoto, Tomokazu Fuji, Kazuya Yasui, Kosei Takagi, Masashi Kayano, Shunsuke Nakamura, Hiroyuki Michiue, Hideki Yamamoto, Nobuhiko Kanaya, Yuhei Kondo, Eiki Miyake, Yusuke Yoshida, Ryohei Shoji, Yoshihiko Kakiuchi, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Scientific reports   15 ( 1 )   26752 - 26752   2025.7

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    RNA editing by adenosine deaminase acting on RNA (ADAR) enzymes plays a role in cancer progression. However, its clinical significance in metastatic colorectal cancer (CRC) remains unclear. This study aimed to evaluate whether ADAR1 expression predicts prognosis and treatment response in colorectal cancer (CRC) with synchronous liver metastasis. This study included 40 patients with stage IV CRC and synchronous liver metastases. ADAR1 expression in tumor tissues was evaluated using immunohistochemistry. Expression levels were quantified using the immunoreactive score, and associations with clinicopathological features, overall survival (OS), and chemotherapy response were examined. High ADAR1 expression was significantly associated with multiple liver metastases (P = 0.0206), lymph node metastasis (P = 0.0241), and reduced response to chemotherapy (P = 0.0224). Significantly shorter OS was observed in patients with high ADAR1 expression in the nucleus (P = 0.0458). ADAR1 expression was an independent prognostic factor comparable to the presence of extrahepatic metastases. Low ADAR1 expression was correlated with a higher likelihood of achieving a response to chemotherapy. ADAR1 expression can reflect tumor aggressiveness and chemotherapy resistance in patients with CRC and synchronous liver metastasis. ADAR1 has considerable potential as a dual-purpose biomarker for stratifying patients based on prognosis and optimizing treatment intensity.

    DOI: 10.1038/s41598-025-11918-7

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  • Oncolytic virus-mediated p53 activation boosts the antitumor immunity of a p53-transduced dendritic cell vaccine. Reviewed International journal

    Motohiko Yamada, Hiroshi Tazawa, Kanto Suemori, Naohiro Okada, Yoshinori Kajiwara, Ryohei Shoji, Yasuo Nagai, Hiroaki Inoue, Naoyuki Hashimoto, Nobuhiko Kanaya, Satoru Kikuchi, Shinji Kuroda, Hiroyuki Michiue, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    NPJ vaccines   10 ( 1 )   158 - 158   2025.7

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    Dendritic cells (DCs) transduced with replication-deficient, wild-type human p53-expressing adenovirus Ad-p53 (Ad-p53 DCs) induce p53-targeting cytotoxic T lymphocytes (CTLs). However, the antitumor efficacy of Ad-p53 DCs is diminished by weak p53 immunogenicity in tumor cells and poor immune responses. We developed a p53-armed oncolytic adenovirus, OBP-702, to induce tumor-specific p53 expression and antitumor immune response, suggesting a role for OBP-702 in enhancing the antitumor efficacy of Ad-p53 DCs. The combined effect of Ad-p53 DCs and OBP-702 was investigated using murine colon cancer (CC) tumor models. Ad-p53 DCs were obtained by stimulating bone marrow-derived cells with granulocyte-macrophage colony-stimulating factor, interleukin-4, and Ad-p53. Subcutaneous tumor models of CT26 (p53 wild-type) and MC38 (p53 mutant-type) murine CC cell lines were used to evaluate the therapeutic potential of combination therapy in the terms of tumor growth, abscopal effect, antitumor immune response, and presentation of p53 peptides in tumor cells. Combination therapy with Ad-p53 DCs and OBP-702 significantly suppressed the growth of p53-intact CT26 tumors at treated and untreated sites by inducing tumor-infiltration of CD8+ CTLs and CD11c+ DCs. OBP-702-infected tumor cells presented human p53 epitopes in the context of major histocompatibility complex molecules, which were recognized by CTLs induced by Ad-p53 DCs. Combination therapy significantly suppressed the growth of p53-mutant MC38 tumors by activating the antitumor immune response. Our results suggest that OBP-702-mediated presentation of p53 epitopes on tumor cells enhances the antitumor efficacy of Ad-p53 DCs against murine CC tumors by attracting p53-targeting CTLs.

    DOI: 10.1038/s41541-025-01219-5

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  • Grafting Islets to a Prevascularized Subcutaneous Site to Improve Transplant Survival and Function: A Mouse Model. Reviewed International journal

    Tsuyoshi Okada, Takashi Kuise, Kenjiro Kumano, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Transplantation proceedings   2025.6

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    BACKGROUND: The subcutaneous space is regarded as a potential site for islet transplantation; however, hypoxic conditions are a major drawback. We hypothesized that islet transplantation into a prevascularized subcutaneous space created using in-body tissue architecture technology would improve islet engraftment and contribute to maintaining the function of transplanted islets. METHODS: Five hundred syngeneic islets were transplanted into the prevascularized subcutaneous space (PSS) constructed by the implantation of a silicone rod for 2 weeks in C57BL/6J diabetic mice. Diabetic mice transplanted with islets into the unmodified subcutaneous space (USS) were used as the controls. After transplantation, nonfasting blood glucose levels were monitored for 8 weeks, and an intraperitoneal glucose tolerance test and histological evaluation were performed. RESULTS: Five of the 10 recipients in the PSS group and two of the nine recipients in the USS group returned to normoglycemia. Engraftment of the transplanted islets was detected in nine of the 10 recipients in the PSS group, and the engraftment rate in the PSS group was significantly higher than that in the USS group (P = .005). Intraperitoneal glucose tolerance test results showed that the glucose tolerance of recipient mice in the PSS group was significantly better than that of the diabetic mice. Histological analysis revealed that the density of capillary vessels in the connective tissue surrounding the engrafted islets in the PSS group was significantly higher than that in the USS group (41.7/mm2 vs 7.2/mm2, P < .01). CONCLUSION: Islet transplantation into the PSS using in-body tissue architecture technology has the potential to improve graft survival.

    DOI: 10.1016/j.transproceed.2025.05.019

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  • Osteosarcoma cell-derived CCL2 facilitates lung metastasis via accumulation of tumor-associated macrophages. Reviewed International journal

    Hiroya Kondo, Hiroshi Tazawa, Tomohiro Fujiwara, Aki Yoshida, Miho Kure, Koji Demiya, Nobuhiko Kanaya, Toshiaki Hata, Koji Uotani, Joe Hasei, Toshiyuki Kunisada, Shunsuke Kagawa, Yusuke Yoshioka, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Cancer immunology, immunotherapy : CII   74 ( 7 )   193 - 193   2025.5

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    Osteosarcoma (OS) is the most common malignant tumor of bone in children and adolescents. Although lung metastasis is a major obstacle to improving the prognosis of OS patients, the underlying mechanism of lung metastasis of OS is poorly understood. Tumor-associated macrophages (TAMs) with M2-like characteristics are reportedly associated with lung metastasis and poor prognosis in OS patients. In this study, we investigated the metastasis-associated tumor microenvironment (TME) in orthotopic OS tumor models with non-metastatic and metastatic OS cells. Non-metastatic and metastatic tumor cells derived from mouse OS (Dunn and LM8) and human OS (HOS and 143B) were used to analyze the TME associated with lung metastasis in orthotopic OS tumor models. OS cell-derived secretion factors were identified by cytokine array and enzyme-linked immunosorbent assay (ELISA). Orthotopic tumor models with metastatic LM8 and 143B cells were analyzed to evaluate the therapeutic potential of a neutralizing antibody in the development of primary and metastatic tumors. Metastatic OS cells developed metastatic tumors with infiltration of M2-like TAMs in the lungs. Cytokine array and ELISA demonstrated that metastatic mouse and human OS cells commonly secreted CCL2, which was partially encapsulated in extracellular vesicles. In vivo experiments demonstrated that while primary tumor growth was unaffected, administration of CCL2-neutralizing antibody led to a significant suppression of lung metastasis and infiltration of M2-like TAMs in the lung tissue. Our results suggest that CCL2 plays a crucial role in promoting the lung metastasis of OS cells via accumulation of M2-like TAMs.

    DOI: 10.1007/s00262-025-04051-x

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  • HIF-PH inhibitors induce pseudohypoxia in T cells and suppress the growth of microsatellite stable colorectal cancer by enhancing antitumor immune responses. Reviewed International journal

    Yuehua Chen, Toshiaki Ohara, Yusuke Hamada, Yuze Wang, Miao Tian, Kazuhiro Noma, Hiroshi Tazawa, Masayoshi Fujisawa, Teizo Yoshimura, Akihiro Matsukawa

    Cancer immunology, immunotherapy : CII   74 ( 7 )   192 - 192   2025.5

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    BACKGROUND: Recent studies have revealed that CD8+ T cells can be activated via genetic upregulation of HIF-1α, thereby augmenting antitumor effector functions. HIF-1α upregulation can be attained by inhibiting HIF-prolyl hydroxylase (HIF-PH) under normoxic conditions, termed pseudohypoxia. This study investigated whether pseudohypoxia induced by HIF-PH inhibitors suppresses Microsatellite stable (MSS) colorectal cancer (CRC) by affecting tumor immune response. METHODS: The HIF-PH inhibitors Roxadustat and Vadadustat were utilized in this study. In vitro, we assessed the effects of HIF-PH inhibitors on human and murine colon cancer cell lines (SW480, HT29, Colon26) and murine T cells. In vivo experiments were performed with mice bearing Colon26 tumors to evaluate the effect of these inhibitors on tumor immune responses. Tumor and spleen samples were analyzed using immunohistochemistry, RT-qPCR, and flow cytometry to elucidate potential mechanisms. RESULTS: HIF-PH inhibitors demonstrated antitumor effects in vivo but not in vitro. These inhibitors enhanced the tumor immune response by increasing the infiltration of CD8+ and CD4+ tumor-infiltrating lymphocytes (TILs). HIF-PH inhibitors induced IL-2 production in splenic and intratumoral CD4+ T cells, promoting T cell proliferation, differentiation, and immune responses. Roxadustat synergistically enhanced the efficacy of anti-PD-1 antibody for MSS cancer by increasing the recruitment of TILs and augmenting effector-like CD8+ T cells. CONCLUSION: Pseudohypoxia induced by HIF-PH inhibitors activates antitumor immune responses, at least in part, through the induction of IL-2 secretion from CD4+ T cells in the spleen and tumor microenvironment, thereby enhancing immune efficacy against MSS CRC.

    DOI: 10.1007/s00262-025-04067-3

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  • [Development of Oncolytic Virus Immunotherapy to Improve the Immunosuppressive Microenvironment in Pancreatic Cancer]. Invited Reviewed

    Kanto Suemori, Hiroshi Tazawa, Motohiko Yamada, Naohiro Okada, Satoru Kikuchi, Shinji Kuroda, Kazuhiro Noma, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Gan to kagaku ryoho. Cancer & chemotherapy   52 ( 5 )   399 - 401   2025.5

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    Immunotherapy resistance in pancreatic ductal adenocarcinoma(PDAC)limits treatment outcomes; therefore, improving the immunosuppressive microenvironment is important for PDAC treatment. We developed an oncolytic adenovirus, OBP-702, carrying the tumor suppressor gene p53, and report its therapeutic potential to induce cytopathic effects and activate antitumor immunity via p53 induction. In the present study, we investigated the therapeutic potential of epigenetic modulators in oncolytic viral immunotherapy combined with a dendritic cell vaccine.

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  • ADAR1-high tumor-associated macrophages induce drug resistance and are therapeutic targets in colorectal cancer. Reviewed International journal

    Hibiki Umeda, Kunitoshi Shigeyasu, Toshiaki Takahashi, Kazuya Moriwake, Yoshitaka Kondo, Kazuhiro Yoshida, Sho Takeda, Shuya Yano, Yuki Matsumi, Hiroyuki Kishimoto, Tomokazu Fuji, Kazuya Yasui, Hideki Yamamoto, Kosei Takagi, Masashi Kayano, Hiroyuki Michiue, Keiichiro Nakamura, Yoshiko Mori, Fuminori Teraishi, Hiroshi Tazawa, Yuzo Umeda, Shunsuke Kagawa, Ajay Goel, Toshiyoshi Fujiwara

    Molecular cancer   24 ( 1 )   116 - 116   2025.4

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    BACKGROUND: Colorectal cancer (CRC) is considered the third most common type of cancer worldwide. Tumor-associated macrophages (TAMs) have been shown to promote drug resistance. Adenosine-to-inosine RNA-editing, as regulated by adenosine deaminase acting on RNA (ADAR), is a process that induces the posttranscriptional modification of critical oncogenes. The aim of this study is to determine whether the signals from cancer cells would induce RNA-editing in macrophages. METHODS: The effects of RNA-editing on phenotypes in macrophages were analyzed using clinical samples and in vitro and in vivo models. RESULTS: The intensity of the RNA-editing enzyme ADAR1 (Adenosine deaminase acting on RNA 1) in cancer and mononuclear cells indicated a strong positive correlation between the nucleus and cytoplasm. The ADAR1-positive mononuclear cells were positive for CD68 and CD163, a marker for M2 macrophages. Cancer cells transport pro-inflammatory cytokines or ADAR1 protein directly to macrophages via the exosomes, promoting RNA-editing in AZIN1 (Antizyme Inhibitor 1) and GLI1 (Glioma-Associated Oncogene Homolog 1) and resulting in M2 macrophage polarization. GLI1 RNA-editing in the macrophages induced by cancer cells promotes the secretion of SPP1, which is supplied to the cancer cells. This activates the NFκB pathway in cancer cells, promoting oxaliplatin resistance. When the JAK inhibitors were administered, oncogenic RNA-editing in the macrophages was suppressed. This altered the macrophage polarization from M2 to M1 and decreased oxaliplatin resistance in cancer cells. CONCLUSIONS: This study revealed that ADAR1-high TAMs are crucial in regulating drug resistance in CRC and that targeting ADAR1 in TAMs could be a promising treatment approach for overcoming drug resistance in CRC.

    DOI: 10.1186/s12943-025-02312-y

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  • Cancer-associated fibroblasts promote pro-tumor functions of neutrophils in pancreatic cancer via IL-8: potential suppression by pirfenidone. Reviewed International journal

    Tomohiko Yagi, Shunsuke Kagawa, Shohei Nogi, Atsuki Taniguchi, Masashi Yoshimoto, Kanto Suemori, Yasuo Nagai, Shuto Fujita, Shinji Kuroda, Satoru Kikuchi, Yoshihiko Kakiuchi, Fuminori Teraishi, Kosei Takagi, Toshiaki Ohara, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Cancer immunology, immunotherapy : CII   74 ( 3 )   96 - 96   2025.2

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    BACKGROUND: The mechanisms by which neutrophils acquire pro-tumor properties remain poorly understood. In pancreatic cancer, cancer-associated fibroblasts (CAFs) may interact with neutrophils, directing them to promote tumor progression. METHODS: To validate the association between CAFs and neutrophils, the localization of neutrophils was examined in clinically resected pancreatic cancer specimens. CAFs were produced by culturing in cancer-conditioned media, and the effects of these CAFs on neutrophils were examined. In vitro migration and invasion assays assess the effect of CAF-activated neutrophils on cancer cells. The factors secreted by the activated neutrophils were also explored. Finally, pirfenidone (PFD) was tested to determine whether it could suppress the pro-tumor functions of activated neutrophils. RESULTS: In pancreatic cancer specimens, neutrophils tended to co-localize with IL-6-positive CAFs. Neutrophils co-cultured with CAFs increased migratory capacity and prolonged life span. CAF-affected neutrophils enhance the migratory and invasive activities of pancreatic cancer cells. IL-8 is the most upregulated cytokine secreted by the neutrophils. PFD suppresses IL-8 secretion from CAF-stimulated neutrophils and mitigates the malignant traits of pancreatic cancer cells. CONCLUSION: CAFs activate neutrophils and enhance the malignant phenotype of pancreatic cancer. The interactions between cancer cells, CAFs, and neutrophils can be disrupted by PFD, highlighting a potential therapeutic approach.

    DOI: 10.1007/s00262-025-03946-z

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  • Novel treatment strategy targeting interleukin-6 induced by cancer associated fibroblasts for peritoneal metastasis of gastric cancer. Reviewed International journal

    Ema Mitsui, Satoru Kikuchi, Tomohiro Okura, Hiroshi Tazawa, Yuta Une, Noriyuki Nishiwaki, Shinji Kuroda, Kazuhiro Noma, Shunsuke Kagawa, Toshiaki Ohara, Junko Ohtsuka, Rieko Ohki, Toshiyoshi Fujiwara

    Scientific reports   15 ( 1 )   3267 - 3267   2025.1

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    Cancer-associated fibroblasts (CAFs) are a crucial component in the tumor microenvironment (TME) of peritoneal metastasis (PM), where they contribute to tumor progression and metastasis via secretion of interleukin-6 (IL-6). Here, we investigated the role of IL-6 in PM of gastric cancer (GC) and assessed whether anti-IL-6 receptor antibody (anti-IL-6R Ab) could inhibit PM of GC. We conducted immunohistochemical analysis of IL-6 and α-smooth muscle (α-SMA) expressions in clinical samples of GC and PM, and investigated the interactions between CAFs and GC cells in vitro. Anti-tumor effects of anti-IL-6R Ab on PM of GC were investigated in an orthotopic murine PM model. IL-6 expression was significantly correlated with α-SMA expression in clinical samples of GC, and higher IL-6 expression in the primary tumor was associated with poor prognosis of GC. Higher IL-6 and α-SMA expressions were also observed in PM of GC. In vitro, differentiation of fibroblasts into CAFs and chemoresistance were observed in GC cells cocultured with fibroblasts. Anti-IL-6R Ab inhibited the progression of PM in GC cells cocultured with fibroblasts in the orthotopic mouse model but could not inhibit the progression of PM consisting of GC cells alone. IL-6 expression in the TME was associated with poor prognosis of GC, and CAFs were associated with establishment and progression of PM via IL-6. Anti-IL-6R Ab could inhibit PM of GC by the blockade of IL-6 secreted by CAFs, which suggests its therapeutic potential for PM of GC.

    DOI: 10.1038/s41598-025-88033-0

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  • がんに対するウイルス療法 臨床応用を目指した創薬研究 Invited Reviewed

    藤原俊義, 黒田新士, 田澤大

    ファルマシア(Web)   61 ( 5 )   2025

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  • Development of Oncolytic Viruses against Cancer Invited Reviewed

    田澤大, 黒田新士, 香川俊輔, 藤原俊義

    癌と化学療法   52 ( 6 )   2025

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    Authorship:Lead author, Corresponding author   Language:Japanese   Publishing type:Research paper (scientific journal)  

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  • Dendritic cell maturation is induced by p53-armed oncolytic adenovirus via tumor-derived exosomes enhancing systemic antitumor immunity. Reviewed International journal

    Tomoko Ohtani, Shinji Kuroda, Nobuhiko Kanaya, Yoshihiko Kakiuchi, Kento Kumon, Masashi Hashimoto, Chiaki Yagi, Ryoma Sugimoto, Satoru Kikuchi, Shunsuke Kagawa, Hiroshi Tazawa, Yasuo Urata, Toshiyoshi Fujiwara

    Cancer immunology, immunotherapy : CII   74 ( 1 )   12 - 12   2024.11

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    Dendritic cells (DCs) are crucial in cancer immunity, because they activate cytotoxic T cells by presenting tumor antigens. Recently, oncolytic virus therapy has been recognized as a systemic immune stimulator. We previously developed a telomerase-specific oncolytic adenovirus (OBP-301) and a p53-armed OBP-301 (OBP-702), demonstrating that these viruses strongly activate systemic antitumor immunity. However, their effects on DCs remained unclear. In the present study, the aim was to elucidate the mechanisms of DC activation by OBP-702, focusing particularly on tumor-derived exosomes. Exosomes (Exo53, Exo301, or Exo702) were isolated from conditioned media of human or murine pancreatic cancer cell lines (Panc-1, MiaPaCa-2, and PAN02) after treatment with Ad-p53, OBP-301, or OBP-702. Exo702 derived from Panc-1 and MiaPaCa-2 cells significantly upregulated CD86, CD80, CD83 (markers of DC maturation), and IFN-γ in DCs in vitro. Similarly, Exo702 derived from PAN02 cells upregulated CD86 and IFN-γ in bone marrow-derived DCs in a bilateral PAN02 subcutaneous tumor model. This DC maturation was inhibited by GW4869, an inhibitor of exosome release, and anti-CD63, an antibody targeting the exosome marker. Intratumoral injection of OBP-702 into PAN02 subcutaneous tumors significantly increased the presence of mature DCs and CD8-positive T cells in draining lymph nodes, leading to long-lasting antitumor effects through the durable activation of systemic antitumor immunity. In conclusion, tumor-derived exosomes play a significant role in DC maturation following OBP-702 treatment and are critical for the systemic activation of antitumor immunity, leading to the abscopal effect.

    DOI: 10.1007/s00262-024-03849-5

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  • 大腸癌に対する樹状細胞ワクチン療法と腫瘍融解アデノウイルスの併用効果 Invited Reviewed

    岡田 尚大, 田澤 大, 山田 元彦, 陶守 貫人, 菊地 覚次, 黒田 新士, 野間 和広, 浦田 泰生, 香川 俊輔, 藤原 俊義

    癌と化学療法   51 ( 10 )   1035 - 1037   2024.10

  • p53-armed oncolytic virotherapy induces abscopal effect in osteosarcoma by promoting immunogenic cell death. Reviewed International journal

    Koji Demiya, Hiroshi Tazawa, Hiroya Kondo, Miho Kure, Yusuke Mochizuki, Tadashi Komatsubara, Aki Yoshida, Koji Uotani, Joe Hasei, Tomohiro Fujiwara, Toshiyuki Kunisada, Yasuo Urata, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Molecular therapy. Oncology   32 ( 3 )   200845 - 200845   2024.9

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    Authorship:Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    Osteosarcoma (OS), the most frequent primary malignant tumor of bone in children and adolescents, is refractory to immune checkpoint inhibitors due to its poor antitumor immune response. Chemotherapy and virotherapy induce immunogenic cell death (ICD) and antitumor immune responses, leading to the abscopal effect in untreated tumors. We previously demonstrated the antitumor activity of the telomerase-specific replication-competent oncolytic adenoviruses OBP-301 and p53-armed OBP-702 in human OS cells. Here, we show the therapeutic potential of chemotherapeutic drugs (doxorubicin, cisplatin) and telomerase-specific oncolytic adenoviruses (OBP-301, p53-armed OBP-702) to induce ICD in human OS cells (U2OS, MNNG/HOS, SaOS-2) and murine OS cells (NHOS). OBP-702 induced more profound ICD via the secretion of adenosine triphosphate (ATP) and high-mobility group box protein B1 (HMGB1) compared with chemotherapy and OBP-301 in human OS cells. Murine NHOS cells were also more sensitive to OBP-702 than OBP-301. Subcutaneous NHOS tumor models demonstrated that intratumoral injection of OBP-702 significantly increased the tumor infiltration of cytotoxic CD8+ T cells and induced the abscopal effect against non-treated tumors compared with OBP-301. Our results suggest that OBP-702 is a promising antitumor reagent to induce ICD with secretion of ATP and HMGB1 and the abscopal effect against OS.

    DOI: 10.1016/j.omton.2024.200845

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  • Near-infrared Photoimmunotherapy Targeting Cancer-Associated Fibroblasts in Patient-Derived Xenografts Using a Humanized Anti-Fibroblast Activation Protein Antibody. Reviewed International journal

    Teruki Kobayashi, Kazuhiro Noma, Seitaro Nishimura, Takuya Kato, Noriyuki Nishiwaki, Toshiaki Ohara, Tomoyoshi Kunitomo, Kento Kawasaki, Masaaki Akai, Satoshi Komoto, Hajime Kashima, Satoru Kikuchi, Hiroshi Tazawa, Yasuhiro Shirakawa, Peter L Choyke, Hisataka Kobayashi, Toshiyoshi Fujiwara

    Molecular cancer therapeutics   23 ( 7 )   1031 - 1042   2024.7

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    Esophageal cancer remains a highly aggressive malignancy with a poor prognosis, despite ongoing advancements in treatments such as immunotherapy. The tumor microenvironment, particularly cancer-associated fibroblasts (CAF), plays a crucial role in driving the aggressiveness of esophageal cancer. In a previous study utilizing human-derived xenograft models, we successfully developed a novel cancer treatment that targeted CAFs with near-infrared photoimmunotherapy (NIR-PIT), as an adjuvant therapy. In this study, we sought to translate our findings toward clinical practice by employing patient-derived xenograft (PDX) models and utilizing humanized mAbs, specifically sibrotuzumab, which is an antihuman fibroblast activation protein (FAP) Ab and already being investigated in clinical trials as monotherapy. PDX models derived from patients with esophageal cancer were effectively established, preserving the expression of key biomarkers such as EGFR and FAP, as observed in primary tumors. The application of FAP-targeted NIR-PIT using sibrotuzumab, conjugated with the photosensitizer IR700DX, exhibited precise binding and selective elimination of FAP-expressing fibroblasts in vitro. Notably, in our in vivo investigations using both cell line-derived xenograft and PDX models, FAP-targeted NIR-PIT led to significant inhibition of tumor progression compared with control groups, all without inducing adverse events such as weight loss. Immunohistologic assessments revealed a substantial reduction in CAFs exclusively within the tumor microenvironment of both models, further supporting the efficacy of our approach. Thus, our study demonstrates the potential of CAF-targeted NIR-PIT employing sibrotuzumab as a promising therapeutic avenue for the clinical treatment of patients with esophageal cancer.

    DOI: 10.1158/1535-7163.MCT-23-0527

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  • Functional remodeling of intraperitoneal macrophages by oncolytic adenovirus restores anti-tumor immunity for peritoneal metastasis of gastric cancer. Reviewed International journal

    Motoyasu Tabuchi, Satoru Kikuchi, Hiroshi Tazawa, Tomohiro Okura, Toshihiro Ogawa, Ema Mitsui, Yuta Une, Shinji Kuroda, Hiroki Sato, Kazuhiro Noma, Shunsuke Kagawa, Toshiaki Ohara, Junko Ohtsuka, Rieko Ohki, Yasuo Urata, Toshiyoshi Fujiwara

    Molecular therapy. Oncology   32 ( 2 )   200806 - 200806   2024.6

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    Intraperitoneal tumor-associated macrophages (TAMs) are involved in evading anti-tumor immunity and promoting the peritoneal metastasis (PM) of gastric cancer (GC). Oncolytic viruses are known to induce the activation of host anti-tumor immunity in addition to tumor lysis. This study investigated whether a wild-type p53-loading telomerase-specific oncolytic adenovirus (OBP-702) could elicit the remodeling of intraperitoneal macrophages and enhance the efficacy of immune therapy. Increased numbers of CD163 TAMs and few CD8+ lymphocytes were immunohistochemically observed in clinical samples with PM, which suggested that TAMs were associated with the suppression of anti-tumor immunity. OBP-702 induced immunogenic cell death and upregulated PD-L1 expression in human and murine GC cell lines. Intraperitoneal administration of OBP-702 increased recruitment of CD8+ lymphocytes into the PM via the functional remodeling of intraperitoneal macrophages from TAM toward a pro-inflammatory phenotype, resulting in significantly suppressed tumor growth for the in vivo model. Furthermore, the combination of intraperitoneal OBP-702 with anti-programmed cell death-1 antibody enhanced anti-tumor immunity and prolonged the survival of mice bearing PM. Intraperitoneal immunotherapy using OBP-702 restores anti-tumor immunity via the remodeling of intraperitoneal macrophages in addition to direct tumor lysis and cooperates with immune checkpoint inhibitors to suppress PM in GC.

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  • Senescent Fibroblasts Potentiate Peritoneal Metastasis of Diffuse-type Gastric Cancer Cells via IL-8-mediated Crosstalk. Reviewed International journal

    Yuncheng Li, Hiroshi Tazawa, Yasuo Nagai, Shuto Fujita, Tomohiro Okura, Ryohei Shoji, Motohiko Yamada, Satoru Kikuchi, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Masahiko Nishizaki, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Anticancer research   44 ( 6 )   2497 - 2509   2024.6

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    BACKGROUND/AIM: Diffuse-type gastric cancer (DGC) often forms peritoneal metastases, leading to poor prognosis. However, the underlying mechanism of DGC-mediated peritoneal metastasis is poorly understood. DGC is characterized by desmoplastic stroma, in which heterogeneous cancer-associated fibroblasts (CAFs), including myofibroblastic CAFs (myCAFs) and senescent CAFs (sCAFs), play a crucial role during tumor progression. This study investigated the CAF subtypes induced by GC cells and the role of sCAFs in peritoneal metastasis of DGC cells. MATERIALS AND METHODS: Conditioned medium of human DGC cells (KATOIII, NUGC-4) and human intestinal-type GC (IGC) cells (MKN-7, N87) was used to induce CAFs. CAF subtypes were evaluated by analyzing the expression of α-smooth muscle actin (α-SMA), senescence-associated β-galactosidase (SA-β-gal), and p16 in human normal fibroblasts (GF, FEF-3). A cytokine array was used to explore the underlying mechanism of GC-induced CAF subtype development. The role of sCAFs in peritoneal metastasis of DGC cells was analyzed using a peritoneally metastatic DGC tumor model. The relationships between GC subtypes and CAF-related markers were evaluated using publicly available datasets. RESULTS: IGC cells significantly induced α-SMA+ myCAFs by secreting transforming growth factor-β, whereas DGC cells induced SA-β-gal+/p16+ sCAFs by secreting interleukin (IL)-8. sCAFs further secreted IL-8 to promote DGC cell migration. In vivo experiments demonstrated that co-inoculation of sCAFs significantly enhanced peritoneal metastasis of NUGC-4 cells, which was attenuated by administration of the IL-8 receptor antagonist navarixin. p16 and IL-8 expression was significantly associated with poor prognosis of DGC patients. CONCLUSION: sCAFs promote peritoneal metastasis of DGC via IL-8-mediated crosstalk.

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  • p53-Armed Oncolytic Virotherapy Improves Radiosensitivity in Soft-Tissue Sarcoma by Suppressing BCL-xL Expression. Reviewed

    Tadashi Komatsubara, Hiroshi Tazawa, Joe Hasei, Toshinori Omori, Kazuhisa Sugiu, Yusuke Mochizuki, Koji Demiya, Aki Yoshida, Tomohiro Fujiwara, Toshiyuki Kunisada, Yasuo Urata, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Acta medica Okayama   78 ( 2 )   151 - 161   2024.4

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    Soft-tissue sarcoma (STS) is a heterogeneous group of rare tumors originating predominantly from the embryonic mesoderm. Despite the development of combined modalities including radiotherapy, STSs are often refractory to antitumor modalities, and novel strategies that improve the prognosis of STS patients are needed. We previously demonstrated the therapeutic potential of two telomerase-specific replication-competent oncolytic adenoviruses, OBP-301 and tumor suppressor p53-armed OBP-702, in human STS cells. Here, we demonstrate in vitro and in vivo antitumor effects of OBP-702 in combination with ionizing radiation against human STS cells (HT1080, NMS-2, SYO-1). OBP-702 synergistically promoted the antitumor effect of ionizing radiation in the STS cells by suppressing the expression of B-cell lymphoma-X large (BCL-xL) and enhancing ionizing radiation-induced apoptosis. The in vivo experiments demonstrated that this combination therapy significantly suppressed STS tumors' growth. Our results suggest that OBP-702 is a promising antitumor reagent for promoting the radiosensitivity of STS tumors.

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  • Long-term activation of anti-tumor immunity in pancreatic cancer by a p53-expressing telomerase-specific oncolytic adenovirus. Reviewed International journal

    Masashi Hashimoto, Shinji Kuroda, Nobuhiko Kanaya, Daisuke Kadowaki, Yusuke Yoshida, Masaki Sakamoto, Yuki Hamada, Ryoma Sugimoto, Chiaki Yagi, Tomoko Ohtani, Kento Kumon, Yoshihiko Kakiuchi, Kazuya Yasui, Satoru Kikuchi, Ryuichi Yoshida, Hiroshi Tazawa, Shunsuke Kagawa, Takahito Yagi, Yasuo Urata, Toshiyoshi Fujiwara

    British journal of cancer   130 ( 7 )   1187 - 1195   2024.4

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    BACKGROUND: Pancreatic cancer is an aggressive, immunologically "cold" tumor. Oncolytic virotherapy is a promising treatment to overcome this problem. We developed a telomerase-specific oncolytic adenovirus armed with p53 gene (OBP-702). METHODS: We investigated the efficacy of OBP-702 for pancreatic cancer, focusing on its long-term effects via long-lived memory CD8 + T cells including tissue-resident memory T cells (TRMs) and effector memory T cells (TEMs) differentiated from effector memory precursor cells (TEMps). RESULTS: First, in vitro, OBP-702 significantly induced adenosine triphosphate (ATP), which is important for memory T cell establishment. Next, in vivo, OBP-702 local treatment to murine pancreatic PAN02 tumors increased TEMps via ATP induction from tumors and IL-15Rα induction from macrophages, leading to TRM and TEM induction. Activation of these memory T cells by OBP-702 was also maintained in combination with gemcitabine+nab-paclitaxel (GN) in a PAN02 bilateral tumor model, and GN + OBP-702 showed significant anti-tumor effects and increased TRMs in OBP-702-uninjected tumors. Finally, in a neoadjuvant model, in which PAN02 cells were re-inoculated after resection of treated-PAN02 tumors, GN + OBP-702 provided long-term anti-tumor effects even after tumor resection. CONCLUSION: OBP-702 can be a long-term immunostimulant with sustained anti-tumor effects on immunologically cold pancreatic cancer.

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  • Fibroblast activation protein-targeted near-infrared photoimmunotherapy depletes immunosuppressive cancer-associated fibroblasts and remodels local tumor immunity. Reviewed International journal

    Masaaki Akai, Kazuhiro Noma, Takuya Kato, Seitaro Nishimura, Hijiri Matsumoto, Kento Kawasaki, Tomoyoshi Kunitomo, Teruki Kobayashi, Noriyuki Nishiwaki, Hajime Kashima, Satoru Kikuchi, Toshiaki Ohara, Hiroshi Tazawa, Peter L Choyke, Hisataka Kobayashi, Toshiyoshi Fujiwara

    British journal of cancer   2024.3

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    BACKGROUND: Cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TME) play a critical role in tumor immunosuppression. However, targeted depletion of CAFs is difficult due to their diverse cells of origin and the resulting lack of specific surface markers. Near-infrared photoimmunotherapy (NIR-PIT) is a novel cancer treatment that leads to rapid cell membrane damage. METHODS: In this study, we used anti-mouse fibroblast activation protein (FAP) antibody to target FAP+ CAFs (FAP-targeted NIR-PIT) and investigated whether this therapy could suppress tumor progression and improve tumor immunity. RESULTS: FAP-targeted NIR-PIT induced specific cell death in CAFs without damaging adjacent normal cells. Furthermore, FAP-targeted NIR-PIT treated mice showed significant tumor regression in the CAF-rich tumor model accompanied by an increase in CD8+ tumor infiltrating lymphocytes (TILs). Moreover, treated tumors showed increased levels of IFN-γ, TNF-α, and IL-2 in CD8+ TILs compared with non-treated tumors, suggesting enhanced antitumor immunity. CONCLUSIONS: Cancers with FAP-positive CAFs in their TME grow rapidly and FAP-targeted NIR-PIT not only suppresses their growth but improves tumor immunosuppression. Thus, FAP-targeted NIR-PIT is a potential therapeutic strategy for selectively targeting the TME of CAF+ tumors.

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  • Fluorescence-guided assessment of bone and soft-tissue sarcomas for predicting the efficacy of telomerase-specific oncolytic adenovirus. Reviewed International journal

    Koji Uotani, Hiroshi Tazawa, Joe Hasei, Tomohiro Fujiwara, Aki Yoshida, Yasuaki Yamakawa, Toshinori Omori, Kazuhisa Sugiu, Tadashi Komatsubara, Hiroya Kondo, Takuya Morita, Masahiro Kiyono, Suguru Yokoo, Toshiaki Hata, Toshiyuki Kunisada, Ken Takeda, Yasuo Urata, Toshiyoshi Fujiwara, Toshifumi Ozaki

    PloS one   19 ( 2 )   e0298292   2024

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    Bone and soft-tissue sarcomas are rare malignancies with histological diversity and tumor heterogeneity, leading to the lack of a common molecular target. Telomerase is a key enzyme for keeping the telomere length and human telomerase reverse transcriptase (hTERT) expression is often activated in most human cancers, including bone and soft-tissue sarcomas. For targeting of telomerase-positive tumor cells, we developed OBP-301, a telomerase-specific replication-competent oncolytic adenovirus, in which the hTERT promoter regulates adenoviral E1 gene for tumor-specific viral replication. In this study, we present the diagnostic potential of green fluorescent protein (GFP)-expressing oncolytic adenovirus OBP-401 for assessing virotherapy sensitivity using bone and soft-tissue sarcomas. OBP-401-mediated GFP expression was significantly associated with the therapeutic efficacy of OBP-401 in human bone and soft-tissue sarcomas. In the tumor specimens from 68 patients, malignant and intermediate tumors demonstrated significantly higher expression levels of coxsackie and adenovirus receptor (CAR) and hTERT than benign tumors. OBP-401-mediated GFP expression was significantly increased in malignant and intermediate tumors with high expression levels of CAR and hTERT between 24 and 48 h after infection. Our results suggest that the OBP-401-based GFP expression system is a useful tool for predicting the therapeutic efficacy of oncolytic virotherapy on bone and soft-tissue sarcomas.

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  • Intraperitoneal Administration of p53-armed Oncolytic Adenovirus Inhibits Peritoneal Metastasis of Diffuse-type Gastric Cancer Cells. Reviewed International journal

    Naoto Hori, Hiroshi Tazawa, Yuncheng Li, Tomohiro Okura, Satoru Kikuchi, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Anticancer research   43 ( 11 )   4809 - 4821   2023.11

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    BACKGROUND/AIM: Diffuse-type gastric cancer (GC) frequently exhibits peritoneal metastasis, leading to poor prognosis. However, efforts to develop antitumor strategies for preventing the peritoneal metastasis of GC have been unsuccessful. As diffuse-type GC cells often carry a genetic alteration in the tumor suppressor p53 gene, p53 restoration may be a potent strategy for preventing peritoneal metastasis of GC. In this study, we investigated the therapeutic potential of p53-expressing adenoviral vectors against peritoneal metastasis of diffuse-type GC cells. MATERIALS AND METHODS: Three diffuse-type human GC cell types with different p53 statuses (p53-wild type NUGC-4, p53-mutant type GCIY, and p53-null type KATOIII) were used to evaluate the therapeutic potential of p53 activation induced by the p53-expressing, replication-deficient adenovirus Ad-p53 and oncolytic adenovirus OBP-702. Viability, apoptosis, and autophagy of virus-treated GC cells were analyzed under normal and sphere-forming culture conditions using the XTT assay and western blot analysis. The in vivo antitumor effects of OBP-702 and Ad-p53 were assessed using xenograft tumor models involving peritoneal metastasis of NUGC-4 and GCIY cells. RESULTS: Under normal and sphere-forming culture conditions, OBP-702 induced a significantly greater antitumor effect in GC cells compared with Ad-p53 by strongly inducing p53-mediated apoptosis and autophagy and receptor tyrosine kinase suppression. In vivo experiments demonstrated that intraperitoneal administration of OBP-702 significantly suppressed the peritoneal metastasis of NUGC-4 and GCIY cells compared with Ad-p53, leading to prolonged survival of mice. CONCLUSION: Intraperitoneal administration of OBP-702 inhibits the peritoneal metastasis of GC cells by inducing p53-mediated cytopathic activity.

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  • 膵臓癌間質に対する腫瘍融解アデノウイルス製剤の治療効果 Invited Reviewed

    永井 康雄, 田澤 大, 菊地 覚次, 黒田 新士, 野間 和広, 浦田 泰生, 香川 俊輔, 藤原 俊義

    癌と化学療法   50 ( 10 )   1102 - 1103   2023.10

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  • Exosomes as a drug delivery tool for cancer therapy: a new era for existing drugs and oncolytic viruses. Invited Reviewed International journal

    Yoshihiko Kakiuchi, Shinji Kuroda, Nobuhiko Kanaya, Shunsuke Kagawa, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Expert opinion on therapeutic targets   1 - 10   2023.9

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    INTRODUCTION: Exosomes are cell-derived nanovesicles involved in cell-to-cell communications. These nanovesicles are generally considered to contain important carriers of information such as DNA and RNA, and show specific tropism. AREAS COVERED: The combination of existing therapeutic agents with exosomes enhances therapeutic effects by increasing uptake into the tumor. Induction of immunogenic cell death (ICD) may also be triggered more strongly than with the drug alone. Oncolytic viruses (OVs) are even more effective as a drug in combination with exosomes. Although OVs are more likely to cause immune activity, combination with exosomes can exert synergistic effects. OVs have potent anti-tumor effects, but many limitations, such as being limited to local administration and vulnerability to attack by antibodies. Incorporation into exosomes can overcome these limitations and may allow effects against distant tumors. EXPERT OPINION: Novel therapies using exosomes are very attractive in terms of enhancing therapeutic efficacy and reducing side effects. This approach also contains elements overcoming disadvantages in OVs, which have not been used clinically until now, and may usher in a new era of cancer treatments.

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  • PD-L1-expressing cancer-associated fibroblasts induce tumor immunosuppression and contribute to poor clinical outcome in esophageal cancer. Reviewed International journal

    Kento Kawasaki, Kazuhiro Noma, Takuya Kato, Toshiaki Ohara, Shunsuke Tanabe, Yasushige Takeda, Hijiri Matsumoto, Seitaro Nishimura, Tomoyoshi Kunitomo, Masaaki Akai, Teruki Kobayashi, Noriyuki Nishiwaki, Hajime Kashima, Naoaki Maeda, Satoru Kikuchi, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    Cancer immunology, immunotherapy : CII   72 ( 11 )   3787 - 3802   2023.9

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    The programmed cell death 1 protein (PD-1)/programmed cell death ligand 1 (PD-L1) axis plays a crucial role in tumor immunosuppression, while the cancer-associated fibroblasts (CAFs) have various tumor-promoting functions. To determine the advantage of immunotherapy, the relationship between the cancer cells and the CAFs was evaluated in terms of the PD-1/PD-L1 axis. Overall, 140 cases of esophageal cancer underwent an immunohistochemical analysis of the PD-L1 expression and its association with the expression of the α smooth muscle actin, fibroblast activation protein, CD8, and forkhead box P3 (FoxP3) positive cells. The relationship between the cancer cells and the CAFs was evaluated in vitro, and the effect of the anti-PD-L1 antibody was evaluated using a syngeneic mouse model. A survival analysis showed that the PD-L1+ CAF group had worse survival than the PD-L1- group. In vitro and in vivo, direct interaction between the cancer cells and the CAFs showed a mutually upregulated PD-L1 expression. In vivo, the anti-PD-L1 antibody increased the number of dead CAFs and cancer cells, resulting in increased CD8+ T cells and decreased FoxP3+ regulatory T cells. We demonstrated that the PD-L1-expressing CAFs lead to poor outcomes in patients with esophageal cancer. The cancer cells and the CAFs mutually enhanced the PD-L1 expression and induced tumor immunosuppression. Therefore, the PD-L1-expressing CAFs may be good targets for cancer therapy, inhibiting tumor progression and improving host tumor immunity.

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  • Dual antiplatelet therapy inhibits neutrophil extracellular traps to reduce liver micrometastases of intrahepatic cholangiocarcinoma. Reviewed International journal

    Masashi Yoshimoto, Shunsuke Kagawa, Hiroki Kajioka, Atsuki Taniguchi, Shinji Kuroda, Satoru Kikuchi, Yoshihiko Kakiuchi, Tomohiko Yagi, Shohei Nogi, Fuminori Teraishi, Kunitoshi Shigeyasu, Ryuichi Yoshida, Yuzo Umeda, Kazuhiro Noma, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Cancer letters   567   216260 - 216260   2023.7

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    The involvement of neutrophil extracellular traps (NETs) in cancer metastasis is being clarified, but the relationship between intrahepatic cholangiocarcinoma (iCCA) and NETs remains unclear. The presence of NETs was verified by multiple fluorescence staining in clinically resected specimens of iCCA. Human neutrophils were co-cultured with iCCA cells to observe NET induction and changes in cellular characteristics. Binding of platelets to iCCA cells and its mechanism were also examined, and their effects on NETs were analyzed in vitro and in in vivo mouse models. NETs were present in the tumor periphery of resected iCCAs. NETs promoted the motility and migration ability of iCCA cells in vitro. Although iCCA cells alone had a weak NET-inducing ability, the binding of platelets to iCCA cells via P-selectin promoted NET induction. Based on these results, antiplatelet drugs were applied to these cocultures in vitro and inhibited the binding of platelets to iCCA cells and the induction of NETs. Fluorescently labeled iCCA cells were injected into the spleen of mice, resulting in the formation of liver micrometastases coexisting with platelets and NETs. These mice were treated with dual antiplatelet therapy (DAPT) consisting of aspirin and ticagrelor, which dramatically reduced micrometastases. These results suggest that potent antiplatelet therapy prevents micrometastases of iCCA cells by inhibiting platelet activation and NET production, and it may contribute to a novel therapeutic strategy.

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  • Conventional Cancer Therapies Can Accelerate Malignant Potential of Cancer Cells by Activating Cancer-Associated Fibroblasts in Esophageal Cancer Models. Reviewed International journal

    Satoshi Komoto, Kazuhiro Noma, Takuya Kato, Teruki Kobayashi, Noriyuki Nishiwaki, Toru Narusaka, Hiroaki Sato, Yuki Katsura, Hajime Kashima, Satoru Kikuchi, Toshiaki Ohara, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Cancers   15 ( 11 )   2023.5

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    Esophageal cancer is one of the most aggressive tumors, and the outcome remains poor. One contributing factor is the presence of tumors that are less responsive or have increased malignancy when treated with conventional chemotherapy, radiotherapy, or a combination of these. Cancer-associated fibroblasts (CAFs) play an important role in the tumor microenvironment. Focusing on conventional cancer therapies, we investigated how CAFs acquire therapeutic resistance and how they affect tumor malignancy. In this study, low-dose chemotherapy or radiotherapy-induced normal fibroblasts showed enhanced activation of CAFs markers, fibroblast activation protein, and α-smooth muscle actin, indicating the acquisition of malignancy in fibroblasts. Furthermore, CAFs activated by radiotherapy induce phenotypic changes in cancer cells, increasing their proliferation, migration, and invasion abilities. In in vivo peritoneal dissemination models, the total number of tumor nodules in the abdominal cavity was significantly increased in the co-inoculation group of cancer cells and resistant fibroblasts compared to that in the co-inoculation group of cancer cells and normal fibroblasts. In conclusion, we demonstrated that conventional cancer therapy causes anti-therapeutic effects via the activation of fibroblasts, resulting in CAFs. It is important to select or combine modalities of esophageal cancer treatment, recognizing that inappropriate radiotherapy and chemotherapy can lead to resistance in CAF-rich tumors.

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  • 【mRNAワクチンやゲノム編集で注目が集まる遺伝子治療】遺伝子治療技術を用いた疾患治療 消化器がんに対する腫瘍融解ウイルス療法 Invited Reviewed

    藤原 俊義, 黒田 新士, 田澤 大

    医学のあゆみ   285 ( 5 )   446 - 452   2023.4

  • Overcoming cancer-associated fibroblast-induced immunosuppression by anti-interleukin-6 receptor antibody. Reviewed International journal

    Noriyuki Nishiwaki, Kazuhiro Noma, Toshiaki Ohara, Tomoyoshi Kunitomo, Kento Kawasaki, Masaaki Akai, Teruki Kobayashi, Toru Narusaka, Hajime Kashima, Hiroaki Sato, Satoshi Komoto, Takuya Kato, Naoaki Maeda, Satoru Kikuchi, Shunsuke Tanabe, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    Cancer immunology, immunotherapy : CII   2023.2

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    Cancer-associated fibroblasts (CAFs) are a critical component of the tumor microenvironment and play a central role in tumor progression. Previously, we reported that CAFs might induce tumor immunosuppression via interleukin-6 (IL-6) and promote tumor progression by blocking local IL-6 in the tumor microenvironment with neutralizing antibody. Here, we explore whether an anti-IL-6 receptor antibody could be used as systemic therapy to treat cancer, and further investigate the mechanisms by which IL-6 induces tumor immunosuppression. In clinical samples, IL-6 expression was significantly correlated with α-smooth muscle actin expression, and high IL-6 cases showed tumor immunosuppression. Multivariate analysis showed that IL-6 expression was an independent prognostic factor. In vitro, IL-6 contributed to cell proliferation and differentiation into CAFs. Moreover, IL-6 increased hypoxia-inducible factor 1α (HIF1α) expression and induced tumor immunosuppression by enhancing glucose uptake by cancer cells and competing for glucose with immune cells. MR16-1, a rodent analog of anti-IL-6 receptor antibody, overcame CAF-induced immunosuppression and suppressed tumor progression in immunocompetent murine cancer models by regulating HIF1α activation in vivo. The anti-IL-6 receptor antibody could be systemically employed to overcome tumor immunosuppression and improve patient survival with various cancers. Furthermore, the tumor immunosuppression was suggested to be induced by IL-6 via HIF1α activation.

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  • ADAR1 is a promising risk stratification biomarker of remnant liver recurrence after hepatic metastasectomy for colorectal cancer. Reviewed International journal

    Nanako Hata, Kunitoshi Shigeyasu, Yuzo Umeda, Shuya Yano, Sho Takeda, Kazuhiro Yoshida, Tomokazu Fuji, Ryuichi Yoshida, Kazuya Yasui, Hibiki Umeda, Toshiaki Takahashi, Yoshitaka Kondo, Hiroyuki Kishimoto, Yoshiko Mori, Fuminori Teraishi, Hideki Yamamoto, Hiroyuki Michiue, Keiichiro Nakamura, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Scientific reports   13 ( 1 )   2078 - 2078   2023.2

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    Adenosine-to-inosine RNA editing is a process mediated by adenosine deaminases that act on the RNA (ADAR) gene family. It has been discovered recently as an epigenetic modification dysregulated in human cancers. However, the clinical significance of RNA editing in patients with liver metastasis from colorectal cancer (CRC) remains unclear. The current study aimed to systematically and comprehensively investigate the significance of adenosine deaminase acting on RNA 1 (ADAR1) expression status in 83 liver metastatic tissue samples collected from 36 patients with CRC. The ADAR1 expression level was significantly elevated in liver metastatic tissue samples obtained from patients with right-sided, synchronous, or RAS mutant-type CRC. ADAR1-high liver metastasis was significantly correlated with remnant liver recurrence after hepatic metastasectomy. A high ADAR1 expression was a predictive factor of remnant liver recurrence (area under the curve = 0.72). Results showed that the ADAR1 expression level could be a clinically relevant predictive indicator of remnant liver recurrence. Patients with liver metastases who have a high ADAR1 expression requires adjuvant chemotherapy after hepatic metastasectomy.

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  • p53-armed oncolytic adenovirus induces autophagy and apoptosis in KRAS and BRAF-mutant colorectal cancer cells. Reviewed International journal

    Shuta Tamura, Hiroshi Tazawa, Naoto Hori, Yuncheng Li, Motohiko Yamada, Satoru Kikuchi, Shinji Kuroda, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    PloS one   18 ( 11 )   e0294491   2023

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    Colorectal cancer (CRC) cells harboring KRAS or BRAF mutations show a more-malignant phenotype than cells with wild-type KRAS and BRAF. KRAS/BRAF-wild-type CRCs are sensitive to epidermal growth factor receptor (EGFR)-targeting agents, whereas KRAS/BRAF-mutant CRCs are resistant due to constitutive activation of the EGFR-downstream KRAS/BRAF signaling pathway. Novel therapeutic strategies to treat KRAS/BRAF mutant CRC cells are thus needed. We recently demonstrated that the telomerase-specific replication-competent oncolytic adenoviruses OBP-301 and p53-armed OBP-702 exhibit therapeutic potential against KRAS-mutant human pancreatic cancer cells. In this study, we evaluated the therapeutic potential of OBP-301 and OBP-702 against human CRC cells with differing KRAS/BRAF status. Human CRC cells with wild-type KRAS/BRAF (SW48, Colo320DM, CACO-2), mutant KRAS (DLD-1, SW620, HCT116), and mutant BRAF (RKO, HT29, COLO205) were used in this study. The antitumor effect of OBP-301 and OBP-702 against CRC cells was analyzed using the XTT assay. Virus-mediated modulation of apoptosis, autophagy, and the EGFR-MEK-ERK and AKT-mTOR signaling pathways was analyzed by Western blotting. Wild-type and KRAS-mutant CRC cells were sensitive to OBP-301 and OBP-702, whereas BRAF-mutant CRC cells were sensitive to OBP-702 but resistant to OBP-301. Western blot analysis demonstrated that OBP-301 induced autophagy and that OBP-702 induced autophagy and apoptosis in human CRC cells. In BRAF-mutant CRC cells, OBP-301 and OBP-702 suppressed the expression of EGFR, MEK, ERK, and AKT proteins, whereas mTOR expression was suppressed only by OBP-702. Our results suggest that p53-armed oncolytic virotherapy is a viable therapeutic option for treating KRAS/BRAF-mutant CRC cells via induction of autophagy and apoptosis.

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  • RNA editing is a valuable biomarker for predicting carcinogenesis in ulcerative colitis. Reviewed International journal

    Kazutaka Takahashi, Kunitoshi Shigeyasu, Yoshitaka Kondo, Kazuyoshi Gotoh, Shuya Yano, Yuzo Umeda, Toshihiro Inokuchi, Caiming Xu, Kazuhiro Yoshida, Hibiki Umeda, Toshiaki Takahashi, Sho Takeda, Ryuichi Yoshida, Fuminori Teraishi, Hiroyuki Kishimoto, Yoshiko Mori, Kazuhiro Noma, Yoshinaga Okugawa, Sakiko Hiraoka, Hiroyuki Michiue, Hiroshi Tazawa, Osamu Matsushita, Ajay Goel, Toshiyoshi Fujiwara

    Journal of Crohn's & colitis   17 ( 5 )   754 - 766   2022.12

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    BACKGROUND AND AIMS: Ulcerative colitis (UC) can develop colitis-associated colorectal neoplasm (CAN). Adenine-to-inosine RNA editing, which is regulated by adenosine deaminase acting on RNA (ADAR), induces the posttranscriptional modification of critical oncogenes, including antizyme inhibitor 1 (AZIN1), leading to colorectal carcinogenesis. Therefore, we hypothesized that ADAR1 might be involved in the development of CAN in UC. METHODS: We systematically analyzed a cohort of 139 UC cases (40 acute phase, 73 remission phase, 26 CAN). The degree of inflammation was evaluated using the Mayo endoscopic score (MES). RESULTS: The type 1 IFN-related inflammation pathway was upregulated in the rectum of active UC, rectum of UC-CAN, and tumor site of UC-CAN patients. ADAR1 expression was upregulated in the entire colon of CAN cases, while it was down-regulated in non-CAN MES0 cases. ADAR1 expression in the rectum predicted the development of CAN better than p53 or β-catenin, with an area under the curve of 0.93. The high expression of ADAR1 and high AZIN1 RNA editing in UC was triggered by type 1 IFN stimulation from UC-specific microbiomes, such as Fusobacterium in vitro analyses. The induction of AZIN1 RNA editing by ADAR1, whose expression is promoted by Fusobacterium, may induce carcinogenesis in UC. CONCLUSIONS: The risk of CAN can be evaluated by assessing ADAR1 expression in the rectum of MES0 UC patients, freeing UC patients from unnecessary colonoscopy and reducing their physical burden. RNA editing may be involved in UC carcinogenesis, and may be used to facilitate the prevention and treatment of CAN in UC.

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  • An oncolytic virus as a promising candidate for the treatment of radioresistant oral squamous cell carcinoma. Reviewed International journal

    Shunsuke Gohara, Kosuke Shinohara, Ryoji Yoshida, Ryusho Kariya, Hiroshi Tazawa, Masashi Hashimoto, Junki Inoue, Ryuta Kubo, Hikaru Nakashima, Hidetaka Arita, Sho Kawaguchi, Keisuke Yamana, Yuka Nagao, Asuka Iwamoto, Junki Sakata, Yuichiro Matsuoka, Hisashi Takeshita, Masatoshi Hirayama, Kenta Kawahara, Masashi Nagata, Akiyuki Hirosue, Yoshikazu Kuwahara, Manabu Fukumoto, Seiji Okada, Yasuo Urata, Toshiyoshi Fujiwara, Hideki Nakayama

    Molecular therapy oncolytics   27   141 - 156   2022.12

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    We evaluated the usefulness of an oncolytic virus (Suratadenoturev; OBP-301) against radioresistant oral squamous cell carcinoma. We confirmed the expression of human telomerase reverse transcriptase and the coxsackievirus and adenovirus receptor in cell lines. Also, we examined the potential presence in a patient who has received existing therapy that is amenable to treatment with OBP-301. We evaluated: (1) the antitumor effects of OBP-301 alone and in combination with radiotherapy on radioresistant cell lines, (2) the molecular mechanism underlying the radiosensitizing effect and cell death increased by the combination therapy, and (3) the antitumor effect of the combination therapy in vivo using xenograft models (a radioresistant cell line-derived xenograft in mouse and a patient-derived xenograft). Human telomerase reverse transcriptase and the coxsackievirus and adenovirus receptor were expressed in all cell lines. OBP-301 decreased the proliferative activity of these cell lines in a concentration-dependent manner, and significantly enhanced the antitumor effect of irradiation. Phosphorylated STAT3 and its downstream molecules, which correlated with apoptosis and autophagy, showed significant changes in expression after treatment with OBP-301. The combination therapy exerted a significant antitumor effect versus radiotherapy alone in both xenograft models. Combination of OBP-301 with radiotherapy exerts a synergistic effect and may represent a promising treatment for radioresistant oral squamous cell carcinoma.

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  • Oncolytic virus-mediated p53 overexpression promotes immunogenic cell death and efficacy of PD-1 blockade in pancreatic cancer. Reviewed International journal

    Hiroyuki Araki, Hiroshi Tazawa, Nobuhiko Kanaya, Yoshinori Kajiwara, Motohiko Yamada, Masashi Hashimoto, Satoru Kikuchi, Shinji Kuroda, Ryuichi Yoshida, Yuzo Umeda, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Molecular therapy oncolytics   27   3 - 13   2022.12

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    Immune checkpoint inhibitors, including anti-programmed cell death 1 (PD-1) antibody, provide improved clinical outcome in certain cancers. However, pancreatic ductal adenocarcinoma (PDAC) is refractory to PD-1 blockade therapy due to poor immune response. Oncolytic virotherapy is a novel approach for inducing immunogenic cell death (ICD). We demonstrated the therapeutic potential of p53-expressing telomerase-specific oncolytic adenovirus OBP-702 to induce ICD and anti-tumor immune responses in human PDAC cells with different p53 status (Capan-2, PK-59, PK-45H, Capan-1, MIA PaCa-2, BxPC-3) and murine PDAC cells (PAN02). OBP-702 significantly enhanced ICD with secretion of extracellular adenosine triphosphate and high-mobility group box protein B1 by inducing p53-mediated apoptosis and autophagy. OBP-702 significantly promoted the tumor infiltration of CD8+ T cells and the anti-tumor efficacy of PD-1 blockade in a subcutaneous PAN02 syngeneic tumor model. Our results suggest that oncolytic adenovirus-mediated p53 overexpression augments ICD and the efficacy of PD-1 blockade therapy against cold PDAC tumors. Further in vivo experiments would be warranted to evaluate the survival benefit of tumor-bearing mice in combination therapy with OBP-702 and PD-1 blockade.

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  • Oncolytic virus-mediated reducing of myeloid-derived suppressor cells enhances the efficacy of PD-L1 blockade in gemcitabine-resistant pancreatic cancer. Reviewed International journal

    Yoshinori Kajiwara, Hiroshi Tazawa, Motohiko Yamada, Nobuhiko Kanaya, Takuro Fushimi, Satoru Kikuchi, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Ryuichi Yoshida, Yuzo Umeda, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Cancer immunology, immunotherapy : CII   72 ( 5 )   1285 - 1300   2022.11

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    Pancreatic ductal adenocarcinoma (PDAC) is often refractory to treatment with gemcitabine (GEM) and immune checkpoint inhibitors including anti-programmed cell death ligand 1 (PD-L1) antibody. However, the precise relationship between GEM-resistant PDAC and development of an immunosuppressive tumor microenvironment (TME) remains unclear. In this study, we investigated the immunosuppressive TME in parental and GEM-resistant PDAC tumors and assessed the therapeutic potential of combination therapy with the telomerase-specific replication-competent oncolytic adenovirus OBP-702, which induces tumor suppressor p53 protein and PD-L1 blockade against GEM-resistant PDAC tumors. Mouse PDAC cells (PAN02) and human PDAC cells (MIA PaCa-2, BxPC-3) were used to establish GEM-resistant PDAC lines. PD-L1 expression and the immunosuppressive TME were analyzed using parental and GEM-resistant PDAC cells. A cytokine array was used to investigate the underlying mechanism of immunosuppressive TME induction by GEM-resistant PAN02 cells. The GEM-resistant PAN02 tumor model was used to evaluate the antitumor effect of combination therapy with OBP-702 and PD-L1 blockade. GEM-resistant PDAC cells exhibited higher PD-L1 expression and produced higher granulocyte-macrophage colony-stimulating factor (GM-CSF) levels compared with parental cells, inducing an immunosuppressive TME and the accumulation of myeloid-derived suppressor cells (MDSCs). OBP-702 significantly inhibited GEM-resistant PAN02 tumor growth by suppressing GM-CSF-mediated MDSC accumulation. Moreover, combination treatment with OBP-702 significantly enhanced the antitumor efficacy of PD-L1 blockade against GEM-resistant PAN02 tumors. The present results suggest that combination therapy involving OBP-702 and PD-L1 blockade is a promising antitumor strategy for treating GEM-resistant PDAC with GM-CSF-induced immunosuppressive TME formation.

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  • Dual-targeted near-infrared photoimmunotherapy for esophageal cancer and cancer-associated fibroblasts in the tumor microenvironment. Reviewed International journal

    Hiroaki Sato, Kazuhiro Noma, Toshiaki Ohara, Kento Kawasaki, Masaaki Akai, Teruki Kobayashi, Noriyuki Nishiwaki, Toru Narusaka, Satoshi Komoto, Hajime Kashima, Yuki Katsura, Takuya Kato, Satoru Kikuchi, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Hisataka Kobayashi, Toshiyoshi Fujiwara

    Scientific reports   12 ( 1 )   20152 - 20152   2022.11

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    Cancer-associated fibroblasts (CAFs) play a significant role in tumor progression within the tumor microenvironment. Previously, we used near-infrared photoimmunotherapy (NIR-PIT), a next-generation cancer cell-targeted phototherapy, to establish CAF-targeted NIR-PIT. In this study, we investigated whether dual-targeted NIR-PIT, targeting cancer cells and CAFs, could be a therapeutic strategy. A total of 132 cases of esophageal cancer were analyzed for epidermal growth factor receptor (EGFR), human epidermal growth factor 2 (HER2), and fibroblast activation protein (FAP) expression using immunohistochemistry. Human esophageal cancer cells and CAFs were co-cultured and treated with single- or dual-targeted NIR-PIT in vitro. These cells were co-inoculated into BALB/c-nu/nu mice and the tumors were treated with single-targeted NIR-PIT or dual-targeted NIR-PIT in vivo. Survival analysis showed FAP- or EGFR-high patients had worse survival than patients with low expression of FAP or EGFR (log-rank, P < 0.001 and P = 0.074, respectively), while no difference was observed in HER2 status. In vitro, dual (EGFR/FAP)-targeted NIR-PIT induced specific therapeutic effects in cancer cells and CAFs along with suppressing tumor growth in vivo, whereas single-targeted NIR-PIT did not show any significance. Moreover, these experiments demonstrated that dual-targeted NIR-PIT could treat cancer cells and CAFs simultaneously with a single NIR light irradiation. We demonstrated the relationship between EGFR/FAP expression and prognosis of patients with esophageal cancer and the stronger therapeutic effect of dual-targeted NIR-PIT than single-targeted NIR-PIT in experimental models. Thus, dual-targeted NIR-PIT might be a promising therapeutic strategy for cancer treatment.

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  • OBP-702を用いたウイルス治療による膵癌の長期抗腫瘍免疫賦活効果 Invited Reviewed

    橋本 将志, 黒田 新士, 金谷 信彦, 垣内 慶彦, 菊地 覚次, 田澤 大, 香川 俊輔, 浦田 泰生, 藤原 俊義

    癌と化学療法   49 ( 10 )   1127 - 1129   2022.10

  • RNA editing facilitates the enhanced production of neoantigens during the simultaneous administration of oxaliplatin and radiotherapy in colorectal cancer. Reviewed International journal

    Yasuhiro Komatsu, Kunitoshi Shigeyasu, Shuya Yano, Sho Takeda, Kazutaka Takahashi, Nanako Hata, Hibiki Umeda, Kazuhiro Yoshida, Yoshiko Mori, Kazuya Yasui, Ryuichi Yoshida, Yoshitaka Kondo, Hiroyuki Kishimoto, Fuminori Teraishi, Yuzo Umeda, Shunsuke Kagawa, Hiroyuki Michiue, Hiroshi Tazawa, Ajay Goel, Toshiyoshi Fujiwara

    Scientific reports   12 ( 1 )   13540 - 13540   2022.8

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    Most cases of colorectal cancers (CRCs) are microsatellite stable (MSS), which frequently demonstrate lower response rates to immune checkpoint inhibitors (ICIs). RNA editing produces neoantigens by altering amino acid sequences. In this study, RNA editing was induced artificially by chemoradiation therapy (CRT) to generate neoantigens in MSS CRCs. Altogether, 543 CRC specimens were systematically analyzed, and the expression pattern of ADAR1 was investigated. In vitro and in vivo experiments were also performed. The RNA editing enzyme ADAR1 was upregulated in microsatellite instability-high CRCs, leading to their high affinity for ICIs. Although ADAR1 expression was low in MSS CRC, CRT including oxaliplatin (OX) treatment upregulated RNA editing levels by inducing ADAR1. Immunohistochemistry analyses showed the upregulation of ADAR1 in patients with CRC treated with CAPOX (capecitabine + OX) radiation therapy relative to ADAR1 expression in patients with CRC treated only by surgery (p < 0.001). Compared with other regimens, CRT with OX effectively induced RNA editing in MSS CRC cell lines (HT29 and Caco2, p < 0.001) via the induction of type 1 interferon-triggered ADAR1 expression. CRT with OX promoted the RNA editing of cyclin I, a neoantigen candidate. Neoantigens can be artificially induced by RNA editing via an OX-CRT regimen. CRT can promote proteomic diversity via RNA editing.

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  • Modulation of p53 expression in cancer-associated fibroblasts prevents peritoneal metastasis of gastric cancer. Reviewed International journal

    Toshihiro Ogawa, Satoru Kikuchi, Motoyasu Tabuchi, Ema Mitsui, Yuta Une, Hiroshi Tazawa, Shinji Kuroda, Kazuhiro Noma, Toshiaki Ohara, Shunsuke Kagawa, Yasuo Urata, Toshiyoshi Fujiwara

    Molecular therapy oncolytics   25   249 - 261   2022.6

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    Cancer-associated fibroblasts (CAFs) in the tumor microenvironment are associated with the establishment and progression of peritoneal metastasis. This study investigated the efficacy of replicative oncolytic adenovirus-mediated p53 gene therapy (OBP-702) against CAFs and peritoneal metastasis of gastric cancer (GC). Higher CAF expression in the primary tumor was associated with poor prognosis of GC, and higher CAF expression was also observed with peritoneal metastasis in immunohistochemical analysis of clinical samples. And, we found transcriptional alteration of p53 in CAFs relative to normal gastric fibroblasts (NGFs). CAFs increased the secretion of cancer-promoting cytokines, including interleukin-6, and gained resistance to chemotherapy relative to NGFs. OBP-702 showed cytotoxicity to both GC cells and CAFs but not to NGFs. Overexpression of wild-type p53 by OBP-702 infection caused apoptosis and autophagy of CAFs and decreased the secretion of cancer-promoting cytokines by CAFs. Combination therapy using intraperitoneal administration of OBP-702 and paclitaxel synergistically inhibited the tumor growth of peritoneal metastases and decreased CAFs in peritoneal metastases. OBP-702, a replicative oncolytic adenovirus-mediated p53 gene therapy, offers a promising biological therapeutic strategy for peritoneal metastasis, modulating CAFs in addition to achieving tumor lysis.

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  • Tumor-targeted fluorescence labeling systems for cancer diagnosis and treatment. Invited Reviewed International journal

    Hiroshi Tazawa, Kunitoshi Shigeyasu, Kazuhiro Noma, Shunsuke Kagawa, Fuminori Sakurai, Hiroyuki Mizuguchi, Hisataka Kobayashi, Takeshi Imamura, Toshiyoshi Fujiwara

    Cancer science   113 ( 6 )   1919 - 1929   2022.6

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    Conventional imaging techniques are available for clinical identification of tumor sites. However, detecting metastatic tumor cells that are spreading from primary tumor sites using conventional imaging techniques remains difficult. In contrast, fluorescence-based labeling systems are useful tools for detecting tumor cells at the single-cell level in cancer research. The ability to detect fluorescent-labeled tumor cells enables investigations of the biodistribution of tumor cells for the diagnosis and treatment of cancer. For example, the presence of fluorescent tumor cells in the peripheral blood of cancer patients is a predictive biomarker for early diagnosis of distant metastasis. The elimination of fluorescent tumor cells without damaging normal tissues is ideal for minimally invasive treatment of cancer. To capture fluorescent tumor cells within normal tissues, however, tumor-specific activated target molecules are needed. This review focuses on recent advances in tumor-targeted fluorescence labeling systems, in which indirect reporter labeling using tumor-specific promoters is applied to fluorescence labeling of tumor cells for the diagnosis and treatment of cancer. Telomerase promoter-dependent fluorescence labeling using replication-competent viral vectors produces fluorescent proteins that can be used to detect and eliminate telomerase-positive tumor cells. Tissue-specific promoter-dependent fluorescence labeling enables identification of specific tumor cells. Vimentin promoter-dependent fluorescence labeling is a useful tool for identifying tumor cells that undergo epithelial-mesenchymal transition (EMT). The evaluation of tumor cells undergoing EMT is important for accurately assessing metastatic potential. Thus, tumor-targeted fluorescence labeling systems represent novel platforms that enable the capture of tumor cells for the diagnosis and treatment of cancer.

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  • Regulatory T cells induce a suppressive immune milieu and promote lymph node metastasis in intrahepatic cholangiocarcinoma. Reviewed International journal

    Daisuke Konishi, Yuzo Umeda, Kazuhiro Yoshida, Kunitoshi Shigeyasu, Shuya Yano, Tomohiro Toji, Sho Takeda, Ryuichi Yoshida, Kazuya Yasui, Tomokazu Fuji, Kazuyuki Matsumoto, Hiroyuki Kishimoto, Hiroyuki Michiue, Fuminori Teraishi, Hironari Kato, Hiroshi Tazawa, Hiroyuki Yanai, Takahito Yagi, Ajay Goel, Toshiyoshi Fujiwara

    British journal of cancer   127 ( 4 )   757 - 765   2022.5

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    BACKGROUND: Emerging evidence indicates that immunogenicity plays an important role in intrahepatic cholangiocarcinoma (ICC). Herein, we systematically evaluated the clinical relevance of immunogenicity in ICC. METHODS: Highly immunogenic ICCs identified in the public dataset and the Cancer Immunome Atlas (TCIA) were assessed to determine the prognostic impact of immunogenicity in ICC and key components after curative resection. We also investigated the clinical relevance of the immune milieu in ICC. RESULTS: Using the Gene Expression Omnibus dataset 89749 and TCIA, we identified CD8+/forkhead box P3 (FoxP3)+ tumour-infiltrating lymphocytes (TILs), T-cell immunoglobulin and mucin domain 3 (TIM-3) and human leukocyte antigen-A (HLA-A) in highly immunogenic ICCs. Immunohistochemical analysis of the in-house cohort showed that intratumoral FoxP3+ TILs correlated with CD8+ TILs (P = 0.045, Fisher's exact test) and that high FoxP3+/CD8+ ratio (FCR) was an important marker for poor survival (P < 0.001, log-rank test). Furthermore, the FCR was higher in tumour-free lymph nodes in ICCs with lymph node metastases than in those without lymph node metastases (P = 0.003, Mann-Whitney U test). CONCLUSIONS: FCR should be considered an important biomarker that represents the immune environment of ICC based on its potentially important role in tumour progression, especially lymph node metastasis.

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  • Overexpression of Adenovirus E1A Reverses Transforming Growth Factor-β-induced Epithelial-mesenchymal Transition in Human Esophageal Cancer Cells. Reviewed

    Tomoya Masuda, Hiroshi Tazawa, Yuuri Hashimoto, Takeshi Ieda, Satoru Kikuchi, Shinji Kuroda, Kazuhiro Noma, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Acta medica Okayama   76 ( 2 )   203 - 215   2022.4

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    The epithelial-mesenchymal transition (EMT), a normal biological process by which epithelial cells acquire a mesenchymal phenotype, is associated with migration, metastasis, and chemoresistance in cancer cells, and with poor prognosis in patients with esophageal cancer. However, therapeutic strategies to inhibit EMT in tumor environments remain elusive. Here, we show the therapeutic potential of telomerase-specific replication- competent oncolytic adenovirus OBP-301 in human esophageal cancer TE4 and TE6 cells with an EMT phenotype. Transforming growth factor-β (TGF-β) administration induced the EMT phenotype with spindleshaped morphology, upregulation of mesenchymal markers and EMT transcription factors, migration, and chemoresistance in TE4 and TE6 cells. OBP-301 significantly inhibited the EMT phenotype via E1 accumulation. EMT cancer cells were susceptible to OBP-301 via massive autophagy induction. OBP-301 suppressed tumor growth and lymph node metastasis of TE4 cells co-inoculated with TGF-β-secreting fibroblasts. Our results suggest that OBP-301 inhibits the TGF-β-induced EMT phenotype in human esophageal cancer cells. OBP-301-mediated E1A overexpression is a promising antitumor strategy to inhibit EMT-mediated esophageal cancer progression.

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  • 【今知っておきたいゲノム医療と遺伝子治療-基礎から臨床まで】がんに対する腫瘍融解ウイルス療法 Invited Reviewed

    藤原 俊義, 谷本 光隆, 野田 卓男, 田澤 大

    小児内科   54 ( 2 )   361 - 364   2022.2

  • 《外科学再興特別企画》癌に対する免疫治療New Era がん微小環境内のマクロファージ、好中球を癌の治療標的として解析する Invited Reviewed

    香川 俊輔, 吉本 匡志, 伊藤 雅典, 梶岡 裕樹, 坂本 修一, 桑田 和也, 吉田 龍一, 野間 和広, 楳田 祐三, 菊地 覚次, 黒田 新士, 矢野 修也, 重安 邦俊, 寺石 文則, 田澤 大, 藤原 俊義

    日本外科学会雑誌   123 ( 1 )   80 - 82   2022.1

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  • Oncolytic virotherapy reverses chemoresistance in osteosarcoma by suppressing MDR1 expression. Reviewed International journal

    Kazuhisa Sugiu, Hiroshi Tazawa, Joe Hasei, Yasuaki Yamakawa, Toshinori Omori, Tadashi Komatsubara, Yusuke Mochizuki, Hiroya Kondo, Shuhei Osaki, Tomohiro Fujiwara, Aki Yoshida, Toshiyuki Kunisada, Koji Ueda, Yasuo Urata, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Cancer chemotherapy and pharmacology   88 ( 3 )   513 - 524   2021.9

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    BACKGROUND: Osteosarcoma (OS) is a malignant bone tumor primarily affecting children and adolescents. The prognosis of chemotherapy-refractory OS patients is poor. We developed a tumor suppressor p53-expressing oncolytic adenovirus (OBP-702) that exhibits antitumor effects against human OS cells. Here, we demonstrate the chemosensitizing effect of OBP-702 in human OS cells. MATERIALS AND METHODS: The in vitro and in vivo antitumor activities of doxorubicin (DOX) and OBP-702 were assessed using parental and DOX-resistant OS cells (U2OS, MNNG/HOS) and a DOX-resistant MNNG/HOS xenograft tumor model. RESULTS: DOX-resistant OS cells exhibited high multidrug resistant 1 (MDR1) expression, which was suppressed by OBP-702 or MDR1 siRNA, resulting in enhanced DOX-induced apoptosis. Compared to monotherapy, OBP-702 and DOX combination therapy significantly suppressed tumor growth in the DOX-resistant MNNG/HOS xenograft tumor model. CONCLUSION: Our results suggest that MDR1 is an attractive therapeutic target for chemoresistant OS. Tumor-specific virotherapy is thus a promising strategy for reversing chemoresistance in OS patients via suppression of MDR1 expression.

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  • CSF1/CSF1R Signaling Inhibitor Pexidartinib (PLX3397) Reprograms Tumor-Associated Macrophages and Stimulates T-cell Infiltration in the Sarcoma Microenvironment. Reviewed International coauthorship International journal

    Tomohiro Fujiwara, Mohamed A Yakoub, Andrew Chandler, Alexander B Christ, Guangli Yang, Ouathek Ouerfelli, Vinagolu K Rajasekhar, Aki Yoshida, Hiroya Kondo, Toshiaki Hata, Hiroshi Tazawa, Yildirim Dogan, Malcolm A S Moore, Toshiyoshi Fujiwara, Toshifumi Ozaki, Ed Purdue, John H Healey

    Molecular cancer therapeutics   20 ( 8 )   1388 - 1399   2021.8

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    Colony-stimulating factor 1 (CSF1) is a primary regulator of the survival, proliferation, and differentiation of monocyte/macrophage that sustains the protumorigenic functions of tumor-associated macrophages (TAMs). Considering current advances in understanding the role of the inflammatory tumor microenvironment, targeting the components of the sarcoma microenvironment, such as TAMs, is a viable strategy. Here, we investigated the effect of PLX3397 (pexidartinib) as a potent inhibitor of the CSF1 receptor (CSF1R). PLX3397 was recently approved by the Food and Drug Administration (FDA) to treat tenosynovial giant cell tumor and reprogram TAMs whose infiltration correlates with unfavorable prognosis of sarcomas. First, we confirmed by cytokine arrays of tumor-conditioned media (TCM) that cytokines including CSF1 are secreted from LM8 osteosarcoma cells and NFSa fibrosarcoma cells. The TCM, like CSF1, stimulated ERK1/2 phosphorylation in bone marrow-derived macrophages (BMDMs), polarized BMDMs toward an M2 (TAM-like) phenotype, and strikingly promoted BMDM chemotaxis. In vitro administration of PLX3397 suppressed pERK1/2 stimulation by CSF1 or TCM, and reduced M2 polarization, survival, and chemotaxis in BMDMs. Systemic administration of PLX3397 to the osteosarcoma orthotopic xenograft model significantly suppressed the primary tumor growth and lung metastasis, and thus improved metastasis-free survival. PLX3397 treatment concurrently depleted TAMs and FOXP3+ regulatory T cells and, surprisingly, enhanced infiltration of CD8+ T cells into the microenvironments of both primary and metastatic osteosarcoma sites. Our preclinical results show that PLX3397 has strong macrophage- and T-cell-modulating effects that may translate into cancer immunotherapy for bone and soft-tissue sarcomas.

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  • Phase I dose-escalation study of endoscopic intratumoral injection of OBP-301 (Telomelysin) with radiotherapy in oesophageal cancer patients unfit for standard treatments. Reviewed International journal

    Yasuhiro Shirakawa, Hiroshi Tazawa, Shunsuke Tanabe, Nobuhiko Kanaya, Kazuhiro Noma, Takeshi Koujima, Hajime Kashima, Takuya Kato, Shinji Kuroda, Satoru Kikuchi, Shunsuke Kagawa, Kuniaki Katsui, Susumu Kanazawa, Yasuo Urata, Toshiyoshi Fujiwara

    European journal of cancer (Oxford, England : 1990)   153   98 - 108   2021.8

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    PURPOSE: OBP-301 (Telomelysin) is an attenuated type-5 adenovirus that contains the human telomerase reverse transcriptase promoter to regulate viral replication. OBP-301 sensitises human cancer cells to ionising radiation by inhibiting DNA repair, and radiation enhances coxsackievirus and adenovirus receptor-mediated OBP-301 infection on the contrary. We assessed OBP-301 with radiotherapy in oesophageal cancer patients unfit for standard chemoradiation treatments. METHODS: A phase I dose-escalation study of OBP-301 with radiotherapy was conducted in 13 histologically confirmed oesophageal cancer patients deemed unfit to undergo surgery or chemotherapy. Study treatment consisted of OBP-301 administration by intratumoural needle injection using a flexible endoscope on days 1, 18 and 32. Radiotherapy was administered concurrently over 6 weeks, beginning on day 4, to a total of 60 Gy. RESULTS: Of the 13 patients, 7, 3 and 3 patients were treated with 1010, 1011 and 1012 virus particles, respectively. Study group comprised 10 males and 3 females, with a median age of 82 years (range, 53-91 years). All patients developed a transient, self-limited lymphopenia. Distribution studies revealed transient virus shedding in the plasma. Eight patients had local complete response (CR); all of them exhibited no pathologically viable malignant cells in biopsy specimens, and 3 patients had a partial response. The objective response rate was 91.7%. The clinical CR rate was 83.3% in stage I and 60.0% in stage II/III. Histopathological examination revealed massive infiltration of CD8+ cells and increased PD-L1 expression. CONCLUSION: Multiple courses of endoscopic intratumoural OBP-301 injection with radiotherapy are feasible and provide clinical benefits in patients with oesophageal cancer unfit for standard treatments.

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  • 【分子標的治療の最前線】ウイルスによるがん治療 食道がんに対するウイルス療法の現状と今後の展望 Invited Reviewed

    藤原 俊義, 田澤 大, 田辺 俊介, 白川 靖博

    腫瘍内科   28 ( 2 )   179 - 184   2021.8

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  • Immuno-hyperthermia effected by antibody-conjugated nanoparticles selectively targets and eradicates individual cancer cells. Reviewed International coauthorship International journal

    Tetsuya Kagawa, Yuki Matsumi, Hiromichi Aono, Toshiaki Ohara, Hiroshi Tazawa, Kunitoshi Shigeyasu, Shuya Yano, Sho Takeda, Yasuhiro Komatsu, Robert M Hoffman, Toshiyoshi Fujiwara, Hiroyuki Kishimoto

    Cell cycle (Georgetown, Tex.)   20 ( 13 )   1 - 11   2021.6

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    Hyperthermia has been used for cancer therapy for along period of time, but has shown limited clinical efficacy. Induction-heating hyperthermia using the combination of magnetic nanoparticles (MNPs) and an alternating magnetic field (AMF), termed magnetic hyperthermia (MHT), has previously shown efficacy in an orthotopic mouse model of disseminated gastric cancer. In the present study, superparamagnetic iron oxide nanoparticles (SPIONs), atype of MNP, were conjugated with an anti-HER2 antibody, trastuzumab and termed anti-HER2-antibody-linked SPION nanoparticles (anti-HER2 SPIONs). Anti-HER2 SPIONs selectively targeted HER2-expressing cancer cells co-cultured along with normal fibroblasts and HER2-negative cancer cells and caused apoptosis only in the HER2-expressing individual cancer cells. The results of the present study show proof-of-concept of anovel hyperthermia technology, immuno-MHT for selective cancer therapy, that targets individual cancer cells.AbbreviationsAMF:alternating magnetic fieldDDW:double distilled waterDMEM:Dulbecco's Modified Eagle's Mediumf:frequencyFBS:fetal bovine serumFITC:Fluorescein isothiocyanateGFP:green fluorescent proteinH:amplitudeHsp:heat shock proteinMHT:magnetic hyperthermiaMNPs:magnetic nanoparticlesPI:propidium iodideRFP:red fluorescent proteinSPION:superparamagnetic iron oxide (Fe3O4) nanoparticle.

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  • Hyperthermia generated by magnetic nanoparticles for effective treatment of disseminated peritoneal cancer in an orthotopic nude-mouse model. Reviewed International coauthorship International journal

    Yuki Matsumi, Tetsuya Kagawa, Shuya Yano, Hiroshi Tazawa, Kunitoshi Shigeyasu, Sho Takeda, Toshiaki Ohara, Hiromichi Aono, Robert M Hoffman, Toshiyoshi Fujiwara, Hiroyuki Kishimoto

    Cell cycle (Georgetown, Tex.)   20 ( 12 )   1 - 12   2021.6

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    Magnetic hyperthermia (MHT), which combines magnetic nanoparticles (MNPs) with an alternating magnetic field (AMF), holds promise as a cancer therapy. There have been many studies about hyperthermia, most of which have been performed by direct injection of MNPs into tumor tissues. However, there have been no reports of treating peritoneal disseminated disease with MHT to date. In the present study, we treated peritoneal metastasis of gastric cancer with MHT using superparamagnetic iron oxide (Fe3O4) nanoparticle (SPION) coated with carboxydextran as an MNP, in an orthotopic mouse model mimicking early peritoneal disseminated disease of gastric cancer. SPIONs of an optimal size were intraperitoneally administered, and an AMF (390 kHz, 28 kAm-1) was applied for 10 minutes, four times every three days. Three weeks after the first MHT treatment, the peritoneal metastases were significantly inhibited compared with the AMF-alone group or the untreated-control group. The results of the present study show that MHT can be applied as a new treatment option for disseminated peritoneal gastric cancer.Abbreviations: AMF: alternating magnetic field; Cy1: cytology-positive; DMEM: Dulbecco's Modified Eagle's Medium; FBS: fetal bovine serum; H&E: hematoxylin and eosin; HIPEC: hyperthermic intraperitoneal chemotherapy; MEM: Minimum Essential Medium; MHT: magnetic hyperthermia; MNPs: magnetic nanoparticles; P0: macroscopic peritoneal dissemination; RFP: red fluorescent protein; SPION: superparamagnetic iron oxide (Fe3O4) nanoparticle.

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  • Local oncolytic adenovirotherapy produces an abscopal effect via tumor-derived extracellular vesicles. Reviewed International journal

    Yoshihiko Kakiuchi, Shinji Kuroda, Nobuhiko Kanaya, Kento Kumon, Tomoko Tsumura, Masashi Hashimoto, Chiaki Yagi, Ryoma Sugimoto, Yuki Hamada, Satoru Kikuchi, Masahiko Nishizaki, Shunsuke Kagawa, Hiroshi Tazawa, Yasuo Urata, Toshiyoshi Fujiwara

    Molecular therapy   29 ( 10 )   2920 - 2930   2021.5

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    Extracellular vesicles (EVs) play important roles in various intercellular communication processes. The abscopal effect is an interesting phenomenon in cancer treatment, in which immune activation is generally considered a main factor. We previously developed a telomerase-specific oncolytic adenovirus, Telomelysin (OBP-301), and occasionally observed therapeutic effects on distal tumors after local treatment in immunodeficient mice. Here, we hypothesized that EVs may be involved in the abscopal effect of OBP-301. EVs isolated from the supernatant of HCT116 human colon carcinoma cells treated with OBP-301 were confirmed to contain OBP-301, and showed cytotoxic activity (apoptosis and autophagy) similar to OBP-301. In bilateral subcutaneous HCT116 and CT26 tumor models, intratumoral administration of OBP-301 produced potent antitumor effects on tumors that were not directly treated with OBP-301, involving direct mediation by tumor-derived EVs containing OBP-301. This indicates that immune activation is not the main factor in this abscopal effect. Moreover, tumor-derived EVs exhibited high tumor tropism in orthotopic HCT116 rectal tumors, in which adenovirus E1A and adenovirus type 5 proteins were observed in metastatic liver tumors after localized rectal tumor treatment. In conclusion, local treatment with OBP-301 has the potential to produce abscopal effects via tumor-derived EVs.

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  • Oncolytic virotherapy promotes radiosensitivity in soft tissue sarcoma by suppressing anti-apoptotic MCL1 expression. Reviewed International journal

    Toshinori Omori, Hiroshi Tazawa, Yasuaki Yamakawa, Shuhei Osaki, Joe Hasei, Kazuhisa Sugiu, Tadashi Komatsubara, Tomohiro Fujiwara, Aki Yoshida, Toshiyuki Kunisada, Yasuo Urata, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    PloS one   16 ( 4 )   e0250643   2021.4

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    Soft tissue sarcoma (STS) is a rare cancer that develops from soft tissues in any part of the body. Despite major advances in the treatment of STS, patients are often refractory to conventional radiotherapy, leading to poor prognosis. Enhancement of sensitivity to radiotherapy would therefore improve the clinical outcome of STS patients. We previously revealed that the tumor-specific, replication-competent oncolytic adenovirus OBP-301 kills human sarcoma cells. In this study, we investigated the radiosensitizing effect of OBP-301 in human STS cells. The in vitro antitumor effect of OBP-301 and ionizing radiation in monotherapy or combination therapy was assessed using highly radiosensitive (RD-ES and SK-ES-1) and moderately radiosensitive (HT1080 and NMS-2) STS cell lines. The expression of markers for apoptosis and DNA damage were evaluated in STS cells after treatment. The therapeutic potential of combination therapy was further analyzed using SK-ES-1 and HT1080 cells in subcutaneous xenograft tumor models. The combination of OBP-301 and ionizing radiation showed a synergistic antitumor effect in all human STS cell lines tested, including those that show different radiosensitivity. OBP-301 was found to enhance irradiation-induced apoptosis and DNA damage via suppression of anti-apoptotic myeloid cell leukemia 1 (MCL1), which was expressed at higher levels in moderately radiosensitive cell lines. The combination of OBP-301 and ionizing radiation showed a more profound antitumor effect compared to monotherapy in SK-ES-1 (highly radiosensitive) and HT1080 (moderately radiosensitive) subcutaneous xenograft tumors. OBP-301 is a promising antitumor reagent to improve the therapeutic potential of radiotherapy by increasing radiation-induced apoptosis in STS.

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  • Nanog is a promising chemo-resistant stemness marker and therapeutic target by iron chelators for esophageal cancer. Reviewed International journal

    Toru Narusaka, Toshiaki Ohara, Kazuhiro Noma, Noriyuki Nishiwaki, Yuki Katsura, Takuya Kato, Hiroaki Sato, Yasuko Tomono, Satoru Kikuchi, Hiroshi Tazawa, Yasuhiro Shirakawa, Akihiro Matsukawa, Toshiyoshi Fujiwara

    International journal of cancer   149 ( 2 )   347 - 357   2021.3

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    Esophageal cancer is a disease showing poor prognosis. Although combination chemotherapy using cisplatin and 5-fluorouracil is standard for unresectable esophageal cancer, the response rate is 35%. Cancer stem cells (CSCs) and inflammation are reportedly responsible for the poor prognosis of esophageal cancer. However, comprehensive analyses have not been conducted and proposals for progress remain lacking. Iron is known to be a key factor in the stemness of CSCs. This study focused on the therapeutic potential of iron control using iron chelators for CSCs in esophageal cancer. Among 134 immunohistochemically analyzed cases, Nanog expression was high in 98 cases and low in 36 cases. High Nanog expression correlated with low overall and disease-free survivals. The iron chelators deferasirox (DFX) and SP10 suppressed the proliferation and expression of stemness markers in TE8 and OE33 cells. DFX and SP10 did not induce compensatory interleukin (IL)-6 secretion, although cisplatin did result in high induction. Moreover, BBI608 and SSZ, as other CSC-targeting drugs, could not suppress the expression of stemness markers. Together, Nanog expression appears related to poor prognosis in esophageal cancer patients, and inhibition of stemness and compensatory IL-6 secretion by iron chelators may offer a novel therapeutic strategy for esophageal cancer.

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  • Role of Tumor-Associated Macrophages in Sarcomas. Invited Reviewed International coauthorship International journal

    Tomohiro Fujiwara, John Healey, Koichi Ogura, Aki Yoshida, Hiroya Kondo, Toshiaki Hata, Miho Kure, Hiroshi Tazawa, Eiji Nakata, Toshiyuki Kunisada, Toshiyoshi Fujiwara, Toshifumi Ozaki

    Cancers   13 ( 5 )   1086   2021.3

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    Sarcomas are complex tissues in which sarcoma cells maintain intricate interactions with their tumor microenvironment. Tumor-associated macrophages (TAMs) are a major component of tumor-infiltrating immune cells in the tumor microenvironment and have a dominant role as orchestrators of tumor-related inflammation. TAMs promote tumor growth and metastasis, stimulate angiogenesis, mediate immune suppression, and limit the antitumor activity of conventional chemotherapy and radiotherapy. Evidence suggests that the increased infiltration of TAMs and elevated expression of macrophage-related genes are associated with poor prognoses in most solid tumors, whereas evidence of this in sarcomas is limited. Based on these findings, TAM-targeted therapeutic strategies, such as inhibition of CSF-1/CSF-1R, CCL2/CCR2, and CD47/SIRPα, have been developed and are currently being evaluated in clinical trials. While most of the therapeutic challenges that target sarcoma cells have been unsuccessful and the prognosis of sarcomas has plateaued since the 1990s, several clinical trials of these strategies have yielded promising results and warrant further investigation to determine their translational benefit in sarcoma patients. This review summarizes the roles of TAMs in sarcomas and provides a rationale and update of TAM-targeted therapy as a novel treatment approach for sarcomas.

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  • Targeting neutrophil extracellular traps with thrombomodulin prevents pancreatic cancer metastasis. Reviewed International journal

    Hiroki Kajioka, Shunsuke Kagawa, Atene Ito, Masashi Yoshimoto, Shuichi Sakamoto, Satoru Kikuchi, Shinji Kuroda, Ryuichi Yoshida, Yuzo Umeda, Kazuhiro Noma, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Cancer letters   497   1 - 13   2021.1

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    Surgery is the only curative treatment option for pancreatic cancer, but patients often develop postoperative recurrence. Surgical invasiveness might be involved in the mechanism of recurrence. The associations among inflammation caused by surgery, neutrophils, and cancer metastasis were investigated. At first, neutrophil extracellular traps (NETs) were examined in clinical specimens, and NETs were observed around metastatic tumors. To explore how NETs were induced, neutrophils were cultured with pancreatic cancer or in cancer-conditioned medium. Neutrophils formed NETs when they were cultured with pancreatic cancer or even its conditioned medium. The effects of NETs on cancer cells were further investigated in vitro and in vivo. NETs induced the epithelial to mesenchymal transition in cancer cells and thereby promoted their migration and invasion. HMGB1 derived from NETs appeared to potentiate the malignancy of cancer cells. In a mouse model of liver metastasis with inflammation, NETs participated in the metastatic process by enhancing extravasation. Interestingly, thrombomodulin degraded HMGB1 and consequently inhibited the induction of NETs, thereby preventing pancreatic cancer metastasis to the liver. In conclusion, NETs interact reciprocally with pancreatic cancer cells, which play a pivotal role in inflammation-associated metastasis. Targeting NETs with thrombomodulin can be a novel strategy to improve the surgical outcome of pancreatic cancer patients.

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  • Extracellular vesicles shed from gastric cancer mediate protumor macrophage differentiation. Reviewed International journal

    Atene Ito, Shunsuke Kagawa, Shuichi Sakamoto, Kazuya Kuwada, Hiroki Kajioka, Masashi Yoshimoto, Satoru Kikuchi, Shinji Kuroda, Ryuichi Yoshida, Hiroshi Tazawa, Toshiyoshi Fujiwara

    BMC cancer   21 ( 1 )   102 - 102   2021.1

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    BACKGROUND: Peritoneal dissemination often develops in gastric cancer. Tumor-associated macrophages (TAMs) are present in the peritoneal cavity of gastric cancer patients with peritoneal dissemination, facilitating tumor progression. However, the mechanism by which macrophages differentiate into tumor-associated macrophages in the peritoneal cavity is not well understood. In this study, the interplay between gastric cancer-derived extracellular vesicles (EVs) and macrophages was investigated. METHODS: The association between macrophages and EVs in peritoneal ascitic fluid of gastric cancer patients, or from gastric cancer cell lines was examined, and their roles in differentiation of macrophages and potentiation of the malignancy of gastric cancer were further explored. RESULTS: Immunofluorescent assays of the ascitic fluid showed that M2 macrophages were predominant along with the cancer cells in the peritoneal cavity. EVs purified from gastric cancer cells, as well as malignant ascitic fluid, differentiated peripheral blood mononuclear cell-derived macrophages into the M2-like phenotype, which was demonstrated by their morphology and expression of CD163/206. The macrophages differentiated by gastric cancer-derived EVs promoted the migration ability of gastric cancer cells, and the EVs carried STAT3 protein. CONCLUSION: EVs derived from gastric cancer play a role by affecting macrophage phenotypes, suggesting that this may be a part of the underlying mechanism that forms the intraperitoneal cancer microenvironment.

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  • Fibroblast activation protein targeted near infrared photoimmunotherapy (NIR PIT) overcomes therapeutic resistance in human esophageal cancer. Reviewed International journal

    Ryoichi Katsube, Kazuhiro Noma, Toshiaki Ohara, Noriyuki Nishiwaki, Teruki Kobayashi, Satoshi Komoto, Hiroaki Sato, Hajime Kashima, Takuya Kato, Satoru Kikuchi, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Hisataka Kobayashi, Toshiyoshi Fujiwara

    Scientific reports   11 ( 1 )   1693 - 1693   2021.1

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    Cancer-associated fibroblasts (CAFs) have an important role in the tumor microenvironment. CAFs have the multifunctionality which strongly support cancer progression and the acquisition of therapeutic resistance by cancer cells. Near-infrared photoimmunotherapy (NIR-PIT) is a novel cancer treatment that uses a highly selective monoclonal antibody (mAb)-photosensitizer conjugate. We developed fibroblast activation protein (FAP)-targeted NIR-PIT, in which IR700 was conjugated to a FAP-specific antibody to target CAFs (CAFs-targeted NIR-PIT: CAFs-PIT). Thus, we hypothesized that the control of CAFs could overcome the resistance to conventional chemotherapy in esophageal cancer (EC). In this study, we evaluated whether EC cell acquisition of stronger malignant characteristics and refractoriness to chemoradiotherapy are mediated by CAFs. Next, we assessed whether the resistance could be rescued by eliminating CAF stimulation by CAFs-PIT in vitro and in vivo. Cancer cells acquired chemoradiotherapy resistance via CAF stimulation in vitro and 5-fluorouracil (FU) resistance in CAF-coinoculated tumor models in vivo. CAF stimulation promoted the migration/invasion of cancer cells and a stem-like phenotype in vitro, which were rescued by elimination of CAF stimulation. CAFs-PIT had a highly selective effect on CAFs in vitro. Finally, CAF elimination by CAFs-PIT in vivo demonstrated that the combination of 5-FU and NIR-PIT succeeded in producing 70.9% tumor reduction, while 5-FU alone achieved only 13.3% reduction, suggesting the recovery of 5-FU sensitivity in CAF-rich tumors. In conclusion, CAFs-PIT could overcome therapeutic resistance via CAF elimination. The combined use of novel targeted CAFs-PIT with conventional anticancer treatments can be expected to provide a more effective and sensible treatment strategy.

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  • Real-Time Fluorescence Image-Guided Oncolytic Virotherapy for Precise Cancer Treatment. Invited Reviewed International coauthorship International journal

    Shuya Yano, Hiroshi Tazawa, Hiroyuki Kishimoto, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M Hoffman

    International journal of molecular sciences   22 ( 2 )   879   2021.1

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    Oncolytic virotherapy is one of the most promising, emerging cancer therapeutics. We generated three types of telomerase-specific replication-competent oncolytic adenovirus: OBP-301; a green fluorescent protein (GFP)-expressing adenovirus, OBP-401; and Killer-Red-armed OBP-301. These oncolytic adenoviruses are driven by the human telomerase reverse transcriptase (hTERT) promoter; therefore, they conditionally replicate preferentially in cancer cells. Fluorescence imaging enables visualization of invasion and metastasis in vivo at the subcellular level; including molecular dynamics of cancer cells, resulting in greater precision therapy. In the present review, we focused on fluorescence imaging applications to develop precision targeting for oncolytic virotherapy. Cell-cycle imaging with the fluorescence ubiquitination cell cycle indicator (FUCCI) demonstrated that combination therapy of an oncolytic adenovirus and a cytotoxic agent could precisely target quiescent, chemoresistant cancer stem cells (CSCs) based on decoying the cancer cells to cycle to S-phase by viral treatment, thereby rendering them chemosensitive. Non-invasive fluorescence imaging demonstrated that complete tumor resection with a precise margin, preservation of function, and prevention of distant metastasis, was achieved with fluorescence-guided surgery (FGS) with a GFP-reporter adenovirus. A combination of fluorescence imaging and laser ablation using a KillerRed-protein reporter adenovirus resulted in effective photodynamic cancer therapy (PDT). Thus, imaging technology and the designer oncolytic adenoviruses may have clinical potential for precise cancer targeting by indicating the optimal time for administering therapeutic agents; accurate surgical guidance for complete resection of tumors; and precise targeted cancer-specific photosensitization.

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  • Telomerase-specific oncolytic immunotherapy for promoting efficacy of PD-1 blockade in osteosarcoma. Reviewed International journal

    Yusuke Mochizuki, Hiroshi Tazawa, Koji Demiya, Miho Kure, Hiroya Kondo, Tadashi Komatsubara, Kazuhisa Sugiu, Joe Hasei, Aki Yoshida, Toshiyuki Kunisada, Yasuo Urata, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Cancer immunology, immunotherapy   70 ( 5 )   1405 - 1417   2020.11

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    Immune checkpoint inhibitors including anti-programmed cell death 1 (PD-1) antibody have recently improved clinical outcome in certain cancer patients; however, osteosarcoma (OS) patients are refractory to PD-1 blockade. Oncolytic virotherapy has emerged as novel immunogenic therapy to augment antitumor immune response. We developed a telomerase-specific replication-competent oncolytic adenovirus OBP-502 that induces lytic cell death via binding to integrins. In this study, we assessed the combined effect of PD-1 blockade and OBP-502 in OS cells. The expression of coxsackie and adenovirus receptor (CAR), integrins αvβ3 and αvβ5, and programmed cell death ligand 1 (PD-L1) was analyzed in two murine OS cells (K7M2, NHOS). The cytopathic activity of OBP-502 in both cells was analyzed using the XTT assay. OBP-502-induced immunogenic cell death was assessed by analyzing the level of extracellular ATP and high-mobility group box protein B1 (HMGB1). Subcutaneous tumor models for K7M2 and NHOS cells were used to evaluate the antitumor effect and number of tumor-infiltrating CD8+ cells in combination therapy. K7M2 and NHOS cells showed high expression of integrins αvβ3 and αvβ5, but not CAR. OBP-502 significantly suppressed the viability of both cells, in which PD-L1 expression and the release of ATP and HMGB1 were significantly increased. Intratumoral injection of OBP-502 significantly augmented the efficacy of PD-1 blockade on subcutaneous K2M2 and NHOS tumor models via enhancement of tumor-infiltrating CD8+  T cells. Our results suggest that telomerase-specific oncolytic virotherapy is a promising antitumor strategy to promote the efficacy of PD-1 blockade in OS.

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  • Boosting Replication and Penetration of Oncolytic Adenovirus by Paclitaxel Eradicate Peritoneal Metastasis of Gastric Cancer. Reviewed International journal

    Wataru Ishikawa, Satoru Kikuchi, Toshihiro Ogawa, Motoyasu Tabuchi, Hiroshi Tazawa, Shinji Kuroda, Kazuhiro Noma, Masahiko Nishizaki, Shunsuke Kagawa, Yasuo Urata, Toshiyoshi Fujiwara

    Molecular therapy oncolytics   18   262 - 271   2020.9

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    Peritoneal metastasis is the most frequent form of distant metastasis and recurrence in gastric cancer, and the prognosis is extremely poor due to the resistance of systemic chemotherapy. Here, we demonstrate that intraperitoneal (i.p.) administration of a green fluorescence protein (GFP)-expressing attenuated adenovirus with oncolytic potency (OBP-401) synergistically suppressed the peritoneal metastasis of gastric cancer in combination with paclitaxel (PTX). OBP-401 synergistically suppressed the viability of human gastric cancer cells in combination with PTX. PTX enhanced the antitumor effect of OBP-401 due to enhanced viral replication in cancer cells. The combination therapy increased induction of mitotic catastrophe, resulting in accelerated autophagy and apoptosis. Peritoneally disseminated nodules were selectively visualized as GFP-positive spots by i.p. administration of OBP-401 in an orthotopic human gastric cancer peritoneal dissemination model. PTX enhanced the deep penetration of OBP-401 into the disseminated nodules. Moreover, a non-invasive in vivo imaging system demonstrated that the combination therapy of i.p. OBP-401 administration with PTX significantly inhibited growth of peritoneal metastatic tumors and the amount of malignant ascites. i.p. virotherapy with PTX may be a promising treatment strategy for the peritoneal metastasis of gastric cancer.

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  • Elimination of MYCN-Amplified Neuroblastoma Cells by Telomerase-Targeted Oncolytic Virus via MYCN Suppression. Reviewed International journal

    Terutaka Tanimoto, Hiroshi Tazawa, Takeshi Ieda, Hiroshi Nouso, Morimichi Tani, Takanori Oyama, Yasuo Urata, Shunsuke Kagawa, Takuo Noda, Toshiyoshi Fujiwara

    Molecular therapy oncolytics   18   14 - 23   2020.9

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    Neuroblastoma (NB) is a primary malignant tumor of the peripheral sympathetic nervous system. High-risk NB is characterized by MYCN amplification and human telomerase reverse transcriptase (hTERT) rearrangement, contributing to hTERT activation and a poor outcome. For targeting hTERT-activated tumors, we developed two oncolytic adenoviruses, OBP-301 and tumor suppressor p53-armed OBP-702, in which the hTERT promoter drives expression of the viral E1 gene for tumor-specific virus replication. In this study, we demonstrate the therapeutic potential of the hTERT-driven oncolytic adenoviruses OBP-301 and OBP-702 using four human MYCN-amplified NB cell lines (IMR-32, CHP-134, NB-1, LA-N-5) exhibiting high hTERT expression. OBP-301 and OBP-702 exhibited a strong antitumor effect in association with autophagy in NB cells. Virus-mediated activation of E2F1 protein suppressed MYCN expression. OBP-301 and OBP-702 significantly suppressed the growth of subcutaneous CHP-134 tumors. Thus, these hTERT-driven oncolytic adenoviruses are promising antitumor agents for eliminating MYCN-amplified NB cells via E2F1-mediated suppression of MYCN protein.

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  • FUCCI Real-Time Cell-Cycle Imaging as a Guide for Designing Improved Cancer Therapy: A Review of Innovative Strategies to Target Quiescent Chemo-Resistant Cancer Cells. Invited Reviewed International coauthorship International journal

    Shuya Yano, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M Hoffman

    Cancers   12 ( 9 )   2655   2020.9

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    Progress in chemotherapy of solid cancer has been tragically slow due, in large part, to the chemoresistance of quiescent cancer cells in tumors. The fluorescence ubiquitination cell-cycle indicator (FUCCI) was developed in 2008 by Miyawaki et al., which color-codes the phases of the cell cycle in real-time. FUCCI utilizes genes linked to different color fluorescent reporters that are only expressed in specific phases of the cell cycle and can, thereby, image the phases of the cell cycle in real-time. Intravital real-time FUCCI imaging within tumors has demonstrated that an established tumor comprises a majority of quiescent cancer cells and a minor population of cycling cancer cells located at the tumor surface or in proximity to tumor blood vessels. In contrast to most cycling cancer cells, quiescent cancer cells are resistant to cytotoxic chemotherapy, most of which target cells in S/G2/M phases. The quiescent cancer cells can re-enter the cell cycle after surviving treatment, which suggests the reason why most cytotoxic chemotherapy is often ineffective for solid cancers. Thus, quiescent cancer cells are a major impediment to effective cancer therapy. FUCCI imaging can be used to effectively target quiescent cancer cells within tumors. For example, we review how FUCCI imaging can help to identify cell-cycle-specific therapeutics that comprise decoy of quiescent cancer cells from G1 phase to cycling phases, trapping the cancer cells in S/G2 phase where cancer cells are mostly sensitive to cytotoxic chemotherapy and eradicating the cancer cells with cytotoxic chemotherapy most active against S/G2 phase cells. FUCCI can readily image cell-cycle dynamics at the single cell level in real-time in vitro and in vivo. Therefore, visualizing cell cycle dynamics within tumors with FUCCI can provide a guide for many strategies to improve cell-cycle targeting therapy for solid cancers.

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  • Oncolytic Virus-Mediated Targeting of the ERK Signaling Pathway Inhibits Invasive Propensity in Human Pancreatic Cancer. Reviewed International journal

    Takeshi Koujima, Hiroshi Tazawa, Takeshi Ieda, Hiroyuki Araki, Takuro Fushimi, Ryohei Shoji, Shinji Kuroda, Satoru Kikuchi, Ryuichi Yoshida, Yuzo Umeda, Fuminori Teraishi, Yasuo Urata, Hiroyuki Mizuguchi, Toshiyoshi Fujiwara

    Molecular therapy oncolytics   17   107 - 117   2020.6

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    Pancreatic ductal adenocarcinoma (PDAC) cells have an exceptional ability to invade nerves through pronounced crosstalk between nerves and cancer cells; however, the mechanism of PDAC cell invasion remains to be elucidated. Here, we demonstrate the therapeutic potential of telomerase-specific oncolytic adenoviruses, OBP-301 and tumor suppressor p53-armed OBP-702, against human PDAC cells. Highly invasive PDAC cells exhibited higher levels of phosphorylated extracellular signal-regulated kinases 1 and 2 (ERK1/2) expression independent of KRAS expression; ERK1/2 inhibitor or small interfering RNA (siRNA) treatment significantly reduced the migration and invasion of PDAC cells, suggesting that the ERK signaling pathway is associated with the invasiveness of PDAC cells. OBP-702 infection suppressed ERK signaling and inhibited PDAC cell migration and invasion more efficiently than OBP-301. OBP-702 also effectively inhibited PDAC cell invasion even when invasiveness was enhanced by administration of motility stimulators, such as nerve and neurosecretory factors. Moreover, noninvasive whole-body imaging analyses showed that OBP-702 significantly suppressed tumor growth in an orthotopic PDAC xenograft model, although both viruses were equally effective against subcutaneous tumors, suggesting that OBP-702 can influence the orthotopic tumor microenvironment. Our data suggest that oncolytic virus-mediated disruption of ERK signaling is a promising antitumor strategy for attenuating the invasiveness of PDAC cells.

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  • 骨肉腫に対する抗PD-1抗体の効果増強をめざした腫瘍融解ウイルス併用複合免疫療法の開発 Invited Reviewed

    望月 雄介, 田澤 大, 出宮 光二, 久禮 美穂, 長谷井 嬢, 中田 英二, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    整形外科   71 ( 7 )   786 - 786   2020.6

  • Immune Modulation by Telomerase-Specific Oncolytic Adenovirus Synergistically Enhances Antitumor Efficacy with Anti-PD1 Antibody. Reviewed International journal

    Nobuhiko Kanaya, Shinji Kuroda, Yoshihiko Kakiuchi, Kento Kumon, Tomoko Tsumura, Masashi Hashimoto, Toshiaki Morihiro, Tetsushi Kubota, Katsuyuki Aoyama, Satoru Kikuchi, Masahiko Nishizaki, Shunsuke Kagawa, Hiroshi Tazawa, Hiroyuki Mizuguchi, Yasuo Urata, Toshiyoshi Fujiwara

    Molecular therapy   28 ( 3 )   794 - 804   2020.3

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    The clinical benefit of monotherapy involving immune checkpoint inhibitors (ICIs) such as anti-programmed death-1 antibody (PD-1 Ab) is limited to small populations. We previously developed a telomerase-specific oncolytic adenovirus, Telomelysin (OBP-301), the safety of which was confirmed in a phase I clinical study. Here, we examined the potential of OBP-502, an OBP-301 variant, as an agent for inducing immunogenic cell death (ICD) and synergistically enhancing the efficacy of OBP-502 with PD-1 Ab using CT26 murine colon cancer and PAN02 murine pancreatic cancer cell lines. OBP-502 induced the release of ICD molecules such as adenosine triphosphate (ATP) and high-mobility group box protein 1 (HMGB1) from CT26 and PAN02 cells, leading to recruitment of CD8-positive lymphocytes and inhibition of Foxp3-positive lymphocyte infiltration into tumors. Combination therapy involving OBP-502 intratumoral administration and PD-1 Ab systemic administration significantly suppressed the growth of not only OBP-502-treated tumors but also tumors not treated with OBP-502 (so-called abscopal effect) in CT26 and PAN02 bilateral subcutaneous tumor models, in which active recruitment of CD8-positve lymphocytes was observed even in tumors not treated with OBP-502. This combined efficacy was similar to that observed in a CT26 rectal orthotopic tumor model involving liver metastases. In conclusion, telomerase-specific oncolytic adenoviruses are promising candidates for combined therapies with ICIs.

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  • Bone and Soft-Tissue Sarcoma: A New Target for Telomerase-Specific Oncolytic Virotherapy. Invited Reviewed International journal

    Hiroshi Tazawa, Joe Hasei, Shuya Yano, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Cancers   12 ( 2 )   478   2020.2

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    Adenovirus serotype 5 (Ad5) is widely and frequently used as a virus vector in cancer gene therapy and oncolytic virotherapy. Oncolytic virotherapy is a novel antitumor treatment for inducing lytic cell death in tumor cells without affecting normal cells. Based on the Ad5 genome, we have generated three types of telomerase-specific replication-competent oncolytic adenoviruses: OBP-301 (Telomelysin), green fluorescent protein (GFP)-expressing OBP-401 (TelomeScan), and tumor suppressor p53-armed OBP-702. These viruses drive the expression of the adenoviral E1A and E1B genes under the control of the hTERT (human telomerase reverse transcriptase-encoding gene) promoter, providing tumor-specific virus replication. This review focuses on the therapeutic potential of three hTERT promoter-driven oncolytic adenoviruses against bone and soft-tissue sarcoma cells with telomerase activity. OBP-301 induces the antitumor effect in monotherapy or combination therapy with chemotherapeutic drugs via induction of autophagy and apoptosis. OBP-401 enables visualization of sarcoma cells within normal tissues by serving as a tumor-specific labeling reagent for fluorescence-guided surgery via induction of GFP expression. OBP-702 exhibits a profound antitumor effect in OBP-301-resistant sarcoma cells via activation of the p53 signaling pathway. Taken together, telomerase-specific oncolytic adenoviruses are promising antitumor reagents that are expected to provide novel therapeutic options for the treatment of bone and soft-tissue sarcomas.

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  • Visualization of epithelial-mesenchymal transition in an inflammatory microenvironment-colorectal cancer network. Reviewed International journal

    Takeshi Ieda, Hiroshi Tazawa, Hiroki Okabayashi, Shuya Yano, Kunitoshi Shigeyasu, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Hiroyuki Kishimoto, Masahiko Nishizaki, Shunsuke Kagawa, Yasuhiro Shirakawa, Takashi Saitou, Takeshi Imamura, Toshiyoshi Fujiwara

    Scientific reports   9 ( 1 )   16378   2019.11

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    Epithelial-mesenchymal transition (EMT) is a biological process by which epithelial cells acquire mesenchymal characteristics. In malignant tumors, EMT is crucial for acquisition of a mesenchymal phenotype with invasive and metastatic properties, leading to tumor progression. An inflammatory microenvironment is thought to be responsible for the development and progression of colorectal cancer (CRC); however, the precise role of inflammatory microenvironments in EMT-related CRC progression remains unclear. Here, we show the spatiotemporal visualization of CRC cells undergoing EMT using a fluorescence-guided EMT imaging system in which the mesenchymal vimentin promoter drives red fluorescent protein (RFP) expression. An inflammatory microenvironment including TNF-α, IL-1β, and cytokine-secreting inflammatory macrophages induced RFP expression in association with the EMT phenotype in CRC cells. In vivo experiments further demonstrated the distribution of RFP-positive CRC cells in rectal and metastatic tumors. Our data suggest that the EMT imaging system described here is a powerful tool for monitoring EMT in inflammatory microenvironment-CRC networks.

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  • トランスレーショナルリサーチとしての外科治療を補完する新たな集学的治療の開発研究 Invited Reviewed

    田澤 大, 田辺俊介, 香川俊輔, 白川靖博, 藤原俊義

    日本外科学会雑誌   120 ( 6 )   735 - 737   2019.11

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  • Intraperitoneal cancer-immune microenvironment promotes peritoneal dissemination of gastric cancer Reviewed International journal

    Shuichi Sakamoto, Shunsuke Kagawa, Kazuya Kuwada, Atene Ito, Hiroki Kajioka, Yoshihiko Kakiuchi, Megumi Watanabe, Tetsuya Kagawa, Ryuichi Yoshida, Satoru Kikuchi, Shinji Kuroda, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Oncoimmunology   8 ( 12 )   e1671760   2019.10

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  • Fluorescence-guided cancer therapy Invited Reviewed

    Medical Science Digest   45 ( 7 )   427 - 429   2019.5

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  • PD-L1 expression combined with microsatellite instability/CD8+ tumor infiltrating lymphocytes as a useful prognostic biomarker in gastric cancer. Reviewed International journal

    Toshiaki Morihiro, Shinji Kuroda, Nobuhiko Kanaya, Yoshihiko Kakiuchi, Tetsushi Kubota, Katsuyuki Aoyama, Takehiro Tanaka, Satoru Kikuchi, Takeshi Nagasaka, Masahiko Nishizaki, Shunsuke Kagawa, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Scientific reports   9 ( 1 )   4633   2019.5

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    DOI: 10.1038/s41598-019-41177-2

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  • Activation of AZIN1 RNA editing is a novel mechanism that promotes invasive potential of cancer-associated fibroblasts in colorectal cancer. Reviewed International coauthorship International journal

    Sho Takeda, Kunitoshi Shigeyasu, Yoshinaga Okugawa, Kazuhiro Yoshida, Yoshiko Mori, Shuya Yano, Kazuhiro Noma, Yuzo Umeda, Yoshitaka Kondo, Hiroyuki Kishimoto, Fuminori Teraishi, Takeshi Nagasaka, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara, Ajay Goel

    Cancer letters   444   127 - 135   2019.3

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    Adenosine-to-inosine (A-to-I) RNA editing is a recently described epigenetic modification, which is believed to constitute a key oncogenic mechanism in human cancers. However, its functional role in cancer-associated fibroblasts (CAFs) within the tumor microenvironment (TME) and its clinical significance remains unclear. Herein, we systematically analyzed a large cohort of 627 colorectal cancer (CRC) specimens, and investigated the expression pattern of ADAR1 and its biological significance on the antizyme inhibitor 1 (AZIN1) RNA editing levels. Both ADAR1 expression and AZIN1 RNA editing levels were significantly elevated in CRC tissues vs. normal mucosa, and these findings correlated with the increased expression of mesenchymal markers, Vimentin (ρ = 0.44) and Fibroblast activation protein (ρ = 0.38). Intriguingly, ADAR1 expression was specifically upregulated in both cancer cells and fibroblasts from cancerous lesions. Conditioned medium from cancer cells led to induction of ADAR1 expression and activation of AZIN1 RNA editing in fibroblasts (p < 0.05). Additionally, edited AZIN1 enhanced the invasive potential of fibroblasts. In conclusion, we provide novel evidence that hyper-editing of AZIN1 enhances the invasive potential of CAFs within the TME in colon and is an important predictor of tumor invasiveness in CRC.

    DOI: 10.1016/j.canlet.2018.12.009

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  • Cancer-associated fibroblasts (CAFs) promote the lymph node metastasis of esophageal squamous cell carcinoma. Reviewed International journal

    Hajime Kashima, Kazuhiro Noma, Toshiaki Ohara, Takuya Kato, Yuki Katsura, Satoshi Komoto, Hiroaki Sato, Ryoichi Katsube, Takayuki Ninomiya, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    International journal of cancer   144 ( 4 )   828 - 840   2019.2

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    Lymph node metastasis is a pathognomonic feature of spreading tumors, and overcoming metastasis is a challenge in attaining more favorable clinical outcomes. Esophageal cancer is an aggressive tumor for which lymph node metastasis is a strong poor prognostic factor, and the tumor microenvironment (TME), and cancer-associated fibroblasts (CAFs) in particular, has been implicated in esophageal cancer progression. CAFs play a central role in the TME and have been reported to provide suitable conditions for the progression of esophageal cancer, similar to their role in other malignancies. However, little is known concerning the relevance of CAFs to the lymph node metastasis of esophageal cancer. Here, we used clinical samples of esophageal cancer to reveal that CAFs promote lymph node metastasis and subsequently verified the intercellular relationships in vitro and in vivo using an orthotopic metastatic mouse model. In the analysis of clinical samples, FAP+ CAFs were strongly associated with lymph node metastasis rather than with other prognostic factors. Furthermore, CAFs affected the ability of esophageal cancer cells to acquire metastatic phenotypes in vitro; this finding was confirmed by data from an in vivo orthotopic metastatic mouse model showing that the number of lymph node metastases increased upon injection of cocultured cancer cells and CAFs. In summary, we verified in vitro and in vivo that the accumulation of CAFs enhances the lymph node metastasis of ESCC. Our data suggest that CAF targeted therapy can reduce lymph node metastasis and improve the prognosis of patients with esophageal cancer in the future.

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  • A Novel Combination Cancer Therapy with Iron Chelator Targeting Cancer Stem Cells via Suppressing Stemness. Reviewed International journal

    Yuki Katsura, Toshiaki Ohara, Kazuhiro Noma, Takayuki Ninomiya, Hajime Kashima, Takuya Kato, Hiroaki Sato, Satoshi Komoto, Toru Narusaka, Yasuko Tomono, Boyi Xing, Yuehua Chen, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Tomonari Kasai, Masaharu Seno, Akihiro Matsukawa, Toshiyoshi Fujiwara

    Cancers   11 ( 2 )   177   2019.2

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    Excess iron causes cancer and is thought to be related to carcinogenesis and cancer progression including stemness, but the details remain unclear. Here, we hypothesized that stemness in cancer is related to iron metabolism and that regulating iron metabolism in cancer stem cells (CSCs) may be a novel therapy. In this study, we used murine induced pluripotent stem cells that expressed specific stem cell genes such as Nanog, Oct3/4, Sox2, Klf4, and c-Myc, and two human cancer cell lines with similar stem cell gene expression. Deferasirox, an orally available iron chelator, suppressed expression of stemness markers and spherogenesis of cells with high stemness status in vitro. Combination therapy had a marked antitumor effect compared with deferasirox or cisplatin alone. Iron metabolism appears important for maintenance of stemness in CSCs. An iron chelator combined with chemotherapy may be a novel approach via suppressing stemness for CSC targeted therapy.

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  • Photoimmunotherapy for cancer-associated fibroblasts targeting fibroblast activation protein in human esophageal squamous cell carcinoma. Reviewed International coauthorship International journal

    Shinichiro Watanabe, Kazuhiro Noma, Toshiaki Ohara, Hajime Kashima, Hiroaki Sato, Takuya Kato, Shinichi Urano, Ryoichi Katsube, Yuuri Hashimoto, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Hisataka Kobayashi, Toshiyoshi Fujiwara

    Cancer biology & therapy   20 ( 9 )   1234 - 1248   2019

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    Cancer-associated fibroblasts (CAFs) are strongly implicated in tumor progression, including in the processes of tumorigenesis, invasion, and metastasis. The targeting of CAFs using various therapeutic approaches is a novel treatment strategy; however, the efficacy of such therapies remains limited. Recently, near-infrared photoimmunotherapy (NIR-PIT), which is a novel targeted therapy employing a cell-specific mAb conjugated to a photosensitizer, has been introduced as a new type of phototherapy. In this study, we have developed a novel NIR-PIT technique to target CAFs, by focusing on fibroblast activation protein (FAP), and we evaluate the treatment efficacy in vitro and in vivo. Esophageal carcinoma cells exhibited enhanced activation of fibroblasts, with FAP over-expressed in the cytoplasm and on the cell surface. FAP-IR700-mediated PIT showed induced rapid cell death specifically for those cells in vitro and in vivo, without adverse effects. This novel therapy for CAFs, designed as local control phototherapy, was safe and showed a promising inhibitory effect on FAP+ CAFs. PIT targeting CAFs via the specific marker FAP may be a therapeutic option for CAFs in the tumor microenvironment in the future.

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  • The epithelial-to-mesenchymal transition induced by tumor-associated macrophages confers chemoresistance in peritoneally disseminated pancreatic cancer Reviewed International journal

    Kazuya Kuwada, Shunsuke Kagawa, Ryuichi Yoshida, Shuichi Sakamoto, Atene Ito, Megumi Watanabe, Takeshi Ieda, Shinji Kuroda, Satoru Kikuchi, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Journal of experimental & clinical cancer research   37 ( 1 )   307 - 307   2018.12

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    Background: The peritoneum is one of the most frequent metastatic sites in pancreatic cancer patients, and peritoneal dissemination makes this disease refractory due to aggressive progression and chemoresistance. Although the role of the tumor microenvironment in cancer development is recognized, the correlation between the peritoneal environment and refractoriness of peritoneal dissemination remains unclear. The intraperitoneal tumor-microenvironment and its potential role in the progression of peritoneal dissemination and chemo-refractoriness, focusing especially on macrophages, were investigated.
    Materials and methods: Peritoneal washes were obtained from pancreatic cancer patients, and cellular components were subjected to immunofluorescence assays. The effects of macrophages induced from monocytic THP-1 cells on pancreatic cancer cells were examined in co-culture conditions. The in vivo effects of macrophages on tumor growth and chemo-sensitivity were investigated by subcutaneously or intraperitoneally co-injecting cancer cells with macrophages into mice.
    Results: CD204-positive macrophages were present along with cancer cells in the peritoneal washes. In in vitro co-culture, tumor-associated macrophages affected pancreatic cancer cells, induced the epithelial-to-mesenchymal transition (EMT), and made them more resistant to chemotherapeutic agents. M2 macrophages promoted growth of both subcutaneous tumors and peritoneal dissemination in mice. Furthermore, co-inoculation of M2 macrophages conferred chemoresistance in the peritoneal dissemination mouse model, which significantly shortened their survival.
    Conclusion: Intraperitoneal tumor-associated macrophages potentially play an important role in promotion of peritoneal dissemination and chemoresistance of pancreatic cancer via EMT induction.

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  • Cancer-Associated Fibroblasts Affect Intratumoral CD8+ and FoxP3+ T Cells Via IL6 in the Tumor Microenvironment. Reviewed International journal

    Takuya Kato, Kazuhiro Noma, Toshiaki Ohara, Hajime Kashima, Yuki Katsura, Hiroaki Sato, Satoshi Komoto, Ryoichi Katsube, Takayuki Ninomiya, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    Clinical cancer research   24 ( 19 )   4820 - 4833   2018.10

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    DOI: 10.1158/1078-0432.CCR-18-0205

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  • Integrated fluorescent cytology with nano-biologics in peritoneally disseminated gastric cancer Reviewed International journal

    Megumi Watanabe, Shunsuke Kagawa, Kazuya Kuwada, Yuuri Hashimoto, Kunitoshi Shigeyasu, Michihiro Ishida, Shuichi Sakamoto, Atene Ito, Satoru Kikuchi, Shinji Kuroda, Hiroyuki Kishimoto, Shuta Tomida, Ryuichi Yoshida, Hiroshi Tazawa, Yasuo Urata, Toshiyoshi Fujiwara

    Cancer science   109 ( 10 )   3263 - 3271   2018.10

  • 癌関連線維芽細胞が及ぼす腫瘍免疫逃避の解明 Reviewed

    加藤 卓也, 野間 和広, 桂 佑貴, 佐藤 浩明, 河本 慧, 二宮 卓之, 大原 利章, 田澤 大, 香川 俊輔, 白川 靖博, 藤原 俊義

    癌と化学療法   45 ( 9 )   1279 - 1281   2018.9

  • HER2-targeted gold nanoparticles potentially overcome resistance to trastuzumab in gastric cancer Reviewed International journal

    Tetsushi Kubota, Shinji Kuroda, Nobuhiko Kanaya, Toshiaki Morihiro, Katsuyuki Aoyama, Yoshihiko Kakiuchi, Satoru Kikuchi, Masahiko Nishizaki, Shunsuke Kagawa, Hiroshi Tazawa, Toshiyoshi Fujiwara

    Nanomedicine : nanotechnology, biology, and medicine   14 ( 6 )   1919 - 1929   2018.8

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    An issue of concern is that no current HER2-targeted therapeutic agent is effective against Trastuzumab (Tmab)-resistant gastric cancer. Gold nanoparticles (AuNPs) are promising drug carriers with unique characteristics of a large surface area available for attachment of materials such as antibodies. Here, we created HER2-targeted AuNPs (T-AuNPs) and examined their therapeutic efficacy and cytotoxic mechanisms using HER2-postive Tmab-resistant (MKN7) or Tmab-sensitive (NCI-N87) gastric cancer cell lines. In vitro, T-AuNPs showed stronger cytotoxic effects than controls against MKN7 and NCI-N87 cells although Tmab had no effect on MKN7 cells. Autophagy played an important role in T-AuNP cytotoxic mechanisms, which was considered to be driven by internalization of T-AuNPs. Finally, T-AuNPs displayed potent antitumor effects against NCI-N87 and MKN7 subcutaneous tumors in in vivo mouse models. In conclusion, HER2-targeted AuNPs with conjugated Tmab is a promising strategy for the development of novel therapeutic agents to overcome Tmab resistance in gastric cancer.

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  • Clinical implementation of oncolytic virotherapy for pancreatic cancer Invited Reviewed

    Takeshi Koujima, Hiroshi Tazawa, Takashi Kuise, Ryuichi Yoshida, Yuzo Umeda, Toshiyoshi Fujiwara

    消化器外科   41 ( 6 )   931 - 938   2018.5

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  • Iron depletion is a novel therapeutic strategy to target cancer stem cells. Reviewed International journal

    Takayuki Ninomiya, Toshiaki Ohara, Kazuhiro Noma, Yuki Katsura, Ryoichi Katsube, Hajime Kashima, Takuya Kato, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Fumiaki Kimura, Ling Chen, Tomonari Kasai, Masaharu Seno, Akihiro Matsukawa, Toshiyoshi Fujiwara

    Oncotarget   8 ( 58 )   98405 - 98416   2017.11

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  • Therapeutic Cell-Cycle-Decoy Efficacy of a Telomerase-Dependent Adenovirus in an Orthotopic Model of Chemotherapy-Resistant Human Stomach Carcinomatosis Peritonitis Visualized With FUCCI Imaging Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroshi Tazawa, Hiroyuki Kishimoto, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M. Hoffman

    JOURNAL OF CELLULAR BIOCHEMISTRY   118 ( 11 )   3635 - 3642   2017.11

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  • Liposome-encapsulated plasmid DNA of telomerase-specific oncolytic adenovirus with stealth effect on the immune system Reviewed International journal

    Katsuyuki Aoyama, Shinji Kuroda, Toshiaki Morihiro, Nobuhiko Kanaya, Tetsushi Kubota, Yoshihiko Kakiuchi, Satoru Kikuchi, Masahiko Nishizaki, Shunsuke Kagawa, Hiroshi Tazawa, Toshiyoshi Fujiwara

    SCIENTIFIC REPORTS   7 ( 1 )   2017.10

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    DOI: 10.1038/s41598-017-14717-x

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  • Role of zoledronic acid in oncolytic virotherapy: Promotion of antitumor effect and prevention of bone destruction Reviewed

    Yasuaki Yamakawa, Hiroshi Tazawa, Joe Hasei, Shuhei Osaki, Toshinori Omori, Kazuhisa Sugiu, Tadashi Komatsubara, Kouji Uotani, Tomohiro Fujiwara, Aki Yoshida, Toshiyuki Kunisada, Yasuo Urata, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER SCIENCE   108 ( 9 )   1870 - 1880   2017.9

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  • Eradication of melanoma in vitro and in vivo via targeting with a Killer-Red-containing telomerase-dependent adenovirus Reviewed International coauthorship International journal

    Kiyoto Takehara, Shuya Yano, Hiroshi Tazawa, Hiroyuki Kishimoto, Nobuhiro Narii, Hiroyuki Mizuguchi, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M. Hoffman

    Cell Cycle   16 ( 16 )   1502 - 1508   2017.8

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  • Impact of Autophagy in Oncolytic Adenoviral Therapy for Cancer Invited Reviewed International journal

    Hiroshi Tazawa, Shinji Kuroda, Joe Hasei, Shunsuke Kagawa, Toshiyoshi Fujiwara

    International Journal of Molecular Sciences   18 ( 7 )   1479   2017.7

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  • GFP labeling kinetics of triple-negative human breast cancer by a killer-reporter adenovirus in 3D GelfoamA (R) histoculture Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Shinji Miwa, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    In Vitro Cellular & Developmental Biology-Animal   53 ( 6 )   479 - 482   2017.6

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  • High-metastatic triple-negative breast-cancer variants selected in vivo become chemoresistant in vitro Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    In Vitro Cellular & Developmental Biology-Animal   53 ( 4 )   285 - 287   2017.4

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  • Cell-cycle-dependent drug-resistant quiescent cancer cells induce tumor angiogenesis after chemotherapy as visualized by real-time FUCCI imaging Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroshi Tazawa, Hiroyuki Kishimoto, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M. Hoffman

    CELL CYCLE   16 ( 5 )   406 - 414   2017.3

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  • Oncolytic virotherapy for osteosarcoma Invited Reviewed

    Pharm stage   16 ( 12 )   54 - 59   2017.3

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  • Enhanced Metastatic Recurrence Via Lymphatic Trafficking of a High-Metastatic Variant of Human Triple-Negative Breast Cancer After Surgical Resection in Orthotopic Nude Mouse Models Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroshi Tazawa, Hiroyuki Kishimoto, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Journal of Cellular Biochemistry   118 ( 3 )   559 - 569   2017.3

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  • OBP-401-GFP telomerase-dependent adenovirus illuminates and kills high-metastatic more effectively than low-metastatic triple-negative breast cancer in vitro Reviewed International coauthorship International journal

    S. Yano, K. Takehara, H. Kishimoto, H. Tazawa, Y. Urata, S. Kagawa, M. Bouvet, T. Fujiwara, R. M. Hoffman

    Cancer Gene Therapy   24 ( 2 )   45 - 47   2017.2

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  • Comparison of in vitro invasiveness of high- and low-metastatic triple-negative human breast cancer visualized by color-coded imaging Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroshi Tazawa, Hiroyuki Kishimoto, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M. Hoffman

    In Vitro Cellular & Developmental Biology-Animal   53 ( 2 )   96 - 98   2017.2

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  • Comparison of Tumor Recurrence After Resection of Highly- and Poorly-Metastatic Triple-negative Breast Cancer in Orthotopic Nude-Mouse Models Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara, Michael Bouvet, Robert M. Hoffman

    Anticancer Research   37 ( 1 )   57 - 60   2017.1

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  • 食道がんに対する放射線併用ウイルス療法の臨床研究 Invited Reviewed

    藤原俊義, 田澤大, 田邊俊介, 香川俊輔, 白川靖博

    日本臨床   75 ( 5 )   746 - 751   2017

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  • HOZOT細胞を用いた腫瘍融解ウイルス製剤のDDS Invited Reviewed

    田澤 大, 大西哲平, 香川俊輔, 中村修治, 藤原俊義

    BIO INDUSTRY   34 ( 4 )   16 - 23   2017

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  • HER2陽性胃癌に対する新たな治療戦略 Reviewed

    金谷信彦, 黒田新士, 久保田哲史, 森廣俊昭, 菊地覚次, 西崎正彦, 田澤大, 香川俊輔, 藤原俊義

    癌と化学療法   44 ( 10 )   883 - 885   2017

  • Tumor-targeting adenovirus OBP-401 inhibits primary and metastatic tumor growth of triple-negative breast cancer in orthotopic nude-mouse models Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Oncotarget   7 ( 51 )   85273 - 85282   2016.12

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    DOI: 10.18632/oncotarget.13296

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  • In Vivo Selection of Intermediately- and Highly-Malignant Variants of Triple-negative Breast Cancer in Orthotopic Nude Mouse Models Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Anticancer Research   36 ( 12 )   6273 - 6277   2016.12

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  • Tumor-specific delivery of biologics by a novel T-cell line HOZOT Reviewed International journal

    Teppei Onishi, Hiroshi Tazawa, Yuuri Hashimoto, Makoto Takeuchi, Takeshi Otani, Shuji Nakamura, Fuminori Sakurai, Hiroyuki Mizuguchi, Hiroyuki Kishimoto, Yuzo Umeda, Yasuhiro Shirakawa, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Scientific Reports   6   38060   2016.11

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  • Fluorescence-guided surgery of a highly-metastatic variant of human triple-negative breast cancer targeted with a cancer-specific GFP adenovirus prevents recurrence Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Shinji Miwa, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Oncotarget   7 ( 46 )   75635 - 75647   2016.11

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    DOI: 10.18632/oncotarget.12314

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  • Iron depletion-induced downregulation of N-cadherin expression inhibits invasive malignant phenotypes in human esophageal cancer Reviewed International journal

    Seishi Nishitani, Kazuhiro Noma, Toshiaki Ohara, Yasuko Tomono, Shinichiro Watanabe, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    International Journal of Oncology   49 ( 4 )   1351 - 1359   2016.10

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    DOI: 10.3892/ijo.2016.3640

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  • 金ナノ粒子を用いた新規HER2標的抗体療法 Reviewed

    久保田 哲史, 黒田 新士, 森廣 俊昭, 田澤 大, 香川 俊輔, 藤原 俊義

    癌と化学療法   43 ( 10 )   1237 - 1239   2016.10

  • Efficacy of a Cell-Cycle Decoying Killer Adenovirus on 3-D Gelfoam (R)-Histoculture and Tumor-Sphere Models of Chemo-Resistant Stomach Carcinomatosis Visualized by FUCCI Imaging Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Hiroshi Tazawa, Hiroyuki Kishimoto, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M. Hoffman

    PLOS ONE   11 ( 9 )   e0162991   2016.9

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  • p53 replacement therapy for cancer Invited Reviewed International journal

    Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Recent Results in Cancer Research   209   1 - 15   2016.9

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    DOI: 10.1007/978-3-319-42934-2_1

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  • In Vivo Isolation of a Highly-aggressive Variant of Triple-negative Human Breast Cancer MDA-MB-231 Using Serial Orthotopic Transplantation Reviewed International coauthorship International journal

    Shuya Yano, Kiyoto Takehara, Shinji Miwa, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Anticancer Research   36 ( 8 )   3817 - 3820   2016.8

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  • Ablation of MCL1 expression by virally induced microRNA-29 reverses chemoresistance in human osteosarcomas Reviewed International journal

    Shuhei Osaki, Hiroshi Tazawa, Joe Hasei, Yasuaki Yamakawa, Toshinori Omori, Kazuhisa Sugiu, Tadashi Komatsubara, Tomohiro Fujiwara, Tsuyoshi Sasaki, Toshiyuki Kunisada, Aki Yoshida, Yasuo Urata, Shunsuke Kagawa, Toshifumi Ozaki, Toshiyoshi Fujiwara

    SCIENTIFIC REPORTS   6   28953   2016.6

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    DOI: 10.1038/srep28953

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  • Iron depletion enhances the effect of sorafenib in hepatocarcinoma Reviewed International journal

    Shinichi Urano, Toshiaki Ohara, Kazuhiro Noma, Ryoichi Katsube, Takayuki Ninomiya, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Fumiaki Kimura, Kazuhiro Nouso, Akihiro Matsukawa, Kazuhide Yamamoto, Toshiyoshi Fujiwara

    Cancer Biology & Therapy   17 ( 6 )   648 - 656   2016.6

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    DOI: 10.1080/15384047.2016.1177677

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  • Eradication of osteosarcoma by fluorescence-guided surgery with tumor labeling by a killer-reporter adenovirus Reviewed International coauthorship International journal

    Shuya Yano, Shinji Miwa, Hiroyuki Kishimoto, Yasuo Urata, Hiroshi Tazawa, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Journal of Orthopaedic Research   34 ( 5 )   836 - 844   2016.5

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    DOI: 10.1002/jor.23073

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  • Fluvoxamine, an anti-depressant, inhibits human glioblastoma invasion by disrupting actin polymerization Reviewed International journal

    Keiichiro Hayashi, Hiroyuki Michiue, Hiroshi Yamada, Katsuyoshi Takata, Hiroki Nakayama, Fan-Yan Wei, Atsushi Fujimura, Hiroshi Tazawa, Akira Asai, Naohisa Ogo, Hiroyuki Miyachi, Tei-ichi Nishiki, Kazuhito Tomizawa, Kohji Takei, Hideki Matsui

    SCIENTIFIC REPORTS   6   23372   2016.3

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    DOI: 10.1038/srep23372

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  • Trastuzumab-Based Photoimmunotherapy Integrated with Viral HER2 Transduction Inhibits Peritoneally Disseminated HER2-Negative Cancer Reviewed International coauthorship International journal

    Michihiro Ishida, Shunsuke Kagawa, Kyoko Shimoyama, Kiyoto Takehara, Kazuhiro Noma, Shunsuke Tanabe, Yasuhiro Shirakawa, Hiroshi Tazawa, Hisataka Kobayashi, Toshiyoshi Fujiwara

    Molecular Cancer Therapeutics   15 ( 3 )   402 - 411   2016.3

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    DOI: 10.1158/1535-7163.MCT-15-0644

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  • テロメラーゼ標的化がん治療・診断用アデノウイルス Invited Reviewed

    田澤 大, 香川俊輔, 重安邦俊, 藤原俊義

    実験医学   34 ( 1 )   13 - 18   2016.1

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  • Targeted Photodynamic Virotherapy Armed with a Genetically Encoded Photosensitizer Reviewed International journal

    Kiyoto Takehara, Hiroshi Tazawa, Naohiro Okada, Yuuri Hashimoto, Satoru Kikuchi, Shinji Kuroda, Hiroyuki Kishimoto, Yasuhiro Shirakawa, Nobuhiro Narii, Hiroyuki Mizuguchi, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Molecular Cancer Therapeutics   15 ( 1 )   199 - 208   2016.1

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    DOI: 10.1158/1535-7163.MCT-15-0344

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  • Anti-high mobility group box 1 monoclonal antibody improves ischemia/reperfusion injury and mode of liver regeneration after partial hepatectomy Reviewed International journal

    Masahiro Sugihara, Hiroshi Sadamori, Masahiro Nishibori, Yasuharu Sato, Hiroshi Tazawa, Susumu Shinoura, Yuzo Umeda, Ryuichi Yoshida, Daisuke Nobuoka, Masashi Utsumi, Kyotaro Ohno, Takeshi Nagasaka, Tadashi Yoshino, Hideo Kohka Takahashi, Takahito Yagi, Toshiyoshi Fujiwara

    American Journal of Surgery   211 ( 1 )   179 - 188   2016.1

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    DOI: 10.1016/j.amjsurg.2015.06.025

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  • 宿主正常細胞である癌関連線維芽細胞を標的とした新たな食道癌治療法の開発 Reviewed

    野間 和広, 賀島 肇, 二宮 卓之, 勝部 亮一, 渡邉 伸一郎, 大原 利章, 田澤 大, 香川 俊輔, 白川 靖博, 藤原 俊義

    癌と化学療法   42 ( 10 )   1228 - 1230   2015.10

  • Genetic and epigenetic alterations of netrin-1 receptors in gastric cancer with chromosomal instability Reviewed International coauthorship International journal

    Keisuke Toda, Takeshi Nagasaka, Yuzo Umeda, Takehiro Tanaka, Takashi Kawai, Tomokazu Fuji, Fumitaka Taniguchi, Kazuya Yasui, Nobuhito Kubota, Yuko Takehara, Hiroshi Tazawa, Shunsuke Kagawa, Dong-Sheng Sun, Naoshi Nishida, Ajay Goel, Toshiyoshi Fujiwara

    CLINICAL EPIGENETICS   7 ( 1 )   73   2015.7

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  • Experimental Curative Fluorescence-guided Surgery of Highly Invasive Glioblastoma Multiforme Selectively Labeled With a Killer-reporter Adenovirus Reviewed International coauthorship International journal

    Shuya Yano, Shinji Miwa, Hiroyuki Kishimoto, Makoto Toneri, Yukihiko Hiroshima, Mako Yamamoto, Michael Bouvet, Yasuo Urata, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara, Robert M. Hoffman

    Molecular Therapy   23 ( 7 )   1182 - 1188   2015.7

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    DOI: 10.1038/mt.2015.63

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  • Targeting tumors with a killer-reporter adenovirus for curative fluorescence-guided surgery of soft-tissue sarcoma Reviewed International coauthorship International journal

    Shuya Yano, Shinji Miwa, Hiroyuki Kishimoto, Fuminari Uehara, Hiroshi Tazawa, Makoto Toneri, Yukihiko Hiroshima, Mako Yamamoto, Yasuo Urata, Shunsuke Kagawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Oncotarget   6 ( 15 )   13133 - 13148   2015.5

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    DOI: 10.18632/oncotarget.3811

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  • MicroRNA as a molecular target for gastrointestinal cancers Invited Reviewed International journal

    Hiroshi Tazawa, Takeshi Nagasaka, Shunsuke Kagawa, Toshiyoshi Fujiwara

    TRANSLATIONAL GASTROINTESTINAL CANCER   4 ( 3 )   219 - 235   2015.5

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    DOI: 10.3978/j.issn.2224-4778.2015.04.01

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  • Fluorescence virus-guided capturing system of human colorectal circulating tumour cells for non-invasive companion diagnostics Reviewed International coauthorship International journal

    Kunitoshi Shigeyasu, Hiroshi Tazawa, Yuuri Hashimoto, Yoshiko Mori, Masahiko Nishizaki, Hiroyuki Kishimoto, Takeshi Nagasaka, Shinji Kuroda, Yasuo Urata, Ajay Goel, Shunsuke Kagawa, Toshiyoshi Fujiwara

    GUT   64 ( 4 )   627 - 635   2015.4

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    DOI: 10.1136/gutjnl-2014-306957

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  • Cancer cells mimic in vivo spatial-temporal cell-cycle phase distribution and chemosensitivity in 3-dimensional Gelfoam (R) histoculture but not 2-dimensional culture as visualized with real-time FUCCI imaging Reviewed International coauthorship International journal

    Shuya Yano, Shinji Miwa, Sumiyuki Mii, Yukihiko Hiroshima, Fuminaru Uehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Ming Zhao, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Cell Cycle   14 ( 6 )   808 - 819   2015.3

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    DOI: 10.1080/15384101.2014.1000685

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  • Biological Ablation of Sentinel Lymph Node Metastasis in Submucosally Invaded Early Gastrointestinal Cancer Reviewed International coauthorship International journal

    Satoru Kikuchi, Hiroyuki Kishimoto, Hiroshi Tazawa, Yuuri Hashimoto, Shinji Kuroda, Masahiko Nishizaki, Takeshi Nagasaka, Yasuhiro Shirakawa, Shunsuke Kagawa, Yasuo Urata, Robert M. Hoffman, Toshiyoshi Fujiwara

    Molecular Therapy   23 ( 3 )   501 - 509   2015.3

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    DOI: 10.1038/mt.2014.244

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  • Loss of p53 in stromal fibroblasts enhances tumor cell proliferation through nitric-oxide-mediated cyclooxygenase 2 activation Reviewed International coauthorship International journal

    S. Wada, Y. Matsushita, H. Tazawa, W. Aoi, Y. Naito, A. Higashi, H. Ohshima, T. Yoshikawa

    Free Radical Research   49 ( 3 )   269 - 278   2015.3

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    DOI: 10.3109/10715762.2014.997230

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  • Viral transduction of the HER2-extracellular domain expands trastuzumab-based photoimmunotherapy for HER2-negative breast cancer cells Reviewed International journal

    Kyoko Shimoyama, Shunsuke Kagawa, Michihiro Ishida, Shinichiro Watanabe, Kazuhiro Noma, Kiyoto Takehara, Hiroshi Tazawa, Yuuri Hashimoto, Shunsuke Tanabe, Junji Matsuoka, Hisataka Kobayashi, Toshiyoshi Fujiwara

    Breast Cancer Research and Treatment   149 ( 3 )   597 - 605   2015.2

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    DOI: 10.1007/s10549-015-3265-y

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  • Multidisciplinary cancer therapy with telomerase-specific oncolytic adenovirus Invited Reviewed International journal

    Toshiyoshi Fujiwara, Shunsuke Kagawa, Hiroshi Tazawa

    Current Cancer Therapy Reviews   11 ( 3 )   178 - 187   2015

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    DOI: 10.2174/1573394712666160128201822

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  • Molecular diagnosis and therapy for occult peritoneal metastasis in gastric cancer patients Invited Reviewed International journal

    Shunsuke Kagawa, Kunitoshi Shigeyasu, Michihiro Ishida, Megumi Watanabe, Hiroshi Tazawa, Takeshi Nagasaka, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    World Journal of Gastroenterology   20 ( 47 )   17796 - 17803   2014.12

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    DOI: 10.3748/wjg.v20.i47.17796

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  • Establishment of a Non-Invasive Semi-Quantitative Bioluminescent Imaging Method for Monitoring of an Orthotopic Esophageal Cancer Mouse Model Reviewed International journal

    Shinji Kuroda, Tetsushi Kubota, Katsuyuki Aoyama, Satoru Kikuchi, Hiroshi Tazawa, Masahiko Nishizaki, Shunsuke Kagawa, Toshiyoshi Fujiwara

    PLOS ONE   9 ( 12 )   e114562   2014.12

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    DOI: 10.1371/journal.pone.0114562

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  • Tumor-targeting Salmonella typhimurium A1-R decoys quiescent cancer cells to cycle as visualized by FUCCI imaging and become sensitive to chemotherapy Reviewed International coauthorship International journal

    Shuya Yano, Yong Zhang, Ming Zhao, Yukihiko Hiroshima, Shinji Miwa, Fuminari Uehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Cell Cycle   13 ( 24 )   3958 - 3963   2014.12

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    DOI: 10.4161/15384101.2014.964115

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  • Spatial-temporal FUCCI imaging of each cell in a tumor demonstrates locational dependence of cell cycle dynamics and chemoresponsiveness Reviewed International coauthorship International journal

    Shuya Yano, Yong Zhang, Shinji Miwa, Yasunori Tome, Yukihiko Hiroshima, Fuminari Uehara, Mako Yamamoto, Atsushi Suetsugu, Hiroyuki Kishimoto, Hiroshi Tazawa, Ming Zhao, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Cell Cycle   13 ( 13 )   2110 - 2119   2014.7

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  • Telomerase-specific oncolytic virotherapy for human cancer Invited Reviewed

    13 ( 6 )   817 - 823   2014.6

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  • Establishment of a pancreatic stem cell line from fibroblast-derived induced pluripotent stem cells Reviewed International journal

    Takashi Kuise, Hirofumi Noguchi, Hiroshi Tazawa, Takashi Kawai, Masaya Iwamuro, Issei Saitoh, Hitomi Usui Kataoka, Masami Watanabe, Yasufumi Noguchi, Toshiyoshi Fujiwara

    Biomedical Engineering Online   13   64   2014.5

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    DOI: 10.1186/1475-925X-13-64

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  • Fascin regulates chronic inflammation-related human colon carcinogenesis by inhibiting cell anoikis Reviewed International journal

    Yusuke Kanda, Tokuichi Kawaguchi, Yasuhiro Kuramitsu, Takao Kitagawa, Tokushige Kobayashi, Norihiko Takahashi, Hiroshi Tazawa, Hasem Habelhah, Jun-ichi Hamada, Masanobu Kobayashi, Mio Hirahata, Kunishige Onuma, Mitsuhiko Osaki, Kazuyuki Nakamura, Tomoyuki Kitagawa, Masuo Hosokawa, Futoshi Okada

    Proteomics   14 ( 9 )   1031 - 1041   2014.5

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    DOI: 10.1002/pmic.201300414

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  • Invading cancer cells are predominantly in G(0)/G(1) resulting in chemoresistance demonstrated by real-time FUCCI imaging Reviewed International coauthorship International journal

    Shuya Yano, Shinji Miwa, Sumiyuki Mii, Yukihiko Hiroshima, Fuminari Uehara, Mako Yamamoto, Hiroyuki Kishimoto, Hiroshi Tazawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    Cell Cycle   13 ( 6 )   953 - 960   2014.3

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  • A Genetically Engineered Oncolytic Adenovirus Decoys and Lethally Traps Quiescent Cancer Stem-like Cells in S/G(2)/M Phases Reviewed International coauthorship International journal

    Shuya Yano, Hiroshi Tazawa, Yuuri Hashimoto, Yasuhiro Shirakawa, Shinji Kuroda, Masahiko Nishizaki, Hiroyuki Kishimoto, Futoshi Uno, Takeshi Nagasaka, Yasuo Urata, Shunsuke Kagawa, Robert M. Hoffman, Toshiyoshi Fujiwara

    CLINICAL CANCER RESEARCH   19 ( 23 )   6495 - 6505   2013.12

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    DOI: 10.1158/1078-0432.CCR-13-0742

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  • Oncolytic Adenovirus-Induced Autophagy: Tumor-Suppressive Effect and Molecular Basis Invited Reviewed International journal

    Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Acta Medica Okayama   67 ( 6 )   333 - 342   2013.12

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    DOI: 10.18926/AMO/52006

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  • Chronic inflammation-derived nitric oxide causes conversion of human colonic adenoma cells into adenocarcinoma cells Reviewed International journal

    Hiroshi Tazawa, Tokuichi Kawaguchi, Tokushige Kobayashi, Yasuhiro Kuramitsu, Sayori Wada, Yoshiko Satomi, Hoyoku Nishino, Masanobu Kobayashi, Yusuke Kanda, Mitsuhiko Osaki, Tomoyuki Kitagawa, Masuo Hosokawa, Futoshi Okada

    EXPERIMENTAL CELL RESEARCH   319 ( 18 )   2835 - 2844   2013.11

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    DOI: 10.1016/j.yexcr.2013.08.006

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  • Advances in adenovirus-mediated p53 cancer gene therapy Invited Reviewed International journal

    Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Expert Opinion on Biological Therapy   13 ( 11 )   1569 - 1583   2013.11

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    DOI: 10.1517/14712598.2013.845662

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  • Dual Programmed Cell Death Pathways Induced by p53 Transactivation Overcome Resistance to Oncolytic Adenovirus in Human Osteosarcoma Cells Reviewed International journal

    Joe Hasei, Tsuyoshi Sasaki, Hiroshi Tazawa, Shuhei Osaki, Yasuaki Yamakawa, Toshiyuki Kunisada, Aki Yoshida, Yuuri Hashimoto, Teppei Onishi, Futoshi Uno, Shunsuke Kagawa, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Molecular Cancer Therapeutics   12 ( 3 )   314 - 325   2013.3

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    DOI: 10.1158/1535-7163.MCT-12-0869

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  • A simple detection system for adenovirus receptor expression using a telomerase-specific replication-competent adenovirus Reviewed International journal

    T. Sasaki, H. Tazawa, J. Hasei, S. Osaki, T. Kunisada, A. Yoshida, Y. Hashimoto, S. Yano, R. Yoshida, S. Kagawa, F. Uno, Y. Urata, T. Ozaki, T. Fujiwara

    GENE THERAPY   20 ( 1 )   112 - 118   2013.1

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    DOI: 10.1038/gt.2011.213

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  • Genetically engineered oncolytic adenovirus induces autophagic cell death through an E2F1-microRNA-7-epidermal growth factor receptor axis Reviewed International journal

    Hiroshi Tazawa, Shuya Yano, Ryosuke Yoshida, Yasumoto Yamasaki, Tsuyoshi Sasaki, Yuuri Hashimoto, Shinji Kuroda, Masaaki Ouchi, Teppei Onishi, Futoshi Uno, Shunsuke Kagawa, Yasuo Urata, Toshiyoshi Fujiwara

    International Journal of Cancer   131 ( 12 )   2939 - 2950   2012.12

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    DOI: 10.1002/ijc.27589

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  • Mechanism of resistance to trastuzumab and molecular sensitization via ADCC activation by exogenous expression of HER2-extracellular domain in human cancer cells Reviewed International journal

    Ryosuke Yoshida, Hiroshi Tazawa, Yuuri Hashimoto, Shuya Yano, Teppei Onishi, Tsuyoshi Sasaki, Yasuhiro Shirakawa, Hiroyuki Kishimoto, Futoshi Uno, Masahiko Nishizaki, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Cancer Immunology Immunotherapy   61 ( 11 )   1905 - 1916   2012.11

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    DOI: 10.1007/s00262-012-1249-x

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  • A novel apoptotic mechanism of genetically engineered adenovirus-mediated tumour-specific p53 overexpression through E1A-dependent p21 and MDM2 suppression Reviewed International journal

    Yasumoto Yamasaki, Hiroshi Tazawa, Yuuri Hashimoto, Toru Kojima, Shinji Kuroda, Shuya Yano, Ryosuke Yoshida, Futoshi Uno, Hiroyuki Mizuguchi, Akira Ohtsuru, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    EUROPEAN JOURNAL OF CANCER   48 ( 14 )   2282 - 2291   2012.9

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    DOI: 10.1016/j.ejca.2011.12.020

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  • Synergistic Interaction of Telomerase-Specific Oncolytic Virotherapy and Chemotherapeutic Agents for Human Cancer Invited Reviewed International journal

    Toshiyoshi Fujiwara, Shunsuke Kagawa, Hiroshi Tazawa

    Current Pharmaceutical Biotechnology   13 ( 9 )   1809 - 1816   2012.7

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    DOI: 10.2174/138920112800958887

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  • A protein transduction method using oligo-arginine (3R) for the delivery of transcription factors into cell nuclei Reviewed International journal

    Takashi Hitsuda, Hiroyuki Michiue, Mizuki Kitamatsu, Atsushi Fujimura, Feifei Wang, Takahiro Yamamoto, Xiao-Jian Han, Hiroshi Tazawa, Atsuhito Uneda, Iori Ohmori, Tei-ichi Nishiki, Kazuhito Tomizawa, Hideki Matsui

    Biomaterials   33 ( 18 )   4665 - 4672   2012.6

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    DOI: 10.1016/j.biomaterials.2012.02.049

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  • The hTERT Promoter Enhances the Antitumor Activity of an Oncolytic Adenovirus under a Hypoxic Microenvironment Reviewed International journal

    Yuuri Hashimoto, Hiroshi Tazawa, Fuminori Teraishi, Toru Kojima, Yuichi Watanabe, Futoshi Uno, Shuya Yano, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    PLOS ONE   7 ( 6 )   e39292   2012.6

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    DOI: 10.1371/journal.pone.0039292

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  • Preclinical Evaluation of Telomerase-Specific Oncolytic Virotherapy for Human Bone and Soft Tissue Sarcomas Reviewed International journal

    Tsuyoshi Sasaki, Hiroshi Tazawa, Jo Hasei, Toshiyuki Kunisada, Aki Yoshida, Yuuri Hashimoto, Shuya Yano, Ryosuke Yoshida, Futoshi Uno, Shunsuke Kagawa, Yuki Morimoto, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    Clinical Cancer Research   17 ( 7 )   1828 - 1838   2011.4

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    DOI: 10.1158/1078-0432.CCR-10-2066

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  • MicroRNAs as potential target gene in cancer gene therapy of gastrointestinal tumors Invited Reviewed International journal

    Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Expert Opinion on Biological Therapy   11 ( 2 )   145 - 155   2011.2

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    DOI: 10.1517/14712598.2011.542749

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  • Telomerase-Dependent Oncolytic Adenovirus Sensitizes Human Cancer Cells to Ionizing Radiation via Inhibition of DNA Repair Machinery Reviewed International journal

    Shinji Kuroda, Toshiya Fujiwara, Yasuhiro Shirakawa, Yasumoto Yamasaki, Shuya Yano, Futoshi Uno, Hiroshi Tazawa, Yuuri Hashimoto, Yuichi Watanabe, Kazuhiro Noma, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Cancer Research   70 ( 22 )   9339 - 9348   2010.11

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    DOI: 10.1158/0008-5472.CAN-10-2333

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  • In Vivo Biological Purging for Lymph Node Metastasis of Human Colorectal Cancer by Telomerase-Specific Oncolytic Virotherapy Reviewed

    Toru Kojima, Yuichi Watanabe, Yuuri Hashimoto, Shinji Kuroda, Yasumoto Yamasaki, Shuya Yano, Masaaki Ouchi, Hiroshi Tazawa, Futoshi Uno, Shunsuke Kagawa, Satoru Kyo, Hiroyuki Mizuguchi, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    ANNALS OF SURGERY   251 ( 6 )   1079 - 1086   2010.6

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    DOI: 10.1097/SLA.0b013e3181deb69d

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  • A simple biological imaging system for detecting viable human circulating tumor cells Reviewed

    Toru Kojima, Yuuri Hashimoto, Yuichi Watanabe, Shunsuke Kagawa, Futoshi Uno, Shinji Kuroda, Hiroshi Tazawa, Satoru Kyo, Hiroyuki Mizuguchi, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    JOURNAL OF CLINICAL INVESTIGATION   119 ( 10 )   3172 - 3181   2009.10

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    DOI: 10.1172/JCI38609

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  • Lipopolysaccharide induces aberrant hypermethylation of Hic-1 in mouse embryonic fibroblasts lacking p53 gene Reviewed

    Masayuki Tatemichi, Harumi Hata, Hiroshi Tazawa, Toshio Nakadate

    ANTICANCER RESEARCH   28 ( 4B )   2101 - 2108   2008.7

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  • Tumor-suppressive miR-34a induces senescence-like growth arrest through modulation of the E2F pathway in human colon cancer cells Reviewed

    Hiroshi Tazawa, Naoto Tsuchiya, Masashi Izumiya, Hitoshi Nakagama

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   104 ( 39 )   15472 - 15477   2007.9

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    DOI: 10.1073/pnas.0707351104

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  • Mouse strain differences in inflammatory responses of colonic mucosa induced by dextran sulfate sodium cause differential susceptibility to PhIP-induced large bowel carcinogenesis Reviewed

    Masako Nakanishi, Hiroshi Tazawa, Naoto Tsuchiya, Takashi Sugimura, Takuji Tanaka, Hitoshi Nakagama

    Cancer Science   98 ( 8 )   1157 - 1163   2007.8

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    DOI: 10.1111/j.1349-7006.2007.00528.x

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  • Oxidative and nitrative stress caused by subcutaneous implantation of a foreign body accelerates sarcoma development in Trp53(+/-) mice Reviewed

    Hiroshi Tazawa, Masayuki Tatemichi, Tomohiro Sawa, Isabelle Gilibert, Ning Ma, Yusuke Hiraku, Lawrence A. Donehower, Hiroko Ohgaki, Shosuke Kawanishi, Hiroshi Ohshima

    CARCINOGENESIS   28 ( 1 )   191 - 198   2007.1

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    DOI: 10.1093/carcin/bgl128

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  • The role of nicotinamide adenine dinucleotide phosphate oxidase-derived reactive oxygen species in the acquisition of metastatic ability of tumor cells Reviewed

    F Okada, M Kobayashi, H Tanaka, T Kobayashi, H Tazawa, Y Iuchi, K Onuma, M Hosokawa, MC Dinauer, NH Hunt

    AMERICAN JOURNAL OF PATHOLOGY   169 ( 1 )   294 - 302   2006.7

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    DOI: 10.2353/ajpath.2006.060073

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  • Prevention of inflammation-mediated acquisition of metastatic properties of benign mouse fibrosarcoma cells by administration of an orally available superoxide dismutase Reviewed

    F Okada, H Shionoya, M Kobayashi, T Kobayashi, H Tazawa, K Onuma, Y Iuchi, N Matsubara, T Ijichi, B Dugas, M Hosokawa

    BRITISH JOURNAL OF CANCER   94 ( 6 )   854 - 862   2006.3

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    DOI: 10.1038/sj.bjc.6603016

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  • Involvement of reactive nitrogen oxides for acquisition of metastatic properties of benign tumors in a model of inflammation-based tumor progression Reviewed

    F Okada, H Tazawa, T Kobayashi, M Kobayashi, M Hosokawa

    NITRIC OXIDE-BIOLOGY AND CHEMISTRY   14 ( 2 )   122 - 129   2006.3

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    DOI: 10.1016/j.niox.2005.06.009

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  • Prevention of human cancer by modulation of chronic inflammatory processes Invited Reviewed

    H Ohshima, H Tazawa, BS Sylla, T Sawa

    MUTATION RESEARCH-FUNDAMENTAL AND MOLECULAR MECHANISMS OF MUTAGENESIS   591 ( 1-2 )   110 - 122   2005.12

  • Increased risk of intestinal type of gastric adenocarcinoma in Japanese women associated with long forms of CCTTT pentanucleotide repeat in the inducible nitric oxide synthase promoter Reviewed

    M Tatemichi, T Sawa, Gilibert, I, H Tazawa, T Katoh, H Ohshima

    CANCER LETTERS   217 ( 2 )   197 - 202   2005.1

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    DOI: 10.1016/j.canlet.2004.09.002

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  • Suppression of thymic lymphomas and increased nonthymic lymphomagenesis in TRP53-deficient mice lacking inducible nitric oxide synthase gene Reviewed

    M Tatemichi, H Tazawa, M Masuda, M Saleem, S Wada, LA Donehower, H Ohgaki, H Ohshima

    INTERNATIONAL JOURNAL OF CANCER   111 ( 6 )   819 - 828   2004.10

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    DOI: 10.1002/ijc.20350

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  • Infiltration of neutrophils is required for acquisition of metastatic phenotype of benign murine fibrosarcoma cells - Implication of inflammation-associated carcinogenesis and tumor progression Reviewed

    H Tazawa, F Okada, T Kobayashi, M Tada, Y Mori, Y Une, F Sendo, M Kobayashi, M Hosokawa

    AMERICAN JOURNAL OF PATHOLOGY   163 ( 6 )   2221 - 2232   2003.12

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    DOI: 10.1016/S0002-9440(10)63580-8

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  • Thymosin-beta 4 regulates motility and metastasis of malignant mouse fibrosarcoma cells Reviewed

    T Kobayashi, F Okada, N Fujii, N Tomita, S Ito, H Tazawa, T Aoyama, SK Choi, T Shibata, H Fujita, M Hosokawa

    AMERICAN JOURNAL OF PATHOLOGY   160 ( 3 )   869 - 882   2002.3

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  • Conversion of human colonic adenoma cells to adenocarcinoma cells through inflammation in nude mice Reviewed

    F Okada, T Kawaguchi, H Habelhah, T Kobayashi, H Tazawa, N Takeichi, T Kitagawa, M Hosokawa

    LABORATORY INVESTIGATION   80 ( 11 )   1617 - 1628   2000.11

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    Other Link: http://orcid.org/0000-0003-4733-1037

  • Inhibitory Effects of Anti-Mouse Neutrophil Monoclonal Antibody on Malignant Progression of Murine Fibrosarcoma Cells Co-implanted with Gelatin Sponge Reviewed

    TAZAWA Hiroshi

    Akita journal of medicine   27 ( 3 )   219 - 230   2000

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  • 分子細胞治療フロンティア2025

    田澤大, 黒田新士, 菊地覚次, 垣内慶彦, 金谷信彦, 橋本将志, 浦田泰生, 香川俊輔, 藤原俊義( Role: Joint author ,  膵臓がんの免疫療法抵抗性を克服するp53武装化腫瘍融解ウイルス療法の開発)

    外科分子細胞治療研究会  2025.4  ( ISBN:9784991346613

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  • 入門腫瘍内科学 改訂第4版

    田澤大( Role: Contributor ,  E 新規治療 1) ウイルス療法, 2) 光免疫療法)

    日本臨床腫瘍学会  2025.3 

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  • 分子細胞治療フロンティア 2020

    香川俊輔, 野間和広, 田澤 大, 藤原俊義( Role: Joint author ,  がん治療の新たなmodalityとしての近赤外線光免疫療法)

    外科分子細胞治療研究会  2020.4  ( ISBN:9784990253196

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    Total pages:243p   Language:Japanese

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  • 分子細胞治療フロンティア 2020

    黒田新士, 金谷信彦, 田澤 大, 浦田泰生, 藤原俊義( Role: Joint author ,  テロメラーゼ特異的腫瘍融解アデノウイルス製剤の臨床開発と今後の展望)

    外科分子細胞治療研究会  2020.4  ( ISBN:9784990253196

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    Total pages:243p   Language:Japanese

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  • いま、本格化する遺伝子治療 遺伝性疾患・がんと戦う新たな一手(実験医学 増刊)

    藤原俊義, 田澤 大, 田邊俊介, 白川靖博( Role: Joint author ,  食道がんに対する放射線併用遺伝子組換えウイルス療法)

    羊土社  2020.2 

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  • 次世代がん治療 : 発症・転移メカニズムからがん免疫療法・ウイルス療法、診断法まで

    田澤 大, 田辺俊介, 香川俊輔, 白川靖博, 藤原俊義( Role: Joint author ,  テロメラーゼ依存性腫瘍融解アデノウイルスTelomelysinの臨床開発)

    エヌ・ティー・エス  2017.6  ( ISBN:9784860435035

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    Total pages:12, ii, 10, 347, 10p   Language:Japanese

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  • 今、着実に実り始めた遺伝子治療 : 最新研究と今後の展開

    藤原俊義, 田澤 大, 香川俊輔, 白川靖博( Role: Joint author ,  食道がんに対する放射線併用アデノウイルス療法の臨床開発)

    メディカルドゥ  2016.6  ( ISBN:9784944157600

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    Total pages:300p   Language:Japanese

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  • 分子細胞治療フロンティア 2015

    長谷井 嬢, 尾崎修平, 山川泰明, 田澤 大, 香川俊輔, 尾崎敏文, 藤原俊義( Role: Joint author ,  骨軟部肉腫に対するテロメラーゼ依存性増殖型腫瘍融解ウイルスを用いた治療戦略)

    外科分子細胞治療研究会  2014.8  ( ISBN:4990253140

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    Total pages:236   Language:Japanese

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  • Pseudohypoxia by HIF-PHD inhibitors activates tumor immune response for MSS colorectal cancer.

    Toshiaki Ohara, Yuehua Chen, Yusuke Hamada, Hajime Kashima, Satoru Kikuchi, Kazuhiro Noma, Hiroshi Tazawa, Masayoshi Fujisawa, Toshiyoshi Fujiwara, Akihiro Matsukawa

    CANCER SCIENCE   116   663 - 663   2025.1

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  • 腫瘍融解アデノウイルス製剤の免疫賦活薬としての有用性と免疫チェックポイント阻害剤との複合免疫療法の可能性

    黒田新士, 金谷信彦, 橋本将志, 垣内慶彦, 菊地覚次, 田澤大, 香川俊輔, 藤原俊義

    日本外科学会定期学術集会(Web)   125th   2025

  • RNA編集酵素ADAR1に基づく大腸癌肝転移の残肝再発リスク層別化の検討

    高橋 利明, 重安 邦俊, 中村 峻輔, 高橋 政史, 萱野 真史, 新田 薫, 森分 和也, 安井 和也, 松三 雄騎, 藤 智和, 近藤 喜太, 寺石 文則, 田澤 大, 藤原 俊義

    日本癌治療学会学術集会抄録集   62回   P80 - 2   2024.10

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  • 潰瘍性大腸炎においてRNA編集解析が発癌予測バイオマーカーとなりうる

    森分 和也, 重安 邦俊, 萱野 真史, 新田 薫, 中村 峻輔, 高橋 利明, 高橋 政史, 金谷 信彦, 松三 雄騎, 近藤 喜太, 寺石 文則, 田澤 大, 藤原 俊義

    日本癌治療学会学術集会抄録集   62回   P43 - 2   2024.10

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  • FAPを標的とした近赤外線光免疫療法によるCAF-rich腫瘍への化学療法抵抗性の克服

    西村 星多郎, 野間 和広, 松本 佑, 竹田 泰茂, 高橋 達也, 松本 聖, 河崎 健人, 國友 知義, 賀島 肇, 加藤 卓也, 菊地 覚次, 大原 利章, 田澤 大, 藤原 俊義

    日本癌治療学会学術集会抄録集   62回   O76 - 2   2024.10

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  • 食道扁平上皮癌オルガノイドの樹立と個別化治療のための薬剤耐性実験モデル

    竹田 泰茂, 野間 和広, 賀島 肇, 清水 彰人, 松本 祐, 高橋 達也, 前田 直見, 田邊 俊介, 大原 利章, 田澤 大, 中川 裕, 藤原 俊義

    日本癌治療学会学術集会抄録集   62回   O75 - 6   2024.10

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  • マクロピノサイトーシスは膵癌関連膵星細胞の腫瘍融解ウイルスへの感受性を増強する

    西山 岳芳, 田澤 大, 永井 康雄, 庄司 良平, 菊地 覚次, 黒田 新士, 大原 利章, 野間 和広, 田中 啓祥, 狩野 光伸, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌治療学会学術集会抄録集   62回   O66 - 6   2024.10

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  • 膵癌が誘導する癌関連線維芽細胞サブタイプは腫瘍融解ウイルスに異なる感受性を示す

    永井 康雄, 田澤 大, 藤田 修斗, 高橋 洋祐, 菊地 覚次, 黒田 新士, 大原 利章, 野間 和広, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌治療学会学術集会抄録集   62回   O66 - 4   2024.10

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  • 間質のコラーゲン産生は胃癌における腫瘍融解ウイルス療法の治療抵抗性を増強する(Stromal collagen type 1 deposition promotes resistance to oncolytic virotherapy in gastric cancer)

    大倉 友博, 田澤 大, 菊地 覚次, 黒田 新士, 大原 利章, 野間 和広, 大塚 旬子, 大木 理恵子, 浦田 泰生, 香川 俊輔, 藤原 俊義, 藤原 俊義

    日本癌学会総会記事   83回   P - 2252   2024.9

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  • HIF-PHD阻害薬による偽性低酸素はMSS大腸癌の充腫瘍免疫応答を増強する(Pseudohypoxia by HIF-PHD inhibitors activates tumor immune response for MSS colorectal cancer)

    大原 利章, 陳 悦華, 濱田 祐輔, 賀島 肇, 菊地 覚次, 野間 和広, 田澤 大, 藤澤 真義, 藤原 俊義, 松川 昭博

    日本癌学会総会記事   83回   E - 2017   2024.9

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  • 局所環境とがん免疫 膵臓癌のMHC低発現を改善するエピジェネティック制御剤の同定と樹状細胞併用p53ウイルス免疫療法への応用

    陶守 貫人, 田澤 大, 山田 元彦, 岡田 尚大, 菊地 覚次, 黒田 新士, 野間 和広, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本がん免疫学会総会・日本バイオセラピィ学会学術集会総会合同大会プログラム・抄録集   28回・37回   78 - 78   2024.6

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  • Establishment of predictive biomarkers for carcinogenesis in ulcerative colitis using RNA editing analyses

    Toshiaki Takahashi, Kunitoshi Shigeyasu, Yoshitaka Kondo, Hibiki Umeda, Kazuya Moriwake, Masashi Kayano, Kaori Nitta, Fuminori Teraishi, Yuzo Umeda, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   84 ( 7 )   2024.4

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    DOI: 10.1158/1538-7445.AM2024-LB360

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  • Cancer associated fibroblasts targeted photoimmunotherapy improves drug delivery

    Seitaro Nishimura, Kazuhiro Noma, Tasuku Matsumoto, Tatsuya Takahashi, Yasushige Takeda, Hijiri Matsumoto, Tomoyoshi Kunitomo, Kento Kawasaki, Hajime Kashima, Takuya Kato, Satoru Kikuchi, Toshiaki Ohara, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   84 ( 6 )   2024.3

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    DOI: 10.1158/1538-7445.AM2024-2897

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  • Pseudohypoxia by HIF-PHD inhibitors activates tumor immune response for MSS colorectal cancer

    Toshiaki Ohara, Yuehua Chen, Yusuke Hamada, Seitaro Nishimura, Hotaka Kawai, Kazuhiro Noma, Hiroshi Tazawa, Toshiyoshi Fujiwara, Akihiro Matsukawa

    CANCER RESEARCH   84 ( 6 )   2024.3

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    DOI: 10.1158/1538-7445.AM2024-5271

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  • Sequential Combination Effects of Oncolytic Virus Therapy and Immunotherapy Utilizing the Long-term Immune Activation

    門脇大輔, 黒田新士, 橋本将志, 片山哲也, 實金悠, 半澤俊哉, 吉田有佑, 坂本真樹, 金谷信彦, 垣内慶彦, 菊地覚次, 野間和広, 田澤大, 香川俊輔, 浦田泰生, 藤原俊義

    日本癌学会学術総会抄録集(Web)   83rd   2024

  • 腫瘍融解アデノウイルスの脊髄腫瘍への適応に関する検討

    鷹取亮, 魚谷弘二, 鉄永倫子, 篠原健介, 小田孔明, 志渡澤央和, 植田昌敬, 浦田泰生, 田澤大, 尾崎敏文

    日本整形外科学会雑誌(CD-ROM)   98 ( 8 )   2024

  • Development of the 3D model of peritoneum structure to explore the biology of gastric cancer peritoneal metastasis

    宇根 悠太, 菊地 覚次, 田澤 大, 黒田 新士, 大原 利章, 野間 和広, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   82回   1858 - 1858   2023.9

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  • Selective depletion of PMN-MDSCs in tumor be ds with near infrared photoimmunotherapy enhances host immune response

    加藤 卓也, 野間 和広, 古澤 あき, 福島 啓司, 高尾 誠一郎, 田澤 大, チョイキー・ピーター, 小林 久隆, 藤原 俊義

    日本癌学会総会記事   82回   1758 - 1758   2023.9

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  • Commensal bacteria and tumor immunity Butyrate enhances the antitumor efficacy of telomerase-specific oncolytic adenoviruses

    坂本 真樹, 黒田 新士, 垣内 慶彦, 橋本 将志, 八木 千晶, 杉本 龍馬, 濱田 侑紀, 吉田 有佑, 門脇 大輔, 半澤 俊哉, 菊地 覚次, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   82回   1660 - 1660   2023.9

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  • HIF-PH inhibitors with iron chelating ability enhance the tumor immune response

    大原 利章, 陳 悦華, 王 宇沢, 濱田 祐輔, 菊地 覚次, 野間 和広, 田澤 大, 藤澤 真義, 藤原 俊義, 松川 昭博

    日本癌学会総会記事   82回   248 - 248   2023.9

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  • Drug delivery improvement of CAFs targeted photoimmunotherapy

    西村 星多郎, 野間 和広, 高橋 達也, 竹田 泰茂, 松本 聖, 國友 知義, 河崎 健人, 赤井 正明, 小林 照貴, 賀島 肇, 加藤 卓也, 菊地 覚次, 大原 利章, 田澤 大, 藤原 俊義

    日本癌学会総会記事   82回   131 - 131   2023.9

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  • テロメラーゼ依存性腫瘍融解アデノウイルスの骨・軟部腫瘍への応用を目指した蛍光タンパクによるウイルスの治療効果予測

    魚谷 弘二, 藤原 智洋, 田澤 大, 植田 昌敬, 志渡澤 央和, 小田 孔明, 鉄永 倫子, 三澤 治夫, 中田 英二, 国定 俊之, 尾崎 敏文

    日本整形外科学会雑誌   97 ( 8 )   S1714 - S1714   2023.8

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  • 膵癌に対するp53誘導腫瘍融解ウイルスと免疫チェックポイント阻害剤を用いた複合免疫療法

    藤田脩斗, 田澤大, 田澤大, 梶原義典, 菊地覚次, 黒田新士, 野間和広, 浦田泰生, 香川俊輔, 藤原俊義

    日本バイオセラピィ学会学術集会総会プログラム・抄録集   36th   2023

  • p53感作樹状細胞ワクチンとp53武装化ウイルス免疫療法の併用によるアブスコパル効果の誘導

    陶守貫人, 田澤大, 田澤大, 山田元彦, 菊地覚次, 黒田新士, 野間和広, 浦田泰生, 香川俊輔, 藤原俊義

    日本バイオセラピィ学会学術集会総会プログラム・抄録集   36th   2023

  • がん治療におけるトランスレーショナルリサーチの新展開 難治性膵臓癌に対するミトコンドリア阻害剤と腫瘍融解アデノウイルスの併用療法

    庄司 良平, 田澤 大, 菊地 覚次, 黒田 新士, 吉田 龍一, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌治療学会学術集会抄録集   60回   WS10 - 6   2022.10

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  • 腸内細菌叢からがんを考える 腸内細菌叢は潰瘍性大腸炎においてRNA編集を介し発癌を促進する

    重安 邦俊, 高橋 一剛, 近藤 喜太, 梅田 響, 田澤 大, 藤原 俊義

    日本癌治療学会学術集会抄録集   60回   WS17 - 4   2022.10

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  • RNA編集は大腸癌の発癌や進展を促進するのみならず免疫療法のターゲットとなり得る

    重安 邦俊, 武田 正, 高橋 一剛, 小松 泰浩, 畑 七々子, 梅田 響, 高橋 利明, 田澤 大, 藤原 俊義

    日本癌治療学会学術集会抄録集   60回   P40 - 5   2022.10

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  • がんの微小環境を考える CAFsを標的にした光免疫療法による薬物動態改善効果の検証

    60回   WS4 - 2   2022.10

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  • 食道癌に対するウイルス治療、ワクチン治療の最前線 抗腫瘍免疫賦活を介した腫瘍融解アデノウイルス製剤による免疫チェックポイント阻害薬治療増強効果の検討

    橋本 将志, 黒田 新士, 金谷 信彦, 田辺 俊介, 前田 直見, 野間 和広, 田澤 大, 白川 靖博, 浦田 泰生, 藤原 俊義

    日本食道学会学術集会プログラム・抄録集   76回   59 - 59   2022.9

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  • 食道癌に対するウイルス治療、ワクチン治療の最前線 食道癌に対する腫瘍融解ウイルス併用放射線療法の臨床研究の成果と展望

    田辺 俊介, 野間 和広, 橋本 将志, 最所 公平, 賀島 肇, 前田 直見, 菊地 覚次, 田澤 大, 白川 靖博, 藤原 俊義

    日本食道学会学術集会プログラム・抄録集   76回   59 - 59   2022.9

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  • 癌細胞と癌関連線維芽細胞は互いにPD-L1を増強させ予後に影響する(Cancer cell and cancer-associated fibroblast mutually enhance PD-L1 expression and affect survival in esophageal cancer)

    河崎 健人, 野間 和広, 西村 星多郎, 松本 聖, 國友 知義, 赤井 正明, 小林 照貴, 菊地 覚次, 大原 利章, 田澤 大, 藤原 俊義

    日本癌学会総会記事   81回   P - 2187   2022.9

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  • p53搭載テロメラーゼ特異的腫瘍融解アデノウイルスの抗腫瘍効果予測スコアリングシステム(Scoring system to predict antitumor effects of p53-armed telomerase-specific oncolytic adenovirus)

    杉本 龍馬, 黒田 新士, 吉田 有佑, 坂本 真樹, 濱田 侑紀, 八木 千晶, 橋本 将志, 垣内 慶彦, 菊地 覚次, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   81回   P - 3347   2022.9

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  • 転移性骨肉腫細胞はCCL2によるM2マクロファージの腫瘍内浸潤を誘導して肺転移を促進する(Metastatic osteosarcoma cells facilitate lung metastasis by inducing CCL2-mediated tumor infiltration of M2 macrophages)

    近藤 宏也, 田澤 大, 久禮 美穂, 藤原 智洋, 国定 俊之, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   81回   J - 2087   2022.9

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  • p53感作樹状細胞ワクチンは大腸癌に対するp53搭載腫瘍融解ウイルスの治療効果を増強する(Ad-p53-transduced dendritic cell vaccine enhances the efficacy of p53-armed oncolytic virotherapy in colorectal cancer)

    山田 元彦, 田澤 大, 庄司 良平, 永井 康雄, 井上 弘章, 菊地 覚次, 黒田 新士, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   81回   P - 2177   2022.9

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  • 癌細胞と癌関連線維芽細胞は互いにPD-L1を増強させ予後に影響する(Cancer cell and cancer-associated fibroblast mutually enhance PD-L1 expression and affect survival in esophageal cancer)

    河崎 健人, 野間 和広, 西村 星多郎, 松本 聖, 國友 知義, 赤井 正明, 小林 照貴, 菊地 覚次, 大原 利章, 田澤 大, 藤原 俊義

    日本癌学会総会記事   81回   P - 2187   2022.9

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  • 腫瘍免疫の改善に関わる、FAPを標的とした光免疫療法の可能性(Fibroblast Activation Protein targeted Near-Infrared Photoimmunotherapy improves tumor immunosuppression)

    赤井 正明, 野間 和広, 大原 利章, 松本 聖, 西村 星多郎, 國友 知義, 河崎 健人, 小林 照貴, 賀島 肇, 菊地 覚次, 田澤 大, 藤原 俊義

    日本癌学会総会記事   81回   J - 3010   2022.9

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  • 血清エクソソームE1A-DNAはテロメラーゼ特異的腫瘍融解アデノウイルスの治療効果予測バイオマーカーとして有用である(Exosomal E1A-DNA in serum as a predictive biomarker of telomerase-specific oncolytic adenovirus)

    八木 千晶, 黒田 新士, 吉田 有佑, 坂本 真樹, 濱田 侑紀, 杉本 龍馬, 橋本 将志, 垣内 慶彦, 菊地 覚次, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   81回   E - 3068   2022.9

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  • 食道癌に対するウイルス治療、ワクチン治療の最前線 食道癌に対する腫瘍融解ウイルス併用放射線療法の臨床研究の成果と展望

    田辺 俊介, 野間 和広, 橋本 将志, 最所 公平, 賀島 肇, 前田 直見, 菊地 覚次, 田澤 大, 白川 靖博, 藤原 俊義

    日本食道学会学術集会プログラム・抄録集   76回   59 - 59   2022.9

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  • 食道癌に対するウイルス治療、ワクチン治療の最前線 抗腫瘍免疫賦活を介した腫瘍融解アデノウイルス製剤による免疫チェックポイント阻害薬治療増強効果の検討

    橋本 将志, 黒田 新士, 金谷 信彦, 田辺 俊介, 前田 直見, 野間 和広, 田澤 大, 白川 靖博, 浦田 泰生, 藤原 俊義

    日本食道学会学術集会プログラム・抄録集   76回   59 - 59   2022.9

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  • EMTバイオセンサーを用いたリアルタイムイメージングによる難治性膵臓癌の治療戦略(Real-time imaging of EMT biosensor provide a therapeutic strategy for refractory pancreatic cancer)

    谷 悠真, 田澤 大, 重安 邦俊, 藤原 俊義

    日本癌学会総会記事   81回   P - 3146   2022.9

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  • 骨・軟部腫瘍の基礎科学のトピックス 転移性骨肉腫は臓器指向性サイトカインの分泌を介して微小環境を変化させ前転移ニッチを形成する

    近藤 宏也, 田澤 大, 藤原 智洋, 近藤 彩奈, 片山 晴喜, 佐藤 浩平, 畑 利彰, 中田 英二, 国定 俊之, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   96 ( 8 )   S1532 - S1532   2022.9

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  • 臓器指向性分泌サイトカイン/細胞外小胞を介したcell-cell communicationによる骨肉腫の新しい肺転移形成機構の同定

    近藤 宏也, 藤原 智洋, 田澤 大, 吉田 晶, 片山 晴喜, 近藤 彩奈, 佐藤 浩平, 畑 利彰, たき平 将太, 中田 英二, 国定 俊之, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   96 ( 6 )   S1424 - S1424   2022.6

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  • トランスレーショナル研究における外科医の役割 外科医が思う「あったらいいな」をTranslational researchで解決する

    垣内 慶彦, 黒田 新士, 橋本 将志, 八木 千晶, 杉本 龍馬, 濱田 侑紀, 坂本 真樹, 吉田 侑佑, 菊地 覚次, 香川 俊輔, 田澤 大, 藤原 俊義

    日本外科学会定期学術集会抄録集   122回   DB - 4   2022.4

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  • 大腸癌肝転移におけるRNA編集酵素ADAR1発現は肝転移切除後の残肝再発を予測するバイオマーカーになる

    畑 七々子, 重安 邦俊, 高橋 一剛, 梅田 響, 武田 正, 矢野 修也, 楳田 祐三, 田澤 大, 藤原 俊義

    日本分子腫瘍マーカー研究会誌   37   23 - 24   2022

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  • Elucidation for the mechanism of lymph node metastasis of esophageal squamous cell carcinoma by extracellular vesicles

    木谷嘉孝, 吉岡祐亮, 賀島肇, 野間和広, 田澤大, 田澤大, 藤原俊義, 永川裕一, 落谷孝広

    日本癌学会学術総会抄録集(Web)   81st   P - 2122   2022

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  • 膵癌のがん関連線維芽細胞(CAF)サブタイプに対する腫瘍融解ウイルス療法の感受性の検討

    永井康雄, 田澤大, 田澤大, 菊地覚次, 黒田新士, 野間和広, 浦田泰生, 香川俊輔, 藤原俊義

    日本バイオセラピィ学会学術集会総会プログラム・抄録集   35th   2022

  • p53を抗原とする樹状細胞ワクチンによる前感作はp53武装化ウイルス免疫療法の治療効果を増強する

    山田元彦, 田澤大, 田澤大, 陶守貫人, 菊地覚次, 黒田新士, 野間和広, 浦田泰生, 香川俊輔, 藤原俊義

    日本バイオセラピィ学会学術集会総会プログラム・抄録集   35th   2022

  • 腫瘍融解アデノウイルス製剤の免疫賦活薬としての有用性とICIとの併用治療の可能性

    門脇大輔, 黒田新士, 橋本将志, 垣内慶彦, 菊地覚次, 野間和広, 田澤大, 田澤大, 香川俊輔, 浦田泰生, 藤原俊義

    日本バイオセラピィ学会学術集会総会プログラム・抄録集   35th   2022

  • 免疫抑制環境を誘導するゲムシタビン耐性膵癌に対する新たな複合免疫療法の開発

    田澤大, 梶原義典, 菊地覚次, 黒田新士, 野間和広, 浦田泰生, 香川俊輔, 藤原俊義

    日本バイオセラピィ学会学術集会総会プログラム・抄録集   35th   2022

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  • 胃癌腹膜播種に対する癌関連線維芽細胞を標的としたp53遺伝子治療

    菊地 覚次, 小川 俊博, 田渕 幹康, 光井 恵麻, 宇根 悠太, 田澤 大, 黒田 新士, 野間 和広, 香川 俊輔, 浦田 泰生, 藤原 俊義

    日本癌治療学会学術集会抄録集   59回   O51 - 3   2021.10

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  • 肝内胆管癌におけるNeutrophil Extracellular Traps産生のための血小板の役割

    吉本 匡志, 香川 俊介, 梶原 義典, 藤 智和, 菊池 覚次, 黒田 新士, 吉田 龍一, 楳田 祐三, 田澤 大, 藤原 俊義

    日本癌治療学会学術集会抄録集   59回   O5 - 1   2021.10

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  • がん免疫療法の新展開-がん免疫療法の今後の展望- テロメラーゼ特異的腫瘍融解ウイルス製剤の創薬研究 がん免疫療法との協働

    藤原 俊義, 黒田 新士, 田辺 俊介, 浦田 泰生, 田澤 大

    日本癌治療学会学術集会抄録集   59回   SSY9 - 2   2021.10

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  • これからのハイパーサーミアに向けた研究のトピックス 同所性ヌードマウスモデルにおける腹膜播種に対する磁性体ナノ粒子を用いた温熱療法

    松三 雄騎, 香川 哲也, 矢野 修也, 田澤 大, 重安 邦俊, 武田 正, 大原 利章, 青野 宏通, Hoffman Robert M., 藤原 俊義, 岸本 浩行

    Thermal Medicine   37 ( Suppl. )   S7 - 2   2021.9

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  • 肺転移能を有する骨肉腫細胞はM2様マクロファージへの分化を強力に誘導する

    近藤 宏也, 田澤 大, 久禮 美穂, 藤原 智洋, 国定 俊之, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   80回   [J14 - 4]   2021.9

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  • 腫瘍融解アデノウイルスによる治療機序の次なる一手 細胞外小胞を介して全身免疫賦活と局所細胞毒性を誘発するウイルス療法

    垣内 慶彦, 黒田 新士, 金谷 信彦, 公文 剣斗, 津村 朋子, 橋本 将志, 八木 千晶, 杉本 龍馬, 濱田 侑紀, 菊地 覚次, 西崎 正彦, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   80回   [IS1 - 6]   2021.9

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  • テロメラーゼ特異的腫瘍融解アデノウイルス製剤の免疫賦活剤としての有用性と抗PD-1抗体との相乗効果

    橋本 将志, 黒田 新士, 金谷 信彦, 津村 朋子, 垣内 慶彦, 菊地 覚次, 田澤 大, 香川 俊輔, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   80回   [IS10 - 6]   2021.9

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  • 大腸癌肝転移におけるRNA編集酵素ADAR1発現は肝転移切除後の残肝再発を予測するバイオマーカーになる

    畑 七々子, 重安 邦俊, 高橋 一剛, 梅田 響, 武田 正, 矢野 修也, 楳田 祐三, 田澤 大, 藤原 俊義

    日本分子腫瘍マーカー研究会プログラム・講演抄録   41回   58 - 59   2021.9

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  • これからのハイパーサーミアに向けた研究のトピックス 同所性ヌードマウスモデルにおける腹膜播種に対する磁性体ナノ粒子を用いた温熱療法

    松三 雄騎, 香川 哲也, 矢野 修也, 田澤 大, 重安 邦俊, 武田 正, 大原 利章, 青野 宏通, Hoffman Robert M., 藤原 俊義, 岸本 浩行

    Thermal Medicine   37 ( Suppl. )   S7 - 2   2021.9

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  • 膵臓癌の代謝サブタイプが腫瘍融解アデノウイルスに対する感受性を運命づける

    庄司 良平, 田澤 大, 梶原 義典, 李 云成, 山田 元彦, 井上 弘章, 永井 康雄, 菊地 覚次, 黒田 新士, 吉田 龍一, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   80回   [P14 - 6]   2021.9

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  • Drug repositioningによる新規がん治療の開発に向けて がん関連線維芽細胞由来IL-6の作用と制御

    國友 知義, 野間 和広, 西脇 紀之, 河崎 健人, 小林 照貴, 菊地 覚次, 大原 利章, 田澤 大, 藤原 俊義

    日本癌学会総会記事   80回   [J13 - 3]   2021.9

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  • 腫瘍溶解性ウイルスを介したp53遺伝子治療は胃癌腹膜播種に対する抗腫瘍効果を増強する

    光井 恵麻, 菊地 覚次, 小川 俊博, 田渕 幹康, 宇根 悠太, 田澤 大, 黒田 新士, 野間 和広, 香川 俊輔, 大塚 旬子, 大木 理恵子, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   80回   [E14 - 1]   2021.9

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  • 骨肉腫における腫瘍関連マクロファージの役割とin vitro実験による検証

    近藤 宏也, 田澤 大, 久禮 美穂, 藤原 智洋, 佐藤 浩平, 畑 利彰, 中田 英二, 国定 俊之, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   95 ( 8 )   S1556 - S1556   2021.8

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  • 細胞外小胞がもたらす腫瘍融解アデノウイルス療法の全身性免疫賦活と局所細胞毒性

    垣内 慶彦, 黒田 新士, 津村 朋子, 橋本 将志, 八木 千晶, 杉本 龍馬, 菊地 覚次, 香川 俊輔, 田澤 大, 藤原 俊義

    日本DDS学会学術集会プログラム予稿集   37回   96 - 96   2021.6

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  • 消化管腫瘍に対する内視鏡治療、現況と展望 食道癌に対する腫瘍融解ウイルス併用放射線療法の臨床研究 高リスク症例の治療成績向上を目指して

    田辺 俊介, 野間 和広, 田澤 大, 白川 靖博, 藤原 俊義

    日本消化器内視鏡学会中国支部例会   126回   32 - 32   2021.6

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  • 転移に関わる上皮間葉移行を制御する薬剤スクリーニングシステムの開発と転移予防効果の検討

    岡林 弘樹, 田澤 大, 家田 偉史, 矢野 修也, 菊地 覚次, 黒田 新士, 西崎 正彦, 香川 俊輔, 今村 健志, 藤原 俊義

    日本外科学会定期学術集会抄録集   121回   SF - 3   2021.4

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  • Oncolytic virus-mediated p53 overexpression interrupts tumor-stromal network in pancreatic tumor microenvironment

    Takeyoshi Nishiyama, Hiroshi Tazawa, Yoshinori Kajiwara, Ryohei Shoji, Satoru Kikuchi, Shinji Kuroda, Kazuhiro Noma, Ryuichi Yoshida, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   112   440 - 440   2021.2

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  • Oncolytic virus-mediated p53 gene therapy enhances anti-tumor immunity against peritoneal metastasis of gastric cancer

    Motoyasu Tabuchi, Satoru Kikuchi, Toshihiro Ogawa, Hiroshi Tazawa, Shinji Kuroda, Kazuhiro Noma, Masahiko Nishizaki, Shunsuke Kagawa, Junko Ohtsuka, Rieko Ohki, Yasuo Urata, Toshiyoshi Fujiwara

    CANCER SCIENCE   112   426 - 426   2021.2

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  • Gemcitabine-resistant pancreatic ductal adenocarcinoma cells promote immunosuppressive tumor microenvironment

    Yoshinori Kajiwara, Hiroshi Tazawa, Takeyoshi Nishiyama, Ryohei Shoji, Takuro Fushimi, Satoru Kikuchi, Shinji Kuroda, Kazuhiro Noma, Ryuichi Yoshida, Masahiko Nishizaki, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   112   560 - 560   2021.2

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  • がん関連線維芽細胞由来IL-6制御による免疫応答の効率化バイオマーカーとしてのIL-6の可能性

    西脇 紀之, 野間 和広, 大原 利章, 河崎 健人, 赤井 正明, 小林 照貴, 加藤 卓也, 前田 直見, 菊地 覚次, 田辺 俊介, 田澤 大, 白川 靖博, 藤原 俊義

    日本分子腫瘍マーカー研究会誌   36   32 - 33   2021

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  • Treatment for colorectal liver metastasis: evolving paradigms and future perspectives

    楳田祐三, 田澤大, 矢野修也, 重安邦俊, 神崎洋光, 寺石文則, 黒田新士, 香川俊輔, 八木孝仁, 平沢晃, 岡田裕之, 藤原俊義

    日本がん転移学会学術集会・総会プログラム抄録集   30th   2021

  • p53発現による線維性微小環境の再プログラム化は膵臓癌における腫瘍融解ウイルス療法の治療効果を増強する

    西山 岳芳, 田澤 大, 梶原 義典, 庄司 良平, 永井 康雄, 菊地 覚次, 黒田 新士, 野間 和広, 吉田 龍一, 西崎 正彦, 田中 啓祥, 狩野 光伸, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   80th   [J14 - 4]   2021

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  • フェルカルボトランを用いた胃癌腹膜播種に対する磁気温熱療法

    松三 雄騎, 岸本 浩行, 香川 哲也, 矢野 修也, 重安 邦俊, 岡林 弘樹, 大原 利章, 田澤 大, 藤原 俊義

    日本消化器外科学会総会   75回   P077 - 3   2020.12

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  • 腫瘍融解ウイルスによるp53の発現増強は骨肉腫に対する全身性の抗腫瘍免疫反応を増強する

    近藤 宏也, 田澤 大, 出宮 光二, 久禮 美穂, 望月 雄介, 長谷井 嬢, 國定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   79回   OE14 - 2   2020.10

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  • 好中球と血小板の相互作用が胆管癌の悪性形質転換を促進する

    吉本 匡志, 香川 俊輔, 梶原 義典, 西山 岳芳, 李 云成, 岡林 弘樹, 菊地 覚次, 黒田 新士, 田澤 大, 藤原 俊義

    日本癌学会総会記事   79回   OJ10 - 2   2020.10

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  • エクソソームを用いた革新的治療法 腫瘍融解アデノウイルス局所療法後に産生されるエクソソームはアブスコパル効果を起こす

    垣内 慶彦, 黒田 新士, 金谷 信彦, 公文 剣斗, 津村 朋子, 橋本 将志, 八木 千晶, 杉本 龍馬, 菊地 覚次, 西崎 正彦, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   79回   IS5 - 7   2020.10

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  • ゲムシタビン耐性膵癌細胞は免疫抑制性の微小環境を増強する

    梶原 義典, 田澤 大, 西山 岳芳, 庄司 良平, 伏見 卓郎, 菊地 覚次, 黒田 新士, 野間 和広, 吉田 龍一, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   79回   OJ17 - 6   2020.10

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  • テロメラーゼ特異的腫瘍融解アデノウイルス製剤の併用による抗PD-1抗体治療効果の増強

    橋本 将志, 黒田 新士, 金谷 信彦, 八木 千晶, 津村 朋子, 公文 剣斗, 垣内 慶彦, 菊地 覚次, 田澤 大, 香川 俊輔, 水口 裕之, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   79回   OE12 - 10   2020.10

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  • 腫瘍融解アデノウイルスで治療した腫瘍から得られる細胞外小胞は樹状細胞を活性化する能力を有する

    津村 朋子, 黒田 新士, 金谷 信彦, 垣内 慶彦, 公文 剣斗, 橋本 将志, 八木 千晶, 杉本 龍馬, 菊地 覚次, 西崎 正彦, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   79回   OJ11 - 2   2020.10

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  • リアルタイムイメージングによる予後不良間葉型大腸癌の治療抵抗性EMTマーカーの発現の時空間的意義

    三村 直毅, 矢野 修也, 田澤 大, 家田 偉史, 岡林 弘樹, 重安 邦俊, 武田 正, 吉田 一博, 寺石 文則, 楳田 祐三, 香川 俊輔, 藤原 俊義

    日本分子腫瘍マーカー研究会プログラム・講演抄録   40回   56 - 58   2020.9

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  • 骨肉腫に対するp53誘導性腫瘍融解ウイルスを用いたアブスコパル効果・ワクチン効果の誘導

    出宮 光二, 田澤 大, 近藤 宏也, 久禮 美穂, 長谷井 嬢, 中田 英二, 国定 俊之, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   94 ( 8 )   S1855 - S1855   2020.9

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  • がん関連線維芽細胞由来IL-6制御による免疫応答の効率化バイオマーカーとしてのIL-6の可能性

    西脇 紀之, 野間 和広, 大原 利章, 河崎 健人, 赤井 正明, 小林 照貴, 加藤 卓也, 前田 直見, 菊地 覚次, 田辺 俊介, 田澤 大, 白川 靖博, 藤原 俊義

    日本分子腫瘍マーカー研究会プログラム・講演抄録   40回   72 - 73   2020.9

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  • 肝内胆管癌における免疫微小環境と治療予後の関連性

    小西 大輔, 吉田 一博, 楳田 祐三, 重安 邦俊, 矢野 修也, 武田 正, 吉田 龍一, 杭瀬 崇, 藤 智和, 安井 和也, 松田 達雄, 田澤 大, 白川 靖博, 八木 孝仁, 藤原 俊義

    日本外科学会定期学術集会抄録集   120回   SF - 3   2020.8

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  • Immuno-Oncologyが変えるがん集学的治療【International】テロメラーゼ特異的腫瘍融解アデノウイルス製剤と抗PD-1抗体を併用した集学的免疫療法(Multidisciplinary immunotherapy with telomerase-specific oncolytic adenovirus and anti-PD-1 antibody)

    黒田 新士, 金谷 信彦, 垣内 慶彦, 公文 剣斗, 津村 朋子, 橋本 将志, 菊地 覚次, 西崎 正彦, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本外科学会定期学術集会抄録集   120回   SY - 5   2020.8

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  • 解熱剤のアスピリン投与によるEMT阻害作用を介した大腸がん腹膜播種の抑制効果

    岡林 弘樹, 田澤 大, 家田 偉史, 菊地 覚次, 黒田 新士, 西崎 正彦, 香川 俊輔, 今村 健志, 藤原 俊義

    日本外科学会定期学術集会抄録集   120回   SF - 8   2020.8

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  • 食道癌患者に対する腫瘍融解ウイルスの内視鏡的投与の実際 病棟実施にむけた他部署連携

    矢野 朋美, 采女 典子, 森 隆弘, 笠原 由美子, 石川 貴子, 田辺 俊介, 黒田 新士, 野間 和広, 田澤 大, 香川 俊輔, 白川 靖博, 藤原 俊義

    日本消化器内視鏡技師会会報   ( 64 )   111 - 112   2020.3

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  • Reversible EMT-MET biosensor-mediated imaging visualizes inducible resistance to chemotherapy with hybrid E/M phase

    三村直毅, 矢野修也, 矢野修也, 田澤大, 家田偉史, 岡林大樹, 重安邦俊, 重安邦俊, 武田正, 吉田一博, 寺石文則, 寺石文則, 楳田祐三, 香川俊輔, 香川俊輔, 藤原俊義

    日本癌学会学術総会抄録集(Web)   79th   2020

  • Perspective and prospective of RNA editing in colorectal cancer microenvironme

    武田正, 重安邦俊, 重安邦俊, 小松泰浩, 高橋一剛, 畑七々子, 吉田一博, 矢野修也, 矢野修也, 近藤喜太, 寺石文則, 寺石文則, 楳田祐三, 田澤大, 香川俊輔, 香川俊輔, 藤原俊義

    日本癌学会学術総会抄録集(Web)   79th   2020

  • 癌微小環境が引き起こす腫瘍免疫抑制の解明“Drug repositioning′′による免疫応答賦活化の可能性

    西脇紀之, 野間和広, 赤井正明, 小林照貴, 鳴坂徹, 河本慧, 加藤卓也, 前田直見, 田辺俊介, 大原利章, 田澤大, 白川靖博, 藤原俊義

    日本外科学会定期学術集会(Web)   120th   2020

  • RNA editing activated by chemoradiation therapy artificially generates neoantigen in colorectal cancer

    小松泰浩, 重安邦俊, 重安邦俊, 武田正, 高橋一剛, 畑七々子, 吉田一博, 矢野修也, 矢野修也, 大原利章, 野間和広, 楳田祐三, 黒田新士, 黒田新士, 近藤喜太, 寺石文則, 寺石文則, 田澤大, 香川俊輔, 香川俊輔, 藤原俊義

    日本癌学会学術総会抄録集(Web)   79th   2020

  • Fibroblast activation protein-α(FAP)を標的とした癌関連線維芽細胞(CAFs)に対する光免疫療法~Sunrise of targeting tumor microenvironment therapy~

    小林照貴, 野間和広, 赤井正明, 西脇紀之, 鳴坂徹, 河本慧, 前田直見, 大原利章, 田辺俊介, 田澤大, 白川靖博, 藤原俊義

    日本外科学会定期学術集会(Web)   120th   2020

  • Overcoming cancer-associated fibroblasts induced immunosuppression by blocking IL-6-Exploring for Drug Repositioning-

    西脇紀之, 野間和広, 大原利章, 小林照貴, 菊地覚次, 菊地覚次, 田澤大, 藤原俊義

    日本癌学会学術総会抄録集(Web)   79th   2020

  • 新世代の外科医の苦悩と挑戦

    西脇紀之, 野間和広, 赤井正明, 小林照貴, 鳴坂徹, 河本慧, 大原利章, 田澤大, 藤原俊義

    日本外科学会定期学術集会(Web)   120th   2020

  • Development of novel photoimmunotherapy targeting cancer associated fibroblasts.

    小林照貴, 野間和広, 河崎健人, 赤井正明, 西脇紀之, 大原利章, 田澤大, 藤原俊義

    日本癌学会学術総会抄録集(Web)   79th   2020

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  • Interplay between gastric cancer subtypes and cancer-associated fibroblasts

    李云成, 田澤大, 野間和広, 大原利章, 黒田新士, 黒田新士, 菊地覚次, 菊地覚次, 香川俊輔, 香川俊輔, 藤原俊義

    日本癌学会学術総会抄録集(Web)   79th   2020

  • Overcoming cancer-associated fibroblasts induced immunosuppression by blocking IL-6: Exploring for Drug Repositioning

    西脇紀之, 野間和広, 大原利章, 大原利章, 河崎健人, 赤井正明, 小林照貴, 加藤卓也, 前田直見, 菊地覚次, 田辺俊介, 田澤大, 白川靖博, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   31st   2020

  • A novel photoimmunotherapy for cancer cells and cancer-associated-fibroblasts

    小林照貴, 野間和広, 大原利章, 河崎健人, 赤井正明, 西脇紀之, 前田直見, 菊地覚次, 矢野修也, 田辺俊介, 田澤大, 白川靖博, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   31st   2020

  • 骨肉腫に対する抗PD-1抗体と腫瘍融解アデノウイルスの複合免疫療法

    望月 雄介, 田澤 大, 出宮 光二, 久禮 美穂, 長谷井 嬢, 中田 英二, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   93 ( 8 )   S1672 - S1672   2019.9

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  • 骨肉腫に対するテロメラーゼ特異的腫瘍融解ウイルスを用いた複合免疫療法(Combination immunotherapy with telomerase-specific oncolytic adenovirus for osteosarcoma)

    出宮 光二, 田澤 大, 望月 雄介, 久禮 美穂, 近藤 宏也, 長谷井 嬢, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   78回   J - 1001   2019.9

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  • 骨肉腫に対するp53誘導性腫瘍融解ウイルス療法のアブスコパル効果

    出宮 光二, 田澤 大, 久禮 美穂, 望月 雄介, 長谷井 嬢, 中田 英二, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   93 ( 8 )   S1673 - S1673   2019.9

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  • 鉄キレート剤による幹細胞性制御による新規食道癌治療法(Stemness control by iron chelator is a novel therapeutic strategy for esophageal cancer treatment)

    鳴坂 徹, 大原 利章, 桂 佑貴, 野間 和広, 西脇 紀之, 河本 慧, 田澤 大, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   78回   P - 1077   2019.9

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  • がん関連線維芽細胞(CAFs)による腫瘍免疫抑制のメカニズムについて(Exploring the mechanism of cancer-associated fibroblasts(CAFs) induced immunosuppression in tumor microenvironment)

    西脇 紀之, 野間 和広, 小林 照貴, 鳴坂 徹, 河本 慧, 大原 利章, 田澤 大, 藤原 俊義

    日本癌学会総会記事   78回   P - 3083   2019.9

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  • がん組織の生体イメージング: 現場を押さえろ! 細胞周期の可視化から見えてきた難治性がん細胞の存在と新規治療戦略(In vivo microscopy of cancer tissues: catch the scene! Fluorescence-guided novel therapeutic strategy for therapy-refractory tumor cells identified by cell cycle imaging)

    矢野 修也, 田澤 大, 重安 邦俊, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   78回   IS3 - 5   2019.9

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  • AZIN1 RNA編集は大腸癌微小環境の再構成を促進し癌の進展に寄与する新たなメカニズムである(AZIN1 RNA editing is a novel mechanism that enhances malignant potential of colorectal cancer microenvironment)

    武田 正, 重安 邦俊, 吉田 一博, 母里 淑子, 矢野 修也, 近藤 喜太, 野間 和広, 寺石 文則, 楳田 祐三, 岸本 浩行, 田澤 大, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   78回   E - 2079   2019.9

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  • 化学放射線療法は線維芽細胞の活性化を介して食道癌細胞の悪性度を向上させる(Chemoradiotherapy promotes malignancy of cancer cells via activating fibroblasts in esophageal squamous cell carcinomas)

    河本 慧, 野間 和広, 小林 照貴, 西脇 紀之, 鳴坂 徹, 大原 利章, 田澤 大, 藤原 俊義

    日本癌学会総会記事   78回   E - 1038   2019.9

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  • 神経芽腫に対するp53発現性腫瘍融解アデノウイルスによる免疫原性細胞死の誘導効果(Induction of immunogenic cell death by p53-armed telomerase-specific oncolytic adenovirus in neuroblastoma)

    谷 守通, 田澤 大, 谷本 光隆, 納所 洋, 浦田 泰生, 香川 俊輔, 野田 卓男, 藤原 俊義

    日本癌学会総会記事   78回   P - 1178   2019.9

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  • 消化器外科領域に応用可能な分子レベルの技術開発 標準治療が困難な食道がん患者に対する低侵襲なテロメラーゼ標的型分子治療法の開発(Molecular Technology Development for Gastroenterological Diseases Minimally invasive telomerase-targeted molecular therapy in esophageal cancer patients unfit for standard treatments)

    田澤 大, 田辺 俊介, 野間 和広, 黒田 新士, 香川 俊輔, 浦田 泰生, 白川 靖博, 藤原 俊義

    日本癌学会総会記事   78回   SST6 - 7   2019.9

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  • 腫瘍融解ウイルス療法にて認められるアブスコパル効果と細胞外小胞の関連性についてのリバーストランスレーショナルリサーチ(Reverse translational research with extracellular vesicles for the abscopal effect of oncolytic adenovirotherapy)

    垣内 慶彦, 黒田 新士, 金谷 信彦, 公文 剣斗, 津村 朋子, 橋本 将志, 菊地 覚次, 西崎 正彦, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   78回   E - 3056   2019.9

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  • テロメラーゼ依存性腫瘍融解ウイルスは化学療法抵抗性の膵臓がん細胞を破壊する(Telomerase-specific oncolytic virus eliminates chemoresistant pancreatic ductal adenocarcinoma cells)

    伏見 卓郎, 田澤 大, 荒木 宏之, 西山 岳芳, 菊地 覚次, 黒田 新士, 野間 和広, 吉田 龍一, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   78回   E - 3003   2019.9

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  • 解熱剤のアスピリンはEMT阻害作用を介して大腸がんの腹膜播種を抑制する(Antipyretic aspirin inhibits peritoneal dissemination of colon cancer cells via suppression of EMT)

    岡林 弘樹, 田澤 大, 家田 偉史, 矢野 修也, 菊地 覚次, 黒田 新士, 西崎 正彦, 香川 俊輔, 今村 健志, 藤原 俊義

    日本癌学会総会記事   78回   J - 2032   2019.9

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  • 癌微小環境での胃癌に対するp53武装化腫瘍溶解アデノウイルスの影響(The impact of p53-arming multi-potent oncolytic adenovirus on gastric cancer cells in tumor microenvironment)

    小川 俊博, 菊地 覚次, 石川 亘, 田澤 大, 田渕 幹康, 黒田 新士, 野間 和広, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   78回   J - 2029   2019.9

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  • 膵癌に対する免疫チェックポイント阻害剤を併用したテロメラーゼ特異的腫瘍融解免疫療法(Telomerase-specific oncolytic immunotherapy combined with immune checkpoint inhibitor against pancreatic cancer)

    荒木 宏之, 田澤 大, 金谷 信彦, 伏見 卓郎, 西山 岳芳, 菊地 覚次, 黒田 新士, 吉田 龍一, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   78回   E - 2110   2019.9

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  • Cureを得るためには 好中球細胞外トラップによるEMTを介した消化器癌肝転移促進メカニズムの解明(Aiming to cure cancer Neutrophil extracellular traps promote liver metastasis of gastrointestinal cancer through the induction of EMT)

    梶岡 裕紀, 香川 俊輔, 田澤 大, 伊藤 雅典, 桑田 和也, 菊池 覚次, 黒田 新士, 藤原 俊義

    日本癌学会総会記事   78回   S8 - 5   2019.9

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  • Cureを得るためには ヒト悪性腫瘍に対する集学的腫瘍融解ウイルス療法 現状と次世代の展望(Aiming to cure cancer Multidisciplinary oncolytic virotherapy for human cancer: current status and next-generation perspective)

    藤原 俊義, 田澤 大, 田辺 俊介, 浦田 泰生, 白川 靖博

    日本癌学会総会記事   78回   S8 - 6   2019.9

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  • Activation of AZIN1 RNA editing facilitates and promotes invasive potential of cancer associated fibroblasts in colorectal cancer

    Sho Takeda, Kunitoshi Shigeyasu, Yoshinaga Okugawa, Kazuhiro Yoshida, Yoshiko Mori, Shuya Yano, Kazuhiro Noma, Yuzo Umeda, Yoshitaka Kondo, Hiroyuki Kishimoto, Fuminori Teraishi, Hiroshi Tazawa, Shunsuke Kagawa, Ajay Goel, Toshiyoshi Fujiwara

    CANCER RESEARCH   79 ( 13 )   2019.7

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    DOI: 10.1158/1538-7445.SABCS18-4330

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  • Boosting replication and penetration of telomerase-specific replicative virus by paclitaxel induces synthetic lethality in peritoneal metastasis of gastric cancer

    Toshihiro Ogawa, Satoru Kikuchi, Wataru Ishikawa, Hiroshi Tazawa, Motoyasu Tabuchi, Shinji Kuroda, Kazuhiro Noma, Masahiko Nishizaki, Shunsuke Kagawa, Yasuo Urata, Toshiyoshi Fujiwara

    CANCER RESEARCH   79 ( 13 )   2019.7

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    DOI: 10.1158/1538-7445.SABCS18-2979

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  • Overcoming resistance of conventional therapies by targeting cancer-associated fibroblasts (CAFs) with near-infrared photoimmunotherapy (NIR-PIT)

    Satoshi Komoto, Kazuhiro Noma, Ryoichi Katsube, Takuya Kato, Toshiaki Ohara, Hiroaki Sato, Toru Narusaka, Noriyuki Nisiwaki, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   79 ( 13 )   2019.7

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    DOI: 10.1158/1538-7445.AM2019-LB-310

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  • Sternness control by iron chelator is a novel therapeutic strategy for esophageal cancer

    Toru Narusaka, Toshiaki Ohara, Kazuhiro Noma, Yuki Katsura, Noriyuki Nishiwaki, Motoyasu Tabuchi, Takuro Fushimi, Toshihiro Ogawa, Sho Takeda, Satoshi Komoto, Hiroaki Sato, Satoru Kikuchi, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   79 ( 13 )   2019.7

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    DOI: 10.1158/1538-7445.AM2019-1155

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  • 胃癌腹膜播種に対する新たな治療戦略としての腹腔内ウイルス療法

    石川 亘, 菊地 覚次, 田澤 大, 桑田 和也, 黒田 新士, 野間 和広, 西崎 正彦, 白川 靖博, 香川 俊輔, 藤原 俊義

    日本消化器外科学会総会   74回   RS20 - 1   2019.7

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  • 腫瘍融解ウイルス療法によるエクソソームを介したアブスコパル効果の可能性

    垣内 慶彦, 黒田 新士, 金谷 信彦, 公文 剣斗, 津村 朋子, 菊地 覚次, 香川 俊輔, 田澤 大, 浦田 泰生, 藤原 俊義

    日本DDS学会学術集会プログラム予稿集   35回   140 - 140   2019.6

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  • トラスツズマブ耐性胃癌に対するHER2標的金ナノ粒子製剤の開発

    公文 剣斗, 黒田 新士, 久保田 哲史, 津村 朋子, 垣内 慶彦, 菊地 覚次, 西崎 正彦, 香川 俊輔, 田澤 大, 藤原 俊義

    日本DDS学会学術集会プログラム予稿集   35回   152 - 152   2019.6

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  • 遺伝子改変ウイルスを用いた胃癌腹膜播種に対する腹腔内治療の可能性

    菊地 覚次, 石川 亘, 小川 俊博, 田澤 大, 黒田 新士, 桑田 和也, 西崎 正彦, 香川 俊輔, 白川 靖博, 藤原 俊義

    日本外科学会定期学術集会抄録集   119回   SF - 6   2019.4

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  • Endoscopic intratumoral injection of OBP-301 (telomelysin) with radiotherapy in esophageal cancer patients unfit for standard treatments.

    Shunsuke Tanabe, Hiroshi Tazawa, Nobuhiko Kanaya, Kazuhiro Noma, Shunsuke Kagawa, Shinji Kuroda, Yasuo Urata, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    JOURNAL OF CLINICAL ONCOLOGY   37 ( 4 )   2019.2

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    DOI: 10.1200/JCO.2019.37.4_suppl.130

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  • Fluorescence-guided novel therapeutic strategy for therapy-refractory tumor cells identified by cell cycle imaging

    矢野修也, 矢野修也, 田澤大, 重安邦俊, 香川俊輔, 藤原俊義

    日本癌学会学術総会抄録集(Web)   78th   2019

  • Minimally invasive telomerase-targeted molecular therapy in esophageal cancer patients unfit for standard treatments

    日本癌学会学術総会抄録集(Web)   78th   2019

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  • Visualization of epithelial-mesenchymal transition in inflammatory microenvironment-colorectal cancer crosstalk

    Hiroshi Tazawa, Takeshi Ieda, Shuya Yano, Kunitoshi Shigeyasu, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Hiroyuki Kishimoto, Masahiko Nishizaki, Shunsuke Kagawa, Takashi Saitou, Takeshi Imamura, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   669 - 669   2018.12

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  • Novel virotherapy for scirrhous gastric cancer with peritoneal metastasis

    Wataru Ishikawa, Satoru Kikuchi, Hiroshi Tazawa, Shinji Kuroda, Kazuhiro Noma, Hiroyuki Kishimoto, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   761 - 761   2018.12

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  • Dual-targeting Photoimmunotherapy for esophageal cancer and cancer-associated fibroblasts in tumor microenvironment

    Hiroaki Sato, Kazuhiro Noma, Toru Narusaka, Satoshi Komoto, Toshiaki Ohara, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   371 - 371   2018.12

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  • Near-infrared photoimmunotherapy using anti-GD2 antibody-photosensitizer conjugate for neuroblastoma

    Hiroshi Nouso, Hiroshi Tazawa, Terutaka Tanimoto, Morimochi Tani, Takanori Oyama, Hiroaki Sato, Kazuhiro Noma, Shunsuke Kagawa, Hisataka Kobayashi, Takuo Noda, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   1140 - 1140   2018.12

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  • Stemness control by iron chelator is a novel strategy for cancer treatment

    Toshiaki Ohara, Yuki Katsura, Kazuhiro Noma, Toru Narusaka, Hiroaki Sato, Satoshi Komoto, Takuya Kato, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   1309 - 1309   2018.12

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  • Cancer-associated fibroblasts affect the intra-tumoral infiltration of CD8+and FoxP3+T cells via IL-6

    Takuya Kato, Kazuhiro Noma, Hiroaki Sato, Satoshi Komoto, Toshiaki Ohara, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   1120 - 1120   2018.12

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  • Oncolytic virotherapy for inhibition of epithelial- mesenchymal transition in esophageal cancer

    Tomoya Masuda, Hiroshi Tazawa, Takeshi Ieda, Yuuri Hashimoto, Shunsuke Tanabe, Kazuhiro Noma, Yasuo Urata, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   868 - 868   2018.12

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  • 癌関連線維芽細胞が放出するIL-6が腫瘍内に浸潤するCD8+ならびにFoxP3+T細胞に影響を与える(Cancer-associated fibroblasts affect the intra-tumoral infiltration of CD8+ and FoxP3+ T cells via IL-6)

    加藤 卓也, 野間 和広, 佐藤 浩明, 河本 慧, 大原 利章, 田澤 大, 白川 靖博, 藤原 俊義

    日本癌学会総会記事   77回   1860 - 1860   2018.9

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  • 骨肉腫に対する抗PD-1抗体とテロメラーゼ特異的ウイルス療法による新規治療戦略(Novel therapeutic strategy with anti-PD-1 antibody and telomerase-specific oncolytic virotherapy in osteosarcoma)

    望月 雄介, 田澤 大, 出宮 光二, 小松原 将, 杉生 和久, 長谷井 嬢, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   77回   1813 - 1813   2018.9

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  • p53誘導性腫瘍融解ウイルス療法は骨肉腫に強力な免疫原性細胞死を誘導する(Oncolytic adenoviral therapy with p53 transactivation induces profound immunogenic cell death in osteosarcoma)

    出宮 光二, 田澤 大, 望月 雄介, 小松原 将, 杉生 和久, 長谷井 嬢, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   77回   2251 - 2251   2018.9

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  • 鉄キレート剤の幹細胞性制御による新規癌治療法(Stemness control by iron chelator is a novel strategy for cancer treatment)

    大原 利章, 桂 佑貴, 野間 和広, 鳴坂 徹, 佐藤 浩明, 河本 慧, 加藤 卓也, 田澤 大, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   77回   2318 - 2318   2018.9

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  • 消化管がん治療の新展開 食道癌におけるがん細胞及びがん関連線維芽細胞に対するDual-targeting Photoimmunotherapy(Developments in gastrointestinal cancer treatments Dual-targeting Photoimmunotherapy for esophageal cancer and cancer-associated fibroblasts in tumor microenvironment)

    佐藤 浩明, 野間 和広, 鳴坂 徹, 河本 慧, 大原 利章, 田澤 大, 藤原 俊義

    日本癌学会総会記事   77回   96 - 96   2018.9

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  • 炎症性微小環境-大腸がんクロストークにおけるEMTイメージング(Visualization of epithelial-mesenchymal transition in inflammatory microenvironment-colorectal cancer crosstalk)

    田澤 大, 家田 偉史, 矢野 修也, 重安 邦俊, 黒田 新士, 大原 利章, 野間 和広, 岸本 浩行, 西崎 正彦, 香川 俊輔, 斎藤 卓, 今村 健志, 藤原 俊義

    日本癌学会総会記事   77回   1204 - 1204   2018.9

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  • 神経芽腫に対する抗GD2抗体-光感受性物質結合体を用いた光線免疫療法(Near-infrared photoimmunotherapy using anti-GD2 antibody-photosensitizer conjugate for neuroblastoma)

    納所 洋, 田澤 大, 谷本 光隆, 谷 守通, 尾山 貴徳, 佐藤 浩明, 野間 和広, 香川 俊輔, 小林 久隆, 野田 卓男, 藤原 俊義

    日本癌学会総会記事   77回   1948 - 1948   2018.9

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  • テロメライシンと抗PD-1抗体を用いた新たな複合免疫療法の開発(Telomelysin as an immunotherapy sensitizing gastrointestinal tumors to anti-PD-1 antibody)

    金谷 信彦, 黒田 新士, 公文 剣斗, 垣内 慶彦, 森廣 俊昭, 久保田 哲史, 菊地 覚次, 田澤 大, 西崎 正彦, 香川 俊輔, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   77回   104 - 104   2018.9

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  • 膵癌に対するp53誘導性腫瘍融解ウイルスによる免疫原性細胞死の誘導効果(Oncolytic adenovirus-mediated p53 transactivation induces profound immunogenic cell death in pancreatic cancer)

    荒木 宏之, 田澤 大, 伏見 卓郎, 金谷 信彦, 菊地 覚次, 黒田 新士, 吉田 龍一, 岸本 浩行, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   77回   949 - 949   2018.9

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  • 腹膜播種を伴うスキルス胃癌に対する斬新なウイルス療法(Novel virotherapy for scirrhous gastric cancer with peritoneal metastasis)

    石川 亘, 菊地 覚次, 田澤 大, 黒田 新士, 野間 和広, 岸本 浩行, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   77回   952 - 952   2018.9

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  • 腹腔内マクロファージはIL6を分泌し胃癌腹膜播種を促進する(IL6 derived from intraperitoneal macrophages is involved in peritoneal dissemination of gastric cancer)

    香川 俊輔, 坂本 修一, 桑田 和也, 伊藤 雅典, 梶岡 裕紀, 黒田 新士, 菊地 覚次, 吉田 龍一, 田澤 大, 藤原 俊義

    日本癌学会総会記事   77回   1020 - 1020   2018.9

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  • 胃癌由来細胞外小胞によるマクロファージ分化誘導を介した腹膜播種の促進(Extracellular vesicles from gastric cancer promote peritoneal dissemination via M2 differentiation of macrophages)

    伊藤 雅典, 香川 俊輔, 梶岡 裕紀, 坂本 修一, クワ田 和也, 菊地 覚次, 黒田 新士, 西崎 正彦, 吉田 龍一, 田澤 大, 藤原 俊義

    日本癌学会総会記事   77回   1021 - 1021   2018.9

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  • 癌関連線維芽細胞が引き起こす腫瘍免疫抑制の解明 腫瘍浸潤リンパ球とIL-6と代謝の観点から

    加藤 卓也, 野間 和広, 賀島 肇, 桂 佑貴, 佐藤 浩明, 河本 慧, 二宮 卓之, 大原 利章, 田澤 大, 白川 靖博, 稲垣 優, 岩垣 博巳, 藤原 俊義

    日本がん免疫学会総会プログラム・抄録集   22回   95 - 95   2018.7

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  • Novel theranostic strategy against peritoneal metastasis of scirrhous gastric cancer: Combination with fluorescence oncolytic adenovirus and chemotherapy

    Wataru Ishikawa, Satoru Kikuchi, Hiroshi Tazawa, Toshiaki Ohara, Shinji Kuroda, Kazuhiro Noma, Hiroyuki Kishimoto, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   78 ( 13 )   2018.7

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    DOI: 10.1158/1538-7445.AM2018-4807

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  • Visualization of epithelial-mesenchymal transition in inflammatory microenvironment-colorectal cancer network in vitro and in vivo

    Hiroshi Tazawa, Takeshi Ieda, Shuya Yano, Satoru Kikuchi, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Hiroyuki Kishimoto, Masahiko Nishizaki, Shunsuke Kagawa, Takashi Saitou, Takeshi Imamura, Toshiyoshi Fujiwara

    CANCER RESEARCH   78 ( 13 )   2018.7

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    DOI: 10.1158/1538-7445.AM2018-1101

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  • Iron depletion suppress the stemness markers and functions of cancer stem cells

    Toshiaki Ohara, Yuki Katsura, Kazuhiro Noma, Toru Narusaka, Takuya Kato, Hiroaki Sato, Satoshi Komoto, Yasuko Tomono, Takayuki Ninomiya, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   78 ( 13 )   2018.7

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    DOI: 10.1158/1538-7445.AM2018-LB-045

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  • Dual-targeting photoimmunotherapy (NIR-PIT) for esophageal cancer cells and cancer-associated fibroblasts (CAFs)

    Hiroaki Sato, Kazuhiro Noma, Toru Narusaka, Satoshi Komoto, Yuki Katsura, Takuya Kato, Takayuki Ninomiya, Toshiaki Ohara, Hiroshi Tazawa, Yasuhiro Shirakawa, Hisataka Kobayashi, Toshiyoshi Fujiwara

    CANCER RESEARCH   78 ( 13 )   2018.7

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    DOI: 10.1158/1538-7445.AM2018-5066

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  • Development of near-infrared photoimmunotherapy targeting GD2-positive neuroblastoma

    Hiroshi Nouso, Hiroshi Tazawa, Terutaka Tanimoto, Morimichi Tani, Takanori Oyama, Hiroaki Sato, Kazuhiro Noma, Shunsuke Kagawa, Hisataka Kobayashi, Takuo Noda, Toshiyoshi Fujiwara

    CANCER RESEARCH   78 ( 13 )   2018.7

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    DOI: 10.1158/1538-7445.AM2018-3831

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  • Cancer-associated fibroblasts regulate intratumoral CD8(+)/FoxP3(+) T cells via interleukin 6 in the tumor immune microenvironment

    Takuya Kato, Kazuhiro Noma, Yuki Katsura, Hiroaki Sato, Satoshi Kohmoto, Toshiaki Ohara, Hiroshi Tazawa, Yasuhiro Shirakawa, Masaru Inagaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   78 ( 13 )   2018.7

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    DOI: 10.1158/1538-7445.AM2018-1741

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  • Transforming growth factor-b-induced epithelial-mesenchymal transition is attenuated by telomerase-specific oncolytic virotherapy in human esophageal cancer

    Tomoya Masuda, Hiroshi Tazawa, Takeshi Ieda, Yuuri Hashimoto, Shunsuke Tanabe, Kazuhiro Noma, Yasuo Urata, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   78 ( 13 )   2018.7

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    DOI: 10.1158/1538-7445.AM2018-2033

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  • 免疫原性がん細胞死を誘導するウイルス製剤と抗PD-1抗体を併用する新たな複合免疫療法の開発

    金谷 信彦, 黒田 新士, 森廣 俊昭, 垣内 慶彦, 菊地 覚次, 西崎 正彦, 浦田 泰生, 田澤 大, 香川 俊輔, 藤原 俊義

    日本消化器外科学会総会   73回   544 - 544   2018.7

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  • 胃癌腹膜播種に対する新たな治療戦略としてのウイルス療法

    石川 亘, 菊地 覚次, 田澤 大, 桑田 和也, 黒田 新士, 野間 和広, 西崎 正彦, 白川 靖博, 香川 俊輔, 藤原 俊義

    日本消化器外科学会総会   73回   1005 - 1005   2018.7

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  • 消化管腫瘍において免疫原性telomelysinは抗PD-1抗体と協働作用する(Immunogenic Telomelysin synergizes with anti-PD-1 antibody in gastrointestinal tumors)

    金谷 信彦, 黒田 新士, 公文 剣斗, 垣内 慶彦, 森廣 俊昭, 久保田 哲史, 菊地 覚次, 西崎 正彦, 浦田 泰生, 田澤 大, 香川 俊輔, 藤原 俊義

    日本がん免疫学会総会プログラム・抄録集   22回   89 - 89   2018.7

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  • 化学放射線療法の現状と新たなる展望〜制癌剤と照射法の工夫〜 腫瘍融解ウイルス併用放射線療法の臨床研究の中間報告

    田辺 俊介, 白川 靖博, 前田 直見, 二宮 卓之, 黒田 新士, 野間 和広, 田澤 大, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本食道学会学術集会プログラム・抄録集   72回   59 - 59   2018.6

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  • ステルス効果を有する腫瘍融解アデノウイルス搭載リポソーム製剤の開発

    垣内 慶彦, 青山 克幸, 黒田 新士, 金谷 信彦, 菊地 覚次, 西崎 正彦, 香川 俊輔, 田澤 大, 藤原 俊義

    日本DDS学会学術集会プログラム予稿集   34回   145 - 145   2018.5

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  • 神経芽腫に対する腫瘍融解ウイルス療法の研究を通して感じた、基礎研究の楽しさ・難しさ

    谷本 光隆, 田澤 大, 納所 洋, 尾山 貴徳, 谷 守通, 野田 卓男, 藤原 俊義

    日本小児外科学会雑誌   54 ( 3 )   640 - 640   2018.5

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  • 外科学の新知見(2)がんの早期診断に向けて がん特異的蛍光ウイルス製剤を用いた簡便な循環がん細胞(CTC)の遺伝子プロファイリング技術の開発

    重安 邦俊, 田澤 大, 橋本 悠里, 母里 淑子, 西崎 正彦, 岸本 浩行, 永坂 岳司, 黒田 新士, 香川 俊輔, 藤原 俊義

    日本外科学会定期学術集会抄録集   118回   282 - 282   2018.4

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  • 腫瘍融解ウイルス併用放射線療法による食道癌治療成績向上への取り組み

    田辺 俊介, 白川 靖博, 前田 直見, 二宮 卓之, 黒田 新士, 野間 和広, 楳田 祐三, 田澤 大, 香川 俊輔, 藤原 俊義

    日本外科学会定期学術集会抄録集   118回   944 - 944   2018.4

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  • Molecular radiosensitization of p53-armed telomerase-dependent oncolytic adenovirus against human soft-tissue sarcoma

    Tadashi Komatsubara, Hiroshi Tazawa, Yusuke Mochizuki, Kazuhisa Sugiu, Toshinori Omori, Yasuaki Yamakawa, Syuhei Osaki, Joe Hasei, Tomohiro Fujiwara, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   454 - 454   2018.1

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  • Novel evidence for AZIN1 RNA editing-mediated oncogenic role in colorectal cancer

    Kunitoshi Shigeyasu, Sho Takeda, Yoshinaga Okugawa, Yuji Toiyama, Takeshi Nagasaka, Hiroshi Tazawa, Shunsuke Kagawa, Ajay Goel, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   529 - 529   2018.1

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  • Focusing on the antitumor effect of iron chelator, specifically suppressing the stemness of cancer stem cell.

    Yuki Katsura, Toshiaki Ohara, Hajime Kashima, Hiroaki Sato, Takuya Kato, Takayuki Ninomiya, Kazuhiro Noma, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   87 - 87   2018.1

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  • Novel theranostic strategy: combination of fluorescence oncolytic virus and chemotherapy for scirrhous gastric cancer

    Wataru Ishikawa, Satoru Kikuchi, Hiroshi Tazawa, Shinji Kuroda, Kazuhiro Noma, Hiroyuki Kishimoto, Takeshi Nagasaka, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   912 - 912   2018.1

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  • Cancer-associated fibroblasts (CAFs) promote to tumor immunosuppression via IL-6 secretion.

    Takuya Kato, Kazuhiro Noma, Hajime Kashima, Yuki Katsura, Hiroaki Sato, Takayuki Ninomiya, Toshiaki Ohara, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   299 - 299   2018.1

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  • Fluorescence-guided live cell imaging system of EMT-tumor microenvironment network in gastrointestinal cancer

    Takeshi Ieda, Hiroshi Tazawa, Satoru Kikuchi, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Hiroyuki Kishimoto, Takeshi Nagasaka, Masahiko Nishizaki, Shunsuke Kagawa, Takeshi Imamura, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   557 - 557   2018.1

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  • Liposomally formulated indocyanine green derivative encapsulating anticancer drugs for photoinduced immunotherapy

    Tetsuya Kagawa, Hiroyuki Kishimoto, Yuki Matsumi, Hiroshi Tazawa, Toshiaki Ohara, Takeshi Nagasaka, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER SCIENCE   109   755 - 755   2018.1

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  • 食道癌におけるがん細胞及びがん関連線維芽細胞に対するDual-targeting Photoimmunotherapy

    佐藤浩明, 野間和宏, 鳴坂徹, 河本慧, 大原利章, 田澤大, 白川靖博, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   29th   2018

  • 鉄キレート剤の幹細胞性制御による新規癌治療法の確立

    大原利章, 桂佑貴, 野間和広, 鳴坂徹, 二宮卓之, 友野靖子, 田澤大, 香川俊輔, 白川靖博, 松川昭博, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   29th   2018

  • 軟部肉腫に対するp53発現腫瘍融解アデノウイルスによるアポトーシス抑制遺伝子発現の制御を介した放射線感受性増感作用の検討

    小松原将, 出宮光二, 望月雄介, 長谷井嬢, 吉田晶, 中田英二, 国定俊之, 浦田泰生, 田澤大, 藤原俊義, 尾崎敏文

    日本整形外科学会雑誌   92 ( 8 )   2018

  • 骨肉腫に対するp53誘導性腫瘍融解ウイルス療法による免疫原性細胞死の誘導効果

    出宮光二, 田澤大, 田澤大, 望月雄介, 小松原将, 長谷井嬢, 中田英二, 国定俊之, 浦田泰生, 藤原俊義, 尾崎敏文

    日本整形外科学会雑誌   92 ( 8 )   2018

  • 骨肉腫におけるテロメラーゼ特異的腫瘍融解ウイルスと抗PD-1抗体を用いた複合免疫療法

    望月雄介, 田澤大, 出宮光二, 小松原将, 長谷井嬢, 中田英二, 国定俊之, 浦田泰生, 藤原俊儀, 尾崎敏文

    日本整形外科学会雑誌   92 ( 6 )   2018

  • 食道癌患者に対する腫瘍融解ウイルスの内視鏡的投与の実際-感染対策の取り組み-

    矢野朋美, 采女典子, 森隆弘, 笠原由美子, 田辺俊介, 黒田新士, 野間和広, 田澤大, 香川俊輔, 白川靖博, 藤原俊義

    日本消化器内視鏡技師学会プログラム・講演抄録   81st   2018

  • Novel therapeutic strategy for human epidermal growth factor receptor 2-positive gastric cancer

    Nobuhiko Kanaya, Shinji Kuroda, Tetsushi Kubota, Toshiaki Morihiro, Satoru Kikuchi, Masahiko Nishizaki, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Japanese Journal of Cancer and Chemotherapy   44 ( 10 )   883 - 885   2017.10

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  • 抗体結合磁性ナノ粒子による温熱療法 癌播種病変への治療応用へ向けて

    香川 哲也, 岸本 浩行, 松三 雄騎, 田澤 大, 大原 利章, 永坂 岳司, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   76回   P - 2368   2017.9

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  • 癌関連線維芽細胞(CAFs)により放出されるIL-6が腫瘍免疫抑制を引き起こす

    加藤 卓也, 野間 和広, 賀島 肇, 桂 佑貴, 佐藤 浩明, 二宮 卓之, 大原 利章, 田澤 大, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   76回   P - 1260   2017.9

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  • バイオイメージングの創薬、診断、治療への展開 EMT-がん微小環境ネットワークの蛍光生細胞イメージングシステム

    家田 偉史, 田澤 大, 菊地 覚次, 黒田 新士, 大原 利章, 野間 和広, 岸本 浩行, 永坂 岳司, 西崎 正彦, 香川 俊輔, 今村 健志, 藤原 俊義

    日本癌学会総会記事   76回   S15 - 7   2017.9

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  • 大腸癌におけるAZIN1のRNA編集に関する新しい知見

    重安 邦俊, 武田 正, 奥川 喜永, 問山 裕二, 永坂 岳司, 田澤 大, 香川 俊輔, Goel Ajay, 藤原 俊義

    日本癌学会総会記事   76回   E - 2079   2017.9

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  • 鉄キレート剤特異的な腫瘍幹細胞性抑制効果の検討

    桂 佑貴, 大原 利章, 賀島 肇, 佐藤 浩明, 加藤 卓也, 二宮 卓之, 野間 和広, 友野 靖子, 田澤 大, 香川 俊輔, 白川 靖博, 藤原 俊義

    日本癌学会総会記事   76回   E - 1014   2017.9

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  • 胃癌患者の腹腔内マクロファージは分化し胃癌細胞の悪性形質を促進する

    坂本 修一, 香川 俊輔, 桑田 和也, 伊藤 雅典, 菊地 覚次, 黒田 新士, 吉田 龍一, 浦田 泰生, 田澤 大, 藤原 俊義

    日本癌学会総会記事   76回   P - 3225   2017.9

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  • 軟部肉腫に対するp53発現テロメラーゼ依存型腫瘍融解アデノウイルスの放射線効果増強

    小松原 将, 田澤 大, 望月 雄介, 杉生 和久, 大森 敏規, 山川 泰明, 尾崎 修平, 長谷井 嬢, 藤原 智洋, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   76回   J - 2008   2017.9

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  • 新規光線力学療法としての蛍光タンパク質KillerRed誘導腫瘍融解ウイルスのin vivo抗腫瘍効果

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    日本癌学会総会記事   76回   P - 3386   2017.9

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  • がん個別化医療の革新を目指す新規治療戦略 がんの脆弱性 MYNC増幅神経芽細胞腫のMYCN依存性を標的とするテロメラーゼ特異的腫瘍融解アデノウイルス療法

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    日本癌学会総会記事   76回   S18 - 4   2017.9

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  • スキルス胃癌に対する蛍光発現腫瘍融解ウイルスと化学療法の併用による新たな診断的治療戦略

    石川 亘, 菊地 覚次, 田澤 大, 黒田 新士, 野間 和広, 岸本 浩行, 永坂 岳司, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   76回   E - 3031   2017.9

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  • 抗PD-1抗体の新たな治療戦略 腫瘍選択的融解アデノウイルス療法との相乗効果の可能性

    金谷 信彦, 黒田 新士, 森廣 俊昭, 久保田 哲史, 田澤 大, 菊地 覚次, 西崎 正彦, 香川 俊輔, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   76回   P - 3178   2017.9

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  • ドキソルビシン耐性骨肉腫細胞に対するp53発現腫瘍融解アデノウイルスによるMDR1発現抑制を介した薬剤耐性克服機序の検討

    杉生 和久, 田澤 大, 望月 雄介, 小松原 将, 大森 敏規, 山川 泰明, 吉田 晶, 長谷井 嬢, 藤原 智洋, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   91 ( 8 )   S1523 - S1523   2017.8

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  • p53発現腫瘍融解アデノウイルスによる軟部肉腫に対する放射線治療併用効果の検討

    小松原 将, 望月 雄介, 杉生 和久, 大森 敏規, 長谷井 嬢, 吉田 晶, 藤原 智洋, 国定 俊之, 浦田 泰生, 田澤 大, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   91 ( 8 )   S1499 - S1499   2017.8

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  • Hyperthermia at the single-cell level for disseminated cancer disease with immuno-magnetic nanoparticles

    Tetsuya Kagawa, Hiroyuki Kishimoto, Toshiaki Ohara, Hiroshi Tazawa, Shunsuke Kagawa, Takeshi Nagasaka, Satoshi Nohara, Ichiro Kato, Adarsh Sandhu, Hiromichi Aono, Toshiyoshi Fujiwara

    American Association for Cancer Research   77 ( 13 )   2017.7

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  • 臨床応用を目指した消化器外科領域の基礎研究・橋渡し研究 膵癌に対するテロメラーゼ特異的腫瘍融解ウイルス療法

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    日本消化器外科学会総会   72回   WS14 - 8   2017.7

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  • Gene expression profiles in BRAF V600E mutant colorectal cancer and association with SFRP2 methylation status

    Kazuya Yasui, Takeshi Nagasaka, Toshiaki Toshima, Takashi Kawai, Kunitoshi Shigeyasu, Yoshiko Mori, Junko Haraga, Keiichiro Nakamura, Yuzo Umeda, Hiroshi Tazawa, Ajay Goel, Toshiyoshi Fujiwara

    CANCER RESEARCH   77   2017.7

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    DOI: 10.1158/1538-7445.AM2017-5711

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  • Tumorigenesis of murine iPS cell is prevented by iron depletion with downregulation of stemness markers

    Yuki Katsura, Toshiaki Ohara, Hajime Kashima, Hiroaki Sato, Takuya Kato, Takayuki Ninomiya, Kazuhiro Noma, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   77   2017.7

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    DOI: 10.1158/1538-7445.AM2017-925

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  • Cancer associated fibroblasts promote tumor metastasis coexisting with cancer cells in blood circulation

    Hajime Kashima, Kazuhiro Noma, Hiroaki Sato, Yuki Katsura, Takuya Kato, Toshiaki Ohara, Hiroshi Tazawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   77   2017.7

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    DOI: 10.1158/1538-7445.AM2017-5905

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  • Fluorescence-guided spatiotemporal dynamics of epithelial-mesenchymal transition under inflammatory microenvironment during colorectal cancer progression

    Takeshi Ieda, Hiroshi Tazawa, Satoru Kikuchi, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Hiroyuki Kishimoto, Takeshi Nagasaka, Masahiko Nishizaki, Shunsuke Kagawa, Takeshi Imamura, Toshiyoshi Fujiwara

    CANCER RESEARCH   77   2017.7

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    DOI: 10.1158/1538-7445.AM2017-5809

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  • Novel theranostic strategy against scirrhous gastric cancer; combination of chemotherapy and fluorescence oncolytic adenovirus

    Wataru Ishikawa, Satoru Kikuchi, Hiroshi Tazawa, Shinji Kuroda, Kazuhiro Noma, Hiroyuki Kishimoto, Takeshi Nagasaka, Masahiko Nishizaki, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   77   2017.7

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    DOI: 10.1158/1538-7445.AM2017-1103

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  • 消化器癌腹膜播種の病態解明と新たな治療戦略 腹腔内腫瘍微小環境におけるマクロファージの消化器癌悪性形質への影響

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    日本消化器外科学会総会   72回   WS03 - 7   2017.7

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  • 癌細胞内特異的蛍光発現製剤による浸潤部の蛍光標識と殺細胞性を兼ね備えた高精度な低侵襲手術の開発

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    日本消化器外科学会総会   72回   RS1 - 3   2017.7

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  • Hyperthermia at the single-cell level for disseminated cancer disease with immuno-magnetic nanoparticles

    Tetsuya Kagawa, Hiroyuki Kishimoto, Toshiaki Ohara, Hiroshi Tazawa, Shunsuke Kagawa, Takeshi Nagasaka, Satoshi Nohara, Ichiro Kato, Adarsh Sandhu, Hiromichi Aono, Toshiyoshi Fujiwara

    CANCER RESEARCH   77   2017.7

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    DOI: 10.1158/1538-7445.AM2017-3101

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  • 食道癌に対する化学療法の新しい展望 標準的治療困難な食道癌症例に対する放射線併用ウイルス療法臨床研究の中間報告

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    日本食道学会学術集会プログラム・抄録集   71回   W2 - 3   2017.6

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  • p53発現腫瘍融解アデノウイルスの薬剤耐性骨肉腫細胞に対する抗腫瘍効果と耐性克服メカニズムの検討

    杉生 和久, 田澤 大, 望月 雄介, 小松原 将, 大森 敏規, 山川 泰明, 吉田 晶, 長谷井 嬢, 藤原 智洋, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   91 ( 6 )   S1385 - S1385   2017.6

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  • 軟部肉腫に対する腫瘍融解アデノウイルスによる放射線治療増感効果の検討

    小松原 将, 大森 敏規, 望月 雄介, 杉生 和久, 長谷井 嬢, 吉田 晶, 藤原 智洋, 国定 俊之, 浦田 泰生, 田澤 大, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   91 ( 6 )   S1385 - S1385   2017.6

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  • テロメラーゼ標的蛍光発現ウイルスを用いた膵癌腹腔内微小環境の解析

    桑田 和也, 香川 俊輔, 坂本 修一, 渡邉 めぐみ, 香川 哲也, 菊地 寛次, 黒田 新士, 吉田 龍一, 浦田 泰生, 田澤 大, 藤原 俊義

    日本外科学会定期学術集会抄録集   117回   SF - 1   2017.4

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  • Trastuzumab抵抗性胃癌に対する金ナノ技術を融合した新規HER2標的抗体療法

    久保田 哲史, 黒田 新士, 金谷 信彦, 森廣 俊昭, 田澤 大, 香川 俊輔, 藤原 俊義

    日本外科学会定期学術集会抄録集   117回   SF - 4   2017.4

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  • 胃癌における組織型とPD-L1発現の患者予後および術後再発予測因子としての有用性

    黒田 新士, 森廣 俊昭, 久保田 哲史, 金谷 信彦, 菊地 覚次, 田澤 大, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本外科学会定期学術集会抄録集   117回   SF - 4   2017.4

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  • 癌関連線維芽細胞は食道癌のリンパ節転移を促進するか~臨床検体の解析と同所移植モデルを用いた検証~

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    日本がん転移学会学術集会・総会プログラム抄録集   26th   2017

  • Real-time in-vivo image-guided cell-cycle perturbation to increase tumor chemosensitivity

    Shuya Yano, Hiroshi Tazawa, Hiroyuki Kishimoto, Shunsuke Kagawa, Yoshihiko Kadowaki, Nobuhiro Ishido, Takahiro Okamoto, Yasuo Urata, Kiyoto Takehara, Robert M. Hoffman, Toshiyoshi Fujiwara

    MOLECULAR CANCER RESEARCH   14   2016.11

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    DOI: 10.1158/1557-3125.CELLCYCLE16-PR14

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  • 高リスク神経芽腫に対するhTERT標的化膿瘍融解ウイルス療法(hTERT-targeted oncolytic virotherapy against high-risk neuroblastomas)

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    日本小児血液・がん学会雑誌   53 ( 4 )   202 - 202   2016.11

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  • Novel HER2-Targeted therapy combined with gold nanoparticles

    Tetsushi Kubota, Shinji Kuroda, Toshiaki Morihiro, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    Japanese Journal of Cancer and Chemotherapy   43 ( 10 )   1237 - 1239   2016.10

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  • p53活性化能を有するテロメラーゼ標的型ウイルス療法による腹腔内胃癌微小環境の浄化作用

    田澤 大, 堀 直人, 國府島 健, 谷本 光隆, 家田 偉史, 渡邉 めぐみ, 黒田 新士, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   75回   E - 2069   2016.10

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  • 食道癌において癌関連繊維芽細胞が腫瘍転移に及ぼす影響の検証

    賀島 肇, 野間 和広, 桂 佑貴, 加藤 卓也, 勝部 亮一, 二宮 卓之, 大原 利章, 田澤 大, 香川 俊輔, 白川 靖博, 藤原 俊義

    日本癌学会総会記事   75回   P - 3151   2016.10

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  • 癌関連線維芽細胞(CAFs)が及ぼす腫瘍免疫逃避の解明 CAFsと腫瘍浸潤リンパ球の検討

    加藤 卓也, 野間 和広, 賀島 肇, 桂 佑貴, 二宮 卓之, 大原 利章, 田澤 大, 香川 俊輔, 白川 靖博, 藤原 俊義

    日本癌学会総会記事   75回   E - 1068   2016.10

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  • 鉄代謝は癌幹細胞の新規治療ターゲットとなり得る

    大原 利章, 二宮 卓之, 桂 佑貴, 賀島 肇, 加藤 卓也, 野間 和広, 田澤 大, 藤原 俊義

    日本癌学会総会記事   75回   E - 1109   2016.10

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  • 炎症性微小環境によって誘導されるEMTの蛍光生細胞イメージングシステム

    家田 偉史, 田澤 大, 菊地 覚次, 黒田 新士, 大原 利章, 野間 和広, 岸本 浩行, 永坂 岳司, 西崎 正彦, 香川 俊輔, 今村 健志, 藤原 俊義

    日本癌学会総会記事   75回   J - 3053   2016.10

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  • 抗体結合磁性ナノ粒子による腫瘍選択的な細胞内温熱療法の開発

    香川 哲也, 岸本 浩行, 田澤 大, 大原 利章, 永坂 岳司, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   75回   P - 3307   2016.10

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  • ウイルスによる遺伝子導入は抗原陰性胃癌に対する光線免疫療法を可能にする

    香川 俊輔, 石田 道拡, 下山 京子, 竹原 清人, 野間 和広, 田辺 俊介, 白川 靖博, 田澤 大, 小林 久隆, 藤原 俊義

    日本癌学会総会記事   75回   E - 2094   2016.10

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  • 胃癌根治切除後におけるPD-L1発現に基づいた予後および再発パターンの予測

    森廣 俊昭, 黒田 新士, 久保田 哲史, 田澤 大, 菊地 覚次, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   75回   E - 3064   2016.10

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  • 蛍光ウイルスによる腹腔内の腫瘍関連マクロファージと膵癌細胞の関連性の解析

    桑田 和也, 香川 俊輔, 坂本 修一, 渡邉 めぐみ, 香川 哲也, 菊地 覚次, 黒田 新士, 吉田 龍一, 浦田 泰生, 田澤 大, 藤原 俊義

    日本癌学会総会記事   75回   P - 1320   2016.10

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  • 腫瘍融解ウイルス療法による骨肉腫のABC Transporterを介した薬剤耐性の克服

    杉生 和久, 田澤 大, 長谷井 嬢, 尾崎 修平, 山川 泰明, 大森 敏規, 小松原 将, 望月 雄介, 藤原 智洋, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   75回   J - 3020   2016.10

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  • 軟部肉腫に対するテロメラーゼ標的型腫瘍融解アデノウイルスの放射線効果増強

    小松原 将, 大森 敏規, 田澤 大, 杉生 和久, 望月 雄介, 山川 泰明, 尾崎 修平, 長谷井 嬢, 藤原 智洋, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   75回   P - 3306   2016.10

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  • 高悪性度神経芽細胞種に対するhTERT標的型腫瘍融解ウイルス療法の抗腫瘍活性

    谷本 光隆, 田澤 大, 家田 偉史, 納所 洋, 尾山 貴徳, 浦田 泰生, 香川 俊輔, 野田 卓男, 藤原 俊義

    日本癌学会総会記事   75回   P - 2312   2016.10

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  • p53発現腫瘍融解アデノウイルスはMDR-1発現を抑制することにより薬剤耐性骨肉腫細胞に対して強力な抗腫瘍効果を示す

    杉生 和久, 望月 雄介, 小松原 将, 大森 敏規, 山川 泰明, 吉田 晶, 長谷井 嬢, 藤原 智洋, 国定 俊之, 田澤 大, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   90 ( 8 )   S1554 - S1554   2016.8

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  • 放射線抵抗性を示す骨・軟部肉腫に対する腫瘍融解アデノウイルスの放射線増感作用

    大森 敏規, 山川 泰明, 長谷井 嬢, 田澤 大, 尾崎 修平, 杉生 和久, 藤原 智洋, 吉田 晶, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   90 ( 8 )   S1564 - S1564   2016.8

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  • Iron control is a novel therapeutic target of cancer stem cells

    Toshiaki Ohara, Takayuki Ninomiya, Kazuhiro Noma, Hajime Kashima, Yuki Katsura, Takuya Kato, Yasuko Tomono, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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    DOI: 10.1158/1538-7445.AM2016-2510

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  • A novel circulating cell free DNA-based assay in colorectal cancer patients during treatment with systematic chemotherapy

    Toshiaki Toshima, Takeshi Nagasaka, Yoshiko Mori, Takashi Kawai, Tomokazu Fuji, Fumitaka Taniguchi, Keisuke Kimura, Kazuya Yasui, Hiroyuki Kishimoto, Yuzo Umeda, Hiroshi Tazawa, Ajay Goel, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • Tumor suppressor p53 reactivation by oncolytic adenovirus reverses chemoresistance in human osteosarcomas

    Kazuhisa Sugiu, Hiroshi Tazawa, Joe Hasei, Shuhei Osaki, Yasuaki Yamakawa, Toshinori Omori, Tadashi Komatsubara, Kouji Uotani, Tomohiro Fujiwara, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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    DOI: 10.1158/1538-7445.AM2016-4677

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  • Suppression of MYCN-driven neuroblastoma malignant phenotype by telomerasetargeted tumor suppressor p53 transactivation

    Terutaka Tanimoto, Hiroshi Tazawa, Hiroshi Noso, Takanori Oyama, Yasuo Urata, Shunsuke Kagawa, Takuo Noda, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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    DOI: 10.1158/1538-7445.AM2016-2448

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  • Micro RNAs as promising therapeutic targets for anti-metastatic therapy in colorectal cancer

    Takashi Kawai, Takeshi Nagasaka, Yoshiko Mori, Tomokazu Fuji, Fumitaka Taniguchi, Keisuke Kimura, Toshiaki Toshima, Kazuya Yasui, Yuzo Umeda, Hiroshi Tazawa, Ajay Goel, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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    DOI: 10.1158/1538-7445.AM2016-1078

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  • Functional analysis of tumor associated macrophage utilizing virus-guided fluorescent imaging of pancreatic cancer cells in the peritoneal cavity

    Kazuya Kuwada, Shunsuke Kagawa, Megumi Watanabe, Shuichi Sakamoto, Satoru Kikuchi, Shinji Kuroda, Ryuichi Yoshida, Hiroshi Tazawa, Tetuya Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • Correlation of FAP(fibroblast activation protein)-expressing cancer associated fibroblasts (CAFs) and tumor metastasis in esophageal carcinoma

    Hajime Kashima, Kazuhiro Noma, Yuki Katsura, Takuya Kato, Ryoichi Katsube, Takayuki Ninomiya, Toshiaki Ohara, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • Virally enhanced p53 reactivation impairs KRAS-driven pancreatic cancer invasion

    Takeshi Koujima, Hiroshi Tazawa, Takeshi Leda, Kazuya Kuwada, Terutaka Tanimoto, Shinji Kuroda, Hiroyuki Kishimoto, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • A novel live imaging system for inflammation-induced epithelial-mesenchymal transition in colorectal cancers

    Takeshi Ieda, Hiroshi Tazawa, Satoru Kikuchi, Shinji Kuroda, Toshiaki Ohara, Kazuhiro Noma, Hiroyuki Kishimoto, Takeshi Nagasaka, Masahiko Nishizaki, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • Prognostic correlation of tumor-infiltrating lymphocytes (TILs) and cancer associated fibroblasts (CAFs) in patients with human esophageal carcinoma

    Takuya Kato, Kazuhiro Noma, Yuki Katsura, Hajime Kashima, Takayuki Ninomiya, Toshiaki Ohara, Hiroshi Tazawa, Shunsuke Kagawa, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • PD-L1 expression as a predictive factor for recurrence pattern and prognosis in curatively resected gastric cancer

    Toshiaki Morihiro, Shinji Kuroda, Tetsushi Kubota, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • Novel HER2-targeted gold nanoparticles; integration of antibody therapy and nanotechnology

    Tetsushi Kubota, Shinji Kuroda, Toshiaki Morihiro, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • PD-1 and PD-L1 expression patterns and DNA mismatch repair status for precision management of patients with gastric cancer

    Keisuke Kimura, Takeshi Nagasaka, Yoshiko Mori, Takashi Kawai, Tomokazu Fuji, Fumitaka Taniguchi, Kazuya Yasui, Toshiaki Toshima, Yuzo Umeda, Hiroshi Tazawa, Ajay Goel, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • Comprehensive analysis of intrahepatic cholangiocarcinoma based on viral infections and mutational status in the IDH1/2 and KRAS genes

    Kazuya Yasui, Takeshi Nagasaka, Yuzo Umeda, Tomokazu Fuji, Fumitaka Taniguchi, Toshiaki Toshima, Keisuke Kimura, Takashi Kawai, Yoshiko Mori, Hiroshi Tazawa, Takahito Yagi, Ajay Goel, Toshiyoshi Fujiwara

    CANCER RESEARCH   76   2016.7

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  • 胃癌腹膜播種の基礎と臨床 新たなエビデンスの創出に向けて 胃癌個別化治療に向けた腹腔内遊離癌細胞イメージング技術の応用

    渡辺 めぐみ, 香川 俊輔, 桑田 和也, 坂本 修一, 菊地 覚次, 黒田 新士, 岸本 浩行, 西崎 正彦, 田澤 大, 藤原 俊義

    日本消化器外科学会総会   71回   WS15 - 6   2016.7

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  • 消化器外科領域における最新のトランスレーショナルリサーチ 食道癌に対する放射線併用ウイルス療法の臨床研究 低用量群(Level 1)の薬理動態解析

    藤原 俊義, 香川 俊輔, 田辺 俊介, 田澤 大, 野間 和広, 黒田 新士, 菊地 覚次, 白川 靖博

    日本消化器外科学会総会   71回   WS5 - 1   2016.7

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  • 明日の食道癌非手術治療 食道癌に対する放射線併用ウイルス療法の臨床研究の中間報告

    田辺 俊介, 白川 靖博, 金谷 信彦, 岡田 剛, 前田 直見, 黒田 新士, 野間 和広, 田澤 大, 香川 俊輔, 藤原 俊義

    日本食道学会学術集会プログラム・抄録集   70回   58 - 58   2016.7

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  • 標的陰性癌に対するPhotoimmunotherapy 抗原修飾による抗原陽転化と不均一性の克服

    香川 俊輔, 石田 道拡, 下山 京子, 竹原 清人, 野間 和広, 田辺 俊介, 渡邉 めぐみ, 田澤 大, 小林 久隆, 藤原 俊義

    日本消化器外科学会総会   71回   SS9 - 8   2016.7

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  • 骨・軟部肉腫に対する腫瘍融解ウイルスの放射線増感作用

    大森 敏規, 山川 泰明, 長谷井 嬢, 田澤 大, 尾崎 修平, 杉生 和久, 藤原 智洋, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   90 ( 6 )   S1260 - S1260   2016.6

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  • 鉄コントロールによる新規がん幹細胞治療

    二宮 卓之, 大原 利章, 加藤 卓也, 賀島 肇, 野間 和広, 田澤 大, 田辺 俊介, 香川 俊輔, 白川 靖博, 藤原 俊義

    日本外科学会定期学術集会抄録集   116回   PS - 8   2016.4

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  • MGMT Inactivation Arrest Tumor Growth and Serves As a Promising Predictive Biomarker for Treatment Response in Colorectal Cancer

    Yoshiko Mori, Takeshi Nagasaka, Hiroshi Tazawa, Yuzo Umeda, Kunitoshi Shigeyasu, Kazuhiro Yoshida, Ajay Goel, Toshiyoshi Fujiwara

    GASTROENTEROLOGY   150 ( 4 )   S1013 - S1013   2016.4

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    DOI: 10.1016/S0016-5085(16)33430-8

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  • 次世代の外科治療における早期探索的医療研究の役割 食道癌外科治療を補完する新たな治療戦略としての腫瘍融解ウイルスと放射線との新規併用療法の臨床研究

    香川 俊輔, 田辺 俊介, 田澤 大, 野間 和広, 國府島 健, 賀島 肇, 加藤 卓也, 黒田 新士, 菊地 覚次, 白川 靖博, 藤原 俊義

    日本外科学会定期学術集会抄録集   116回   WS - 5   2016.4

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  • 胃癌におけるPD-L1の臨床病理学的特徴

    黒田 新士, 森廣 俊昭, 久保田 哲史, 田中 健大, 坂本 修一, 菊地 覚次, 田澤 大, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本外科学会定期学術集会抄録集   116回   PS - 4   2016.4

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  • 腹腔内播種に対する取り組み 外科医の役割 腹膜内播種に関する洞察のための胃がん細胞の蛍光誘導によるイメージング(Challenge to peritoneal dissemination: Role of surgeons Fluorescence-guided imaging of gastric cancer cells for an insight into peritoneal dissemination)

    Kagawa Shunsuke, Watanabe Megumi, Kuwata Kazuya, Kikuchi Satoru, Kuroda Shinji, Sakamoto Shuichi, Nishizaki Masahiko, Tazawa Hiroshi, Fujiwara Toshiyoshi

    日本胃癌学会総会記事   88回   180 - 180   2016.3

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  • スキルス胃癌細胞に対するテロメラーゼ依存的腫瘍融解ウイルス治療の前臨床評価

    堀 直人, 田澤 大, 西崎 正彦, 渡邉 めぐみ, 田村 周太, 國府島 健, 黒田 新士, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本胃癌学会総会記事   88回   452 - 452   2016.3

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  • 癌関連線維芽細胞が食道癌の浸潤と転移に及ぼす影響の検証

    賀島肇, 野間和広, 桂佑貴, 加藤卓也, 大原利章, 田澤大, 白川靖博, 香川俊輔, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   27th   2016

  • 鉄コントロールによる新規がん幹細胞治療

    二宮 卓之, 大原 利章, 勝部 亮一, 賀島 肇, 加藤 卓也, 野間 和広, 田澤 大, 香川 俊輔, 水谷 昭文, 笠井 智成, 妹尾 昌治, 藤原 俊義

    日本癌学会総会記事   74回   IS4 - 6   2015.10

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  • ヒト癌細胞におけるEMT可視化生体イメージング技術の開発

    家田 偉史, 田澤 大, 菊池 覚次, 黒田 新士, 大原 利章, 野間 和広, 岸本 浩行, 永坂 岳司, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   74回   P - 2028   2015.10

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  • 遊走能・浸潤能を有する膵臓癌細胞に対する新たな腫瘍融解ウイルス療法の開発

    國府島 健, 田澤 大, 堀 直人, 田村 周太, 黒田 新士, 岸本 浩行, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   74回   E - 1064   2015.10

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  • 分化型胃癌細胞による癌関連線維芽細胞の活性化機構

    李 云成, 田澤 大, 西崎 正彦, 橋本 悠里, 堀 直人, 勝部 亮一, 黒田 新士, 野間 和広, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   74回   P - 3127   2015.10

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  • 胃癌個別化治療に向けた、蛍光ウイルスによる腹腔内遊離胃癌細胞の検出技術の開発

    渡邉 めぐみ, 香川 俊輔, 桑田 和也, 橋本 悠里, 堀 直人, 菊地 覚次, 黒田 新士, 岸本 浩行, 西崎 正彦, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   74回   E - 1291   2015.10

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  • ナノ技術と抗体療法の融合による新規HER2標的金ナノ製剤の開発と治療効果の検討

    久保田 哲史, 黒田 新士, 森廣 俊昭, 青山 克幸, 田澤 大, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   74回   E - 1332   2015.10

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  • 骨軟部肉腫細胞に対する腫瘍融解ウイルスの放射線増感作用

    大森 敏規, 山川 泰明, 長谷井 嬢, 田澤 大, 尾崎 修平, 佐々木 剛, 杉生 和久, 魚谷 弘二, 藤原 智洋, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   74回   E - 1276   2015.10

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  • 骨肉腫に対するドキソルビシンとp53発現腫瘍融解アデノウイルス製剤の併用療法

    杉生 和久, 田澤 大, 長谷井 嬢, 尾崎 修平, 山川 泰明, 大森 敏規, 小松原 将, 魚谷 弘二, 藤原 智洋, 国定 俊之, 浦田 泰生, 尾崎 敏文, 藤原 俊義

    日本癌学会総会記事   74回   P - 1382   2015.10

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  • スキルス胃癌細胞に対する腫瘍特異的p53遺伝子治療の前臨床評価

    堀 直人, 田澤 大, 西崎 正彦, 渡邉 めぐみ, 田村 周太, 國府島 健, 黒田 新士, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   74回   E - 1272   2015.10

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  • 基礎研究の外科臨床への応用 早期消化管がんに対する新規リンパ節転移治療の可能性

    菊地 覚次, 岸本 浩行, 田澤 大, 黒田 新士, 西崎 正彦, 香川 俊輔, 浦田 泰生, Hoffman Robert M., 藤原 俊義

    日本癌学会総会記事   74回   S16 - 3   2015.10

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  • KRAS/BRAF変異を持つ大腸癌に対する新たな腫瘍融解ウイルス療法の開発

    田村 周太, 田澤 大, 堀 直人, 國府島 健, 菊地 覚次, 黒田 新士, 岸本 浩行, 永坂 岳司, 西崎 正彦, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   74回   E - 1066   2015.10

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  • 新規免疫療法と化学療法 食道癌に対する放射線療法との併用におけるテロメラーゼ標的腫瘍溶解性ウイルス、OBP-301の内視鏡的腫瘍内投与の第1/2相研究(Novel Immunotherapy and Chemothnorty A phase I/II study of endoscopic intratumoral administration of a telomerase targeted oncolytic virus, OBP-301, in combination with radiotherapy for esophageal cancer)

    Kagawa Shunsuke, Tanabe Shunsuke, Tazawa Hiroshi, Noma Kazuhiro, Koujima Takeshi, Kashima Hajime, Kato Takuya, Kuroda Shinji, Kikuchi Satoru, Shirakawa Yasuhiro, Fujiwara Toshiyoshi

    日本癌治療学会誌   50 ( 3 )   1116 - 1116   2015.9

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  • 食道癌と胃癌2 トランスレーショナル研究 新規HER2標的療法としてのtrastuzumab結合金ナノ粒子(Esophageal and Gastric Cancer: Translational Research Trastuzumab-conjugated gold nanoparticles as a novel HER2-targeted therapy)

    Kuroda Shinji, Kubota Tetsushi, Morihiro Toshiaki, Kikuchi Satoru, Tazawa Hiroshi, Nishizaki Masahiko, Kagawa Shunsuke, Fujiwara Toshiyoshi

    日本癌治療学会誌   50 ( 3 )   1076 - 1076   2015.9

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  • 骨肉腫に対する化学療法とp53発現腫瘍融解アデノウイルス治療の併用効果

    杉生 和久, 小松原 将, 大森 敏規, 山川 泰明, 吉田 晶, 藤原 智洋, 武田 健, 国定 俊之, 田澤 大, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   89 ( 8 )   S1799 - S1799   2015.9

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  • 骨肉腫に対するテロメラーゼ依存性腫瘍融解アデノウイルスと骨周囲環境制御による新規治療戦略

    山川 泰明, 長谷井 嬢, 田澤 大, 杉生 和久, 魚谷 弘二, 大森 敏規, 尾崎 修平, 吉田 晶, 藤原 智洋, 武田 健, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   89 ( 8 )   S1798 - S1798   2015.9

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  • 骨・軟部肉腫に対する腫瘍融解アデノウイルスと放射線療法の併用効果

    大森 敏規, 山川 泰明, 長谷井 嬢, 田澤 大, 尾崎 修平, 杉生 和久, 藤原 智洋, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   89 ( 8 )   S1673 - S1673   2015.9

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  • 胃 胃がんのPDL-1発現と免疫療法 胃癌組織におけるPD-L1発現と予後との関連

    黒田 新士, 森廣 俊昭, 久保田 哲史, 菊地 覚次, 田澤 大, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本癌治療学会誌   50 ( 3 )   141 - 141   2015.9

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  • 新規免疫療法と化学療法 早期消化管癌患者のリンパ節転移に対する生物学的アブレーションの利用可能性(Novel Immunotherapy and Chemothnorty The possibility of biological ablation of lymphatic metastasis for early gastrointestinal cancer patients)

    Kikuchi Satoru, Kishimoto Hiroyuki, Tazawa Hiroshi, Kuroda Shinji, Nishizaki Masahiko, Kagawa Shunsuke, Urata Yasuo, Hoffman Robert M., Fujiwara Toshiyoshi

    日本癌治療学会誌   50 ( 3 )   1117 - 1117   2015.9

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  • Phase I/II trial of endoscopic intratumoral administration of OBP-301, a novel telomerase-specific oncolytic virus, with radiation in elderly esophageal cancer patients

    Shunsuke Tanabe, Hiroshi Tazawa, Shunsuke Kagawa, Kazuhiro Noma, Kiyoto Takehara, Takeshi Koujima, Hajime Kashima, Takuya Kato, Shinji Kuroda, Satoru Kikuchi, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-CT123

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  • A novel tumor-specific oncolytic biological therapy against invasive pancreatic cancer

    Takeshi Koujima, Hiroshi Tazawa, Naoto Hori, Shuta Tamura, Shinji Kuroda, Hiroyuki Kishimoto, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-3535

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  • Virus-guided fluorescence imaging of intraperitoneal free gastric cancer cells: a preliminary clinical study as a potential clinical biomarker

    Megumi Watanabe, Shunsuke Kagawa, Kazuya Kuwata, Michihiro Ishida, Yuuri Hashimoto, Naoto Hori, Satoru Kikuchi, Shinji Kuroda, Hiroyuki Kishimoto, Masahiko Nishizaki, Hiroshi Tazawa, Yasuo Urata, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-3412

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  • HER2-targeted gold nanoparticles produce potent antitumor effects on human gastric cancer cells

    Tetsushi Kubota, Shinji Kuroda, Katsuyuki Aoyama, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-5520

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  • A novel photoimmunotherapy targeting cancer-associated fibroblasts (CAFs) overcomes therapeutic resistance in human esophageal cancer

    Ryoichi Katsube, Kazuhiro Noma, Shinichiro Watanabe, Shinichi Urano, Takayuki Ninomiya, Toshiaki Ohara, Hiroshi Tazawa, Shunsuke Kagawa, Hisataka Kobayashi, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-401

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  • Preclinical evaluation of radiotherapy in combination with radio-sensitizing telomerase-specific oncolytic virus for human bone and soft tissue sarcomas

    Toshinori Omori, Yasuaki Yamakawa, Joe Hasei, Hiroshi Tazawa, Shuhei Osaki, Tusyoshi Sasaki, Kazuhisa Sugiu, Tomohiro Fujiwara, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-1794

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  • Iron control is a novel therapeutic target of cancer stem cells

    Takayuki Ninomiya, Toshiaki Ohara, Hajime Kashima, Ryoichi Katsube, Kazuhiro Noma, Yasuko Tomono, Akifumi Mizutani, Tomonari Kasai, Masaharu Seno, Shinji Kuroda, Hiroyuki Kishimoto, Hiroshi Tazawa, Yasuhiro Shirakawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-4243

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  • Differentiated gastric cancer cells have a potential to induce cancer-associated fibroblasts

    Yuncheng Li, Hiroshi Tazawa, Nishizaki Masahiko, Yuuri Hashimoto, Naoto Hori, Ryoichi Katsube, Shinji Kuroda, Kazuhiro Noma, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-2368

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  • Preclinical study of telomerase-specific p53 tumor suppressor gene overexpression in human scirrhous gastric cancer cells with different p53 status

    Naoto Hori, Hiroshi Tazawa, Masahiko Nishizaki, Satoru Kikuchi, Shuya Yano, Michihiro Ishida, Megumi Watanabe, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-5338

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  • Companion diagnostics-based telomerase-specific oncolytic virotherapy: preclinical evaluation in human colorectal cancer cell lines differentially affected in the RAS/RAF/MEK signaling pathway

    Shuta Tamura, Hiroshi Tazawa, Naoto Hori, Takeshi Koujima, Satoru Kikuchi, Shinji Kuroda, Hiroyuki Kishimoto, Takeshi Nagasaka, Masahiko Nishizaki, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   75   2015.8

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    DOI: 10.1158/1538-7445.AM2015-3531

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  • Color-coding cancer and stromal cells with genetic reporters in a patient-derived orthotopic xenograft (PDOX) model of pancreatic cancer enhances fluorescence-guided surgery

    S. Yano, Y. Hiroshima, A. Maawy, H. Kishimoto, A. Suetsugu, S. Miwa, M. Toneri, M. Yamamoto, M. H. G. Katz, J. B. Fleming, Y. Urata, H. Tazawa, S. Kagawa, M. Bouvet, T. Fujiwara, R. M. Hoffman

    CANCER GENE THERAPY   22 ( 7 )   344 - 350   2015.7

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  • 食道癌に対する放射線併用ウイルス療法の臨床研究 レベル1投与量群の中間報告

    田邊 俊介, 白川 靖博, 加藤 卓也, 竹原 清人, 前田 直見, 黒田 新士, 野間 和広, 田澤 大, 香川 俊輔, 藤原 俊義

    日本消化器外科学会総会   70回   O - 6   2015.7

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  • 胃癌腹膜播種の病態と診断・治療 腫瘍特異的蛍光発現virus試薬による腹腔洗浄液中の遊離胃癌細胞診断の臨床的意義

    香川 俊輔, 渡邉 めぐみ, 石田 道拡, 桑田 和也, 黒田 新士, 菊地 覚次, 香川 哲也, 西崎 正彦, 田澤 大, 藤原 俊義

    日本消化器外科学会総会   70回   WS - 4   2015.7

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  • 骨・軟部肉腫に対する腫瘍融解アデノウイルスと放射線療法の併用効果

    大森 敏規, 山川 泰明, 長谷井 嬢, 田澤 大, 尾崎 修平, 杉生 和久, 藤原 智洋, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   89 ( 6 )   S1244 - S1244   2015.6

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  • リポソームを用いたテロメラーゼ特異的全身ウイルス療法の可能性

    森廣 俊昭, 青山 克幸, 久保田 哲史, 黒田 新士, 田澤 大, 香川 俊輔, 藤原 俊義

    日本DDS学会学術集会プログラム予稿集   31回   200 - 200   2015.6

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  • 金ナノ粒子を用いたHER2標的抗体療法 新標的化技術の応用

    久保田 哲史, 黒田 新士, 青山 克幸, 森廣 俊昭, 田澤 大, 藤原 俊義

    日本DDS学会学術集会プログラム予稿集   31回   153 - 153   2015.6

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  • ゾレドロン酸とテロメラーゼ依存性腫瘍融解アデノウイルスの併用療法は骨肉腫に対する抗腫瘍効果を増強し、骨破壊を抑制する

    山川 泰明, 長谷井 嬢, 田澤 大, 杉生 和久, 魚谷 弘二, 尾崎 修平, 吉田 晶, 藤原 智洋, 武田 健, 国定 俊之, 浦田 泰生, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   89 ( 6 )   S1244 - S1244   2015.6

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  • 上部消化管 超高齢者食道癌手術への取り組みと放射線併用ウイルス療法の可能性

    田辺 俊介, 白川 靖博, 賀島 肇, 国府島 健, 前田 直見, 大原 利章, 黒田 新士, 櫻間 教文, 野間 和広, 田澤 大, 香川 俊輔, 藤原 俊義

    日本外科学会定期学術集会抄録集   115回   OP - 2   2015.4

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  • その他 鉄コントロールによるがん幹細胞に対する新規治療

    二宮 卓之, 大原 利章, 浦野 真一, 勝部 亮一, 野間 和広, 田澤 大, 白川 靖博, 香川 俊輔, 藤原 俊義

    日本外科学会定期学術集会抄録集   115回   OP - 7   2015.4

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  • Cancer cells mimic in vivo spatial-temporal cell-cycle phase distribution and chemosensitivity in 3-dimensional Gelfoam (R) histoculture but not 2-dimensional culture as visualized with real-time FUCCI imaging (vol 14, pg 808, 2015)

    Shuya Yano, Shinji Miwa, Sumiyuki Mii, Yukihiko Hiroshima, Fuminaru Uehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Ming Zhao, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    CELL CYCLE   14 ( 8 )   1338 - 1338   2015.4

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  • 上部消化管 胃癌に対する腹膜洗浄術についての蛍光発現ウイルスTelomescanによる新規細胞学的診断(Novel cytological diagnosis of peritoneal wash for gastric cancer by fluorescence-emitting virus TelomeScan)

    香川 俊輔, 渡邉 めぐみ, 石田 道拡, 黒田 新士, 菊地 覚次, 田澤 大, 岸本 浩行, 桑田 和也, 久保田 哲史, 堀 直人, 田邊 俊介, 西崎 正彦, 浦田 泰生, 藤原 俊義

    日本外科学会定期学術集会抄録集   115回   IS - 6   2015.4

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  • 上部消化管 HER2陰性癌細胞に対するHER2細胞外ドメインによる非機能性HER2抗原遺伝子修飾とTrastuzumabを用いた分子標的光免疫療法を併用した治療戦略

    石田 道拡, 香川 俊輔, 下山 京子, 竹原 清人, 渡邉 めぐみ, 菊地 覚次, 黒田 新士, 野間 和広, 岸本 浩行, 田澤 大, 田邊 俊介, 小林 久隆, 藤原 俊義

    日本外科学会定期学術集会抄録集   115回   OP - 3   2015.4

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  • 非機能性HER2抗原で遺伝子修飾したHER2陰性癌細胞に対する分子標的光免疫療法

    石田 道拡, 香川 俊輔, 下山 京子, 竹原 清人, 渡邉 めぐみ, 菊地 覚次, 黒田 新士, 野間 和広, 岸本 浩行, 西崎 正彦, 田澤 大, 田邊 俊介, 小林 久隆, 藤原 俊義

    日本胃癌学会総会記事   87回   402 - 402   2015.3

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  • 腹腔内の遊離胃がん細胞のウイルス標識による蛍光イメージング(Virus-guided fluorescence imaging of intraperitoneal free gastric cancer cells)

    Watanabe Megumi, Kagawa Shunsuke, Ishida Michihiro, Hashimoto Yuuri, Hori Naoto, Kikuchi Satoru, Kuroda Shinji, Kishimoto Hiroyuki, Nishizaki Masahiko, Tazawa Hiroshi, Urata Yasuo, Fujiwara Toshiyoshi

    日本胃癌学会総会記事   87回   497 - 497   2015.3

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  • 骨・軟部肉腫に対する腫瘍融解アデノウイルスと放射線療法の併用効果

    大森 敏規, 山川 泰明, 長谷井 嬢, 田澤 大, 尾崎 修平, 杉生 和久, 藤原 智洋, 国定 俊之, 浦田 泰夫, 藤原 俊義

    日本整形外科学会雑誌   89 ( 2 )   S142 - S142   2015.3

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  • 食道癌におけるFAP(fibroblast activation protein)陽性癌関連線維芽細胞の発現と癌転移の関係

    賀島肇, 野間和広, 加藤卓也, 勝部亮一, 二宮卓之, 大原利章, 田澤大, 白川靖博, 香川俊輔, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   26th   2015

  • 癌関連線維芽細胞を標的とした新規食道癌治療法の開発

    勝部亮一, 野間和広, 賀島肇, 加藤卓也, 二宮卓之, 大原利章, 田澤大, 白川靖博, 香川俊輔, 小林久隆, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   26th   2015

  • Salmonella typhimurium A1-R decoys quiescent cancer cells to cycle rendering them chemosensitive

    S. Yano, Y. Zhang, M. Zhao, Y. Hiroshima, S. Miwa, F. Uehara, H. Kishimoto, H. Tazawa, T. Fujiwara, R. M. Hoffman

    EUROPEAN JOURNAL OF CANCER   50   96 - 96   2014.11

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  • Real-time FUCCI imaging demonstrates targeting dormant cancer cells

    Shuya Yano, Ming Zhao, Hiroshi Tazawa, Robert M. Hoffman, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-1975

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  • A novel photodynamic therapy with virus-mediated delivery of photosensitive cytotoxic fluorescent protein KillerRed for human cancers

    Kiyoto Takehara, Hiroshi Tazawa, Yuuri Hashimoto, Hiroyuki Kishimoto, Toshiyoshi Fujiwara, Nobuhiro Narii, Hiroyuki Mizuguchi

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-706

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  • Real-time FUCCI imaging of cell cycle phase in tumors demonstrates why cancer chemotherapy is not effective in solid cancers

    Shuya Yano, Yasunori Tome, Yong Zhang, Yukihiko Hiroshima, Shinji Miwa, Fuminari Uehara, Atsushi Suetsugu, Hiroyuki Kishimoto, Hiroshi Tazawa, Ming Zhao, Toshiyoshi Fujiwara, Robert M. Hoffman

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-5095

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  • Combination therapy of telomerase-specific oncolytic adenovirus and zoledronic acid in human osteosarcoma cells

    Yasuaki Yamakawa, Joe Hasei, Hiroshi Tazawa, Toshinori Omori, Shuhei Osaki, Tsuyoshi Sasaki, Aki Yoshida, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-725

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  • Telomerase-dependent oncolytic adenovirus sensitizes human osteosarcoma cells to chemotherapy through Mcl-1 downregulation

    Shuhei Osaki, Toshinori Omori, Hiroshi Tazawa, Joe Hasei, Yasuaki Yamakawa, Tsuyoshi Sasaki, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-342

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  • Novel combination therapy of adenoviral gene transfer of HER2-extracellular domain and trastuzumab-based photoimmunotherapy for HER2 negative cancer cells

    Michihiro Ishida, Shunsuke Kagawa, Kyoko Shimoyama, Kiyoto Takehara, Kazuhiro Noma, Shunsuke Tanabe, Hiroshi Tazawa, Junji Matsuoka, Hisataka Kobayashi, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-2615

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  • Telomerase-specific GFP-expressing adenovirus enables fluorescence-guided surgery (FGS) for patient-derived orthotopic xenograft (PDOX) in nude mice

    Shuya Yano, Yukihiko Hiroshima, Ali Maawy, Matthew H. G. Katz, Jason B. Fleming, Hiroyuki Kishimoto, Atsushi Suetsugu, Fuminari Uehara, Shinji Miwa, Hiroshi Tazawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-1218

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  • Iron chelation therapy increased the anticancer effect of sorafenib in hepatocarcinoma

    Shinichi Urano, Toshiaki Ohara, Ryoichi Katsube, Shinichiro Watanabe, Kazuhiro Noma, Yasuko Tomono, Hiroshi Tazawa, Kazuhiro Nouso, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-1681

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  • Invading cancer cells are mostly in G0/G1 and resist chemotherapy demonstrated by real-time FUCCI imaging of cell-cycle kinetics in Gelfoam (R) histoculture

    Shuya Yano, Shinji Miwa, Sumiyuki Mii, Yukihiko Hiroshima, Fuminari Uehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Ming Zhao, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-1982

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  • Virus-guided fluorescence imaging of intraperitoneal free gastric cancer cells as a potential clinical biomarker

    Megumi Watanabe, Shunsuke Kagawa, Michihiro Ishida, Naoto Hori, Satoru Kikuchi, Shinji Kuroda, Hiroyuki Kishimoto, Masahiko Nishizaki, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-4726

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  • REAL TIME COLOR CODED IMAGING OF CELL CYCLE PHASE DEMONSTRATES WHY INVASIVE METASTATIC CANCER CELLS ARE DRUG RESISTANT

    Robert M. Hoffman, Shuya Yano, Shinji Miwa, Sumiyuki Mii, Yukihiko Hiroshima, Fuminari Uehara, Mako Yamamoto, Hiroyuki Kishimoto, Hiroshi Tazawa, Toshiyoshi Fujiwara

    ANNALS OF ONCOLOGY   25   2014.10

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    DOI: 10.1093/annonc/mdu435.28

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  • Three-dimensional Gelfoam (R) histoculture enables cancer cells to mimic in vivo cancer cell cycling as visualized with FUCCI imaging

    Shuya Yano, Shinji Miwa, Sumiyuki Mii, Yukihiko Hiroshima, Fuminari Uehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Ming Zhao, Toshiyoshi Fujiwara, Robert M. Hoffman

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-1979

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  • Combination strategy of endoscopic resection and telomerase-targeting oncolytic virus for eradicating lymph node metastasis of submucosal invasive colorectal cancer

    Naoto Hori, Satoru Kikuchi, Hiroyuki Kishimoto, Hiroshi Tazawa, Yuuri Hashimoto, Shinji Kuroda, Shunsuke Kagawa, Yasuo Urata, Robert M. Hoffman, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-4025

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  • Salmonella typhimurium A1-R induces quiescent FUCCI-expressing cancer cells to cycle and become chemosensitive

    Shuya Yano, Yong Zhang, Ming Zhao, Yukihiko Hiroshima, Shinji Miwa, Fuminari Uehara, Hiroyuki Kishimoto, Hiroshi Tazawa, Toshiyoshi Fujiwara, Robert M. Hoffman

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-711

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  • Development of systemically-deliverable telomerase-specific oncolytic adenovirus

    Katsuyuki Aoyama, Shinji Kuroda, Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   74 ( 19 )   2014.10

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    DOI: 10.1158/1538-7445.AM2014-719

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  • 鉄コントロールによるがん幹細胞の新規治療法(Iron control is a potent novel therapeutic for cancer stem cells)

    二宮 卓之, 大原 利章, 浦野 真一, 勝部 亮一, 野間 和広, 田澤 大, 香川 俊輔, 水谷 昭文, 笠井 智成, 妹尾 昌治, 藤原 俊義

    日本癌学会総会記事   73回   P - 1187   2014.9

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  • 食道癌の悪性化に対するCAF標的光免疫療法の開発(Development of novel strategy of targeting cancer associated fibroblast (CAFs) for resistant esophageal cancer)

    勝部 亮一, 野間 和広, 渡邉 伸一郎, 浦野 真一, 二宮 卓之, 大原 利章, 白川 靖博, 田澤 大, 香川 俊輔, 小林 久隆, 藤原 俊義

    日本癌学会総会記事   73回   P - 3157   2014.9

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  • 鉄キレート療法は肝癌におけるソラフェニブの抗腫瘍効果を増強する(Iron chelation therapy enhances the anticancer effect of sorafenib in hepatocarcinoma)

    浦野 真一, 大原 利章, 勝部 亮一, 野間 和広, 友野 靖子, 田澤 大, 能祖 一裕, 白川 靖博, 藤原 俊義

    日本癌学会総会記事   73回   P - 2328   2014.9

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  • ヒト大腸腺腫細胞の大腸癌細胞への進展における慢性炎症由来一酸化窒素の証明とfascinの同定(Nitric oxide from chronic inflammation and fascin in conversion of human colonic adenoma cells into adenocarcinoma cells)

    神田 裕介, 河口 徳一, 田澤 大, 平畑 美緒, 小沼 邦重, 北川 知行, 尾崎 充彦, 岡田 太

    日本癌学会総会記事   73回   P - 1025   2014.9

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  • 全身送達を目指したリポソーム抱合テロメラーゼ特異的腫瘍融解アデノウイルスプラスミドDNA(Telomerase-specific oncolytic adenoviral plasmid DNA conjugated with liposome for systemic delivery)

    青山 克幸, 黒田 新士, 田澤 大, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   73回   P - 3420   2014.9

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  • HER2抗原で修飾された癌細胞に対するTrastuzumabを用いた近赤外線光線免疫療法の効果(Genetic decoration with HER2-antigen makes cancer cells vulnerable to trastuzumab-based photoimmunotherapy)

    石田 道拡, 香川 俊輔, 下山 京子, 竹原 清人, 野間 和広, 田澤 大, 黒田 新士, 岸本 浩行, 田邊 俊介, 小林 久隆, 藤原 俊義

    日本癌学会総会記事   73回   E - 3040   2014.9

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  • 蛍光発現ウイルスを用いた腹腔内がん細胞の検出技術の開発(A FEASIBILITY STUDY TO VISUALIZE INTRAPERITONEAL DESSEMINATED GASTRIC CANCER BY FLUORESCENCE-EMITTING VIRUS, TELOMESCAN)

    渡邉 めぐみ, 香川 俊輔, 石田 道拡, 橋本 悠里, 堀 直人, 菊地 覚次, 黒田 新士, 岸本 浩行, 西崎 正彦, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   73回   E - 2019   2014.9

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  • テロメラーゼ依存性増殖型アデノウイルス製剤を用いた早期大腸癌の微小リンパ節転移制御(The eradication of lymph node metastasis of early colorectal cancers using telomerase-dependent replicating adenovirus)

    菊地 覚次, 岸本 浩行, 田澤 大, 黒田 新士, 西崎 正彦, 香川 俊輔, 浦田 泰生, ロバート・ホフマン, 藤原 俊義

    日本癌学会総会記事   73回   E - 1115   2014.9

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  • ヒトスキルス胃癌細胞に対する腫瘍融解アデノウイルスの抗腫瘍効果(Antitumor effect of tumor-specific oncolytic adenovirus in human scirrhous gastric cancer cells)

    堀 直人, 田澤 大, 西崎 正彦, 菊地 覚次, 矢野 修也, 石田 道拡, 渡辺 めぐみ, 浦田 泰生, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   73回   P - 2355   2014.9

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  • 腫瘍融解アデノウイルスと放射線療法を併用した骨・軟部肉腫に対する新規治療戦略

    大森 敏規, 長谷井 嬢, 杉生 和久, 山川 泰明, 尾崎 修平, 藤原 智洋, 武田 健, 吉田 晶, 国定 俊之, 田澤 大, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   88 ( 8 )   S1362 - S1362   2014.8

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  • 骨転移におけるゾレドロン酸と腫瘍融解アデノウイルスの併用治療

    山川 泰明, 長谷井 嬢, 杉生 和久, 大森 敏規, 尾崎 修平, 吉田 晶, 藤原 智洋, 国定 俊之, 浦田 泰生, 田澤 大, 藤原 俊義, 尾崎 敏文

    日本整形外科学会雑誌   88 ( 8 )   S1684 - S1684   2014.8

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  • ONCOLYTIC ADENOVIRUS INHIBITS TRANSFORMING GROWTH FACTOR-beta-INDUCED EPITHELIAL-MESENCHYMAL TRANSITION IN HUMAN CANCER CELLS

    Yuuri Hashimoto, Hiroshi Tazawa, Ryosuke Yoshida, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    JOURNAL OF GENE MEDICINE   16 ( 7-8 )   244 - 245   2014.7

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  • MiCRORNA-7 INHIBITS THE STEM-LIKE PROPERTIES OF CD133(+) HUMAN GASTRIC CANCER CELLS

    Teppei Onishi, Hiroshi Tazawa, Shuya Yano, Yuuri Hashimoto, Ryosuke Yoshida, Shunsuke Kagawa, Toshiyoshi Fujiwara

    JOURNAL OF GENE MEDICINE   16 ( 7-8 )   266 - 266   2014.7

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  • MECHANISM OF RESISTANCE TO TRASTUZUMAB AND MOLECULAR SENSITIZATION VIA ADCC ACTIVATION BY EXOGENOUS EXPRESSION OF HER2 EXTRACELLULAR DOMAIN

    Ryosuke Yoshida, Hiroshi Tazawa, Yuuri Hashimoto, Futoshi Uno, Masahiko Nishizaki, Shunsuke Kagawa, Toshiyoshi Fujiwara

    JOURNAL OF GENE MEDICINE   16 ( 7-8 )   277 - 278   2014.7

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  • リポソームを用いた全身投与可能なテロメラーゼ特異的腫瘍融解ウイルス製剤の開発

    青山 克幸, 黒田 新士, 田澤 大, 香川 俊輔, 藤原 俊義

    日本DDS学会学術集会プログラム予稿集   30回   221 - 221   2014.7

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  • ANTITUMOR EFFECT OF TELOMERASE-SPECIFIC ONCOLYTIC ADENOVIRUS ON HUMAN BONE AND SOFT TISSUE SARCOMA CELLS

    Hiroshi Tazawa, Tsuyoshi Sasaki, Jo Hasei, Yuuri Hashimoto, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    JOURNAL OF GENE MEDICINE   16 ( 7-8 )   261 - 262   2014.7

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  • ウイルスを用いたHER2陰性胃癌の強制的HER2標識化とTrastuzumabによる分子標的光免疫療法

    香川 俊輔, 石田 道拡, 田澤 大, 下山 京子, 竹原 清人, 野間 和広, 渡辺 めぐみ, 田辺 俊介, 小林 久隆, 藤原 俊義

    日本消化器外科学会総会   69回   O - 4   2014.7

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  • 慢性炎症に伴う一酸化窒素生成はヒト大腸腺腫細胞から大腸癌細胞を誘導する

    田澤大, 河口徳一, 蔵満保宏, 神田裕介, 尾崎充彦, 藤原俊義, 北川知行, 岡田太

    日本NO学会学術集会プログラム抄録集   14th   60   2014.5

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  • Molecular surgery using a novel biological agent, OBP-301, for lymph node micrometastasis in human colorectal cancer.

    Satoru Kikuchi, Hiroyuki Kishimoto, Hiroshi Tazawa, Shunsuke Kagawa, Yasuo Urata, Robert M. Hoffman, Toshiyoshi Fujiwara

    JOURNAL OF CLINICAL ONCOLOGY   32 ( 15 )   2014.5

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  • OP-048-7 テロメラーゼ依存性増殖型アデノウイルス製剤を用いた早期大腸癌に対する低侵襲治療の開発(OP-048 大腸 その他,一般演題,第114回日本外科学会定期学術集会)

    菊地 覚次, 岸本 浩行, 田澤 大, 西崎 正彦, 香川 俊輔, 浦田 泰生, Hoffman Robert, 藤原 俊義

    日本外科学会雑誌   115 ( 2 )   401 - 401   2014.3

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  • PS-052-4 がん関連線維芽細胞(Cancer Associated Fibroblasts)を標的とした新規癌治療法の開発(PS-052 食道 基礎-2,ポスターセッション,第114回日本外科学会定期学術集会)

    野間 和広, 白川 靖博, 二宮 卓之, 勝部 亮一, 前田 直見, 田辺 俊介, 大原 利章, 田澤 大, 香川 俊輔, 藤原 俊義

    日本外科学会雑誌   115 ( 2 )   678 - 678   2014.3

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  • PS-113-5 大腸癌におけるproenostic factorとしてのmiRNA(PS-113 大腸 基礎-1,ポスターセッション,第114回日本外科学会定期学術集会)

    久保田 暢人, 永坂 岳司, 母里 淑子, 森川 達也, 吉田 一博, 横道 直佑, 稲田 涼, 竹原 裕子, 竹原 清人, 河合 毅, 藤 智和, 楳田 祐三, 田澤 大, 藤原 俊義

    日本外科学会雑誌   115 ( 2 )   801 - 801   2014.3

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  • OP-001-6 温阻血再灌流+肝切除モデルにおけるHMGB1制御による再灌流障害および肝再生への影響解析(OP-001 肝 基礎-1,一般演題,第114回日本外科学会定期学術集会)

    杉原 正大, 貞森 裕, 西堀 正洋, 佐藤 康晴, 田澤 大, 吉田 龍一, 楳田 祐三, 篠浦 先, 永坂 岳司, 八木 孝仁, 藤原 俊義

    日本外科学会雑誌   115 ( 2 )   313 - 313   2014.3

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  • 大腸癌におけるprognostic factorとしてのmiRNA

    久保田 暢人, 永坂 岳司, 母里 淑子, 森川 達也, 吉田 一博, 横道 直佑, 稲田 涼, 竹原 裕子, 竹原 清人, 河合 毅, 藤 智和, 楳田 祐三, 田澤 大, 藤原 俊義

    日本外科学会雑誌   115 ( 臨増2 )   801 - 801   2014.3

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  • がん関連線維芽細胞(Cancer Associated Fibroblasts)を標的とした新規癌治療法の開発

    野間 和広, 白川 靖博, 二宮 卓之, 勝部 亮一, 前田 直見, 田辺 俊介, 大原 利章, 田澤 大, 香川 俊輔, 藤原 俊義

    日本外科学会雑誌   115 ( 臨増2 )   678 - 678   2014.3

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  • 温阻血再灌流+肝切除モデルにおけるHMGB1制御による再灌流障害および肝再生への影響解析

    杉原 正大, 貞森 裕, 西堀 正洋, 佐藤 康晴, 田澤 大, 吉田 龍一, 楳田 祐三, 篠浦 先, 永坂 岳司, 八木 孝仁, 藤原 俊義

    日本外科学会雑誌   115 ( 臨増2 )   313 - 313   2014.3

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  • HER2陰性胃癌におけるウイルスベクターを用いたHER2標識化とそれに対する分子標的光免疫療法

    石田 道拡, 香川 俊輔, 田澤 大, 下山 京子, 竹原 清人, 黒田 新士, 野間 和広, 岸本 浩行, 西崎 正彦, 小林 久隆, 藤原 俊義

    日本胃癌学会総会記事   86回   316 - 316   2014.3

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  • テロメラーゼ依存性増殖型アデノウイルス製剤を用いた早期大腸癌に対する低侵襲治療の開発

    菊地 覚次, 岸本 浩行, 田澤 大, 西崎 正彦, 香川 俊輔, 浦田 泰生, Hoffman Robert, 藤原 俊義

    日本外科学会雑誌   115 ( 臨増2 )   401 - 401   2014.3

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  • 慢性炎症に伴うNO生成はアノイキス抵抗性を介し大腸腺腫細胞から大腸癌細胞を誘導する

    田澤大, 河口徳一, 蔵満保宏, 神田裕介, 尾崎充彦, 藤原俊義, 北川知行, 岡田太

    日本消化器癌発生学会総会プログラム・抄録集   25th   102   2014

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  • Telomerase-targeting oncolytic adenovirus as a thetherapeutic and diagnostic agent

    Shunsuke Kagawa, Hiroshi Tazawa, Kunitoshi Shigeyasu, Hiroyuki Kishimoto, Shinji Kuroda, Toshiyoshi Fujiwara

    HUMAN GENE THERAPY   24 ( 12 )   A13 - A13   2013.12

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  • FUCCI cell cycle imaging identifies drug-resistant quiescent cancer cells within tumors

    Shuya Yano, Yasunori Tome, Yong Zhang, Shinji Miwa, Atsushi Suetsugu, Hiroyuki Kishimoto, Hiroshi Tazawa, Michael Bouvet, Toshiyoshi Fujiwara, Robert M. Hoffman

    MOLECULAR CANCER THERAPEUTICS   12 ( 11 )   2013.11

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    DOI: 10.1158/1535-7163.TARG-13-B60

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  • がん関連線維芽細胞を標的とした新たな癌治療法の可能性 光線免疫療法を用いて(Novel cancer therapy targeting cancer-associated fibroblasts(CAFs) by targeted infrared photoimmunotherapy(PIT))

    勝部 亮一, 野間 和広, 渡邉 伸一郎, 浦野 真一, 大原 利章, 白川 靖博, 田澤 大, 香川 俊輔, 小林 久隆, 藤原 俊義

    日本癌学会総会記事   72回   349 - 350   2013.10

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  • 鉄欠乏状態は肝細胞癌におけるソラフェニブの感受性を改善しうる(Iron depletion status has a possibility to improve the sensitivity of sorafenib in HCC)

    浦野 真一, 大原 利章, 勝部 亮一, 渡邉 伸一郎, 野間 和広, 友野 靖子, 田澤 大, 能祖 一裕, 白川 靖博, 貞森 裕, 藤原 俊義

    日本癌学会総会記事   72回   345 - 345   2013.10

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  • 新規光線力学療法を目指したウイルスを用いた光感受性細胞傷害性蛍光タンパク質KillerRedの治療効果(Virus-mediated delivery system of photosensitive cytotoxic fluorescent protein KillerRed for novel photodynamic therapy)

    竹原 清人, 田澤 大, 橋本 悠里, 岸本 浩行, 水口 裕之, 藤原 俊義

    日本癌学会総会記事   72回   503 - 503   2013.10

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  • HER2遺伝子導入技術を用いたHER2陰性癌細胞に対する分子標的光免疫療法(Neotargeting HER2 negative cancer cells with photoimmunotherapy by virally transduction of HER2- extracellular domain)

    石田 道拡, 香川 俊輔, 下山 京子, 竹原 清人, 野間 和広, 田澤 大, 黒田 新士, 岸本 浩行, 田邊 俊介, 松岡 順治, 小林 久隆, 篠原 俊義

    日本癌学会総会記事   72回   495 - 495   2013.10

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  • 胃癌患者の腹腔洗浄液における蛍光発現ウイルス試薬による新たな生物学的診断(Biological assessment of peritoneal lavage cytology of gastric cancer by fluorescence-expressing virus TelomeScan)

    香川 俊輔, 石田 道拡, 渡邉 めぐみ, 田澤 大, 黒田 新士, 岸本 浩行, 橋本 悠里, 西崎 正彦, 藤原 俊義

    日本癌学会総会記事   72回   187 - 187   2013.10

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  • 早期大腸癌のリンパ節転移制御に向けた新規治療(Novel strategy for eradicating lymph node metastasis of earlystage colorectal cancers)

    菊地 覚次, 岸本 浩行, 田澤 大, 橋本 悠里, 宇野 太, 西崎 正彦, 香川 俊輔, 浦田 泰生, ロバート・ホフマン, 藤原 俊義

    日本癌学会総会記事   72回   178 - 178   2013.10

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  • 蛍光標識による血中遊離癌細胞のLiquid Biopsy技術のバイオマーカー解析への応用

    重安 邦俊, 橋本 悠里, 竹原 清人, 宇野 太, 永坂 岳司, 田澤 大, 香川 俊輔, 浦田 泰生, 藤原 俊義

    日本癌治療学会誌   48 ( 3 )   2759 - 2759   2013.9

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  • がん選択的生物製剤を用いた早期大腸癌の低侵襲治療の開発

    菊地 覚次, 岸本 浩行, 田澤 大, 西崎 正彦, 香川 俊輔, 浦田 泰生, Hoffman Robert M., 藤原 俊義

    日本癌治療学会誌   48 ( 3 )   1918 - 1918   2013.9

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  • Iron-controlled cancer therapy: A new concept for anti-angiogenic drug (bevacizumab and sorafenib)

    T. Ohara, K. Noma, S. Urano, R. Katsube, T. Ninomiya, S. Tanabe, Y. Tomono, H. Tazawa, Y. Shirakawa, T. Fujiwara

    EUROPEAN JOURNAL OF CANCER   49   S639 - S639   2013.9

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  • 温阻血再灌流+70%肝切除におけるHMGB1の動態解析と制御

    杉原 正大, 貞森 裕, 佐藤 太祐, 吉田 龍一, 楳田 祐三, 篠浦 先, 田澤 大, 永坂 岳司, 八木 孝仁, 藤原 俊義

    日本消化器外科学会総会   68回 ( Supplement1 )   RS - 54   2013.7

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  • 癌特異的蛍光発現ウイルスによる胃癌症例腹腔洗浄液中での癌細胞検出法とその意義

    香川 俊輔, 重安 邦俊, 田澤 大, 宇野 太, 岸本 浩行, 黒田 新士, 石田 道拡, 渡邉 めぐみ, 西崎 正彦, 藤原 俊義

    日本消化器外科学会総会   68回   O - 6   2013.7

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  • StageIII大腸癌根治術後の再発予測におけるMGMTプロモーター領域のメチル化解析の有用性

    母里 淑子, 永坂 岳司, 竹原 裕子, 吉田 一博, 重安 邦俊, 楳田 祐三, 田澤 大, 貞森 裕, 藤原 俊義

    日本消化器外科学会総会   68回   O - 2   2013.7

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  • テロメラーゼ依存性増殖型アデノウイルス製剤を用いた早期大腸癌の低侵襲治療の開発

    菊地 覚次, 岸本 浩行, 田澤 大, 橋本 悠里, 宇野 太, 西崎 正彦, 香川 俊輔, 浦田 泰生, ロバート・ホフマン, 藤原 俊義

    日本消化器外科学会総会   68回   RS - 2   2013.7

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  • MGMT Methylation As a Novel Biomarker for the Identification of Stage III Colorectal Cancers At High-Risk of Disease Recurrence Following Curative Surgery

    Yoshiko Mori, Takeshi Nagasaka, Hiroshi Tazawa, Yuzo Umeda, Tatsuya Morikawa, Nobuhito Kubota, Kazuhiro Yoshida, Yuko Takehara, Naosuke Yokomichi, Kiyoto Takehara, Kunitoshi Shigeyasu, Akihiro Nyuya, Rikiya Shiwaku, Manabu Suno, Naoshi Nishida, Toshiyoshi Fujiwara, Ajay Goel

    GASTROENTEROLOGY   144 ( 5 )   S85 - S85   2013.5

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  • Novel photoimmunotherapy (PIT) targeting cancer-associated fibroblasts (CAFs) for esophageal cancer.

    Shinichiro Watanabe, Kazuhiro Noma, Shinichi Urano, Toshiaki Ohara, Yuuri Hashimoto, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   73 ( 8 )   2013.4

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    DOI: 10.1158/1538-7445.AM2013-4946

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  • Combined effect of zoledronic acid and telomerase-specific oncolytic virotherapy for human osteosarcoma cells.

    Yasuaki Yamakawa, Joe Hasei, Hiroshi Tazawa, Shuhei Osaki, Tsuyoshi Sasaki, Toshiyuki Kunisada, Aki Yoshida, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   73 ( 8 )   2013.4

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    DOI: 10.1158/1538-7445.AM2013-3320

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  • Iron depletion by deferasirox have a synergistic effect on sorafenib in hepatocellular carcinoma.

    Shinichi Urano, Toshiaki Ohara, Shinichiro Watanabe, Kazuhiro Noma, Yasuko Tomono, Hiroshi Tazawa, Masafumi Kataoka, Nouso Kazuhiro, Yasuhiro Shirakawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   73 ( 8 )   2013.4

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    DOI: 10.1158/1538-7445.AM2013-5608

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  • Cytotoxic effect of photosensitive fluorescent protein KillerRed-expressing adenovirus against human cancer cells

    Kiyoto Takehara, Hiroshi Tazawa, Yuuri Hashimoto, Hiroyuki Kishimoto, Nobuhiro Narii, Hiroyuki Mizuguchi, Toshiyoshi Fujiwara

    CANCER RESEARCH   73 ( 8 )   2013.4

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    DOI: 10.1158/1538-7445.AM2013-3318

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  • Oncolytic adenovirus-armed p53 induces apoptosis significantly through upregulating miR-93 and 106b in human osteosarcoma cells

    Joe Hasei, Tsuyoshi Sasaki, Hiroshi Tazawa, Yuuri Hashimoto, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   73 ( 8 )   2013.4

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    DOI: 10.1158/1538-7445.AM2013-3316

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  • WS-17-7 テロメラーゼ活性を指標とする血中遊離癌細胞の高感度検出法の開発と遺伝子解析技術への応用(WS ワークショップ,第113回日本外科学会定期学術集会)

    重安 邦俊, 橋本 悠里, 宇野 太, 永坂 岳司, 田澤 大2), 香川 俊輔, 水口 裕之, 浦田 泰生, 藤原 俊義

    日本外科学会雑誌   114 ( 2 )   338 - 338   2013.3

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  • PS-067-5 テロメラーゼ依存性増殖型アデノウイルス製剤を用いた早期大腸癌の低侵襲治療の開発(PS ポスターセッション,第113回日本外科学会定期学術集会)

    菊地 覚次, 岸本 浩行, 田澤 大, 橋本 悠里, 宇野 太, 西崎 正彦, 香川 俊輔, 浦田 泰生, Hoffman Robert, 藤原 俊義

    日本外科学会雑誌   114 ( 2 )   612 - 612   2013.3

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  • PS-084-5 温阻血再灌流+肝切除モデルにおけるHMGBIの動態解析および肝再生機序の解明(PS ポスターセッション,第113回日本外科学会定期学術集会)

    杉原 正大, 貞森 裕, 西堀 正洋, 佐藤 康晴, 田澤 大, 吉田 龍一, 楳田 祐三, 篠浦 先, 永坂 岳司, 八木 孝仁, 藤原 俊義

    日本外科学会雑誌   114 ( 2 )   637 - 637   2013.3

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  • 消化器癌における血中遊離癌細胞の検出と臨床応用 テロメラーゼ活性を指標とする血中遊離癌細胞の高感度検出法の開発と遺伝子解析技術への応用

    重安 邦俊, 橋本 悠里, 宇野 太, 永坂 岳司, 田澤 大, 香川 俊輔, 水口 裕之, 浦田 泰生, 藤原 俊義

    日本外科学会雑誌   114 ( 臨増2 )   338 - 338   2013.3

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  • 温阻血再灌流+肝切除モデルにおけるHMGB1の動態解析および肝再生機序の解明

    杉原 正大, 貞森 裕, 西堀 正洋, 佐藤 康晴, 田澤 大, 吉田 龍一, 楳田 祐三, 篠浦 先, 永坂 岳司, 八木 孝仁, 藤原 俊義

    日本外科学会雑誌   114 ( 臨増2 )   637 - 637   2013.3

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  • テロメラーゼ依存性増殖型アデノウイルス製剤を用いた早期大腸癌の低侵襲治療の開発

    菊地 覚次, 岸本 浩行, 田澤 大, 橋本 悠里, 宇野 太, 西崎 正彦, 香川 俊輔, 浦田 泰生, Robert Hoffman, 藤原 俊義

    日本外科学会雑誌   114 ( 臨増2 )   612 - 612   2013.3

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  • Genetically engineered oncolytic adenovirus induces autophagic cell death through an E2F1-microRNA-7-epidermal growth factor receptor axis

    125 ( 3 )   195 - 199   2013

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  • 癌微小リンパ節転移を標的とするテロメラーゼ特異的制限増殖型ウイルス製剤の開発.

    児島 亨, 渡邉雄一, 橋本悠里, 黒田新士, 山崎泰源, 矢野修也, 田澤 大, 宇野 太, 香川俊輔, 田中紀章, 浦田泰生, 藤原俊義

    岡山医学会雑誌   125 ( 1 )   9 - 12   2013

  • 鉄代謝を利用した新規分子標的薬併用療法

    浦野真一, 大原利章, 白川靖博, 野間和広, 前田直見, 田辺俊介, 櫻間教文, 田澤大, 藤原俊儀

    日本消化器癌発生学会総会プログラム・抄録集   24th   2013

  • 予後および病態評価が可能な新規食道癌同所移植性モデル

    大原利章, 白川靖博, 野間和広, 浦野真一, 前田直見, 田辺俊介, 櫻間教文, 田澤大, 藤原俊義

    日本消化器癌発生学会総会プログラム・抄録集   24th   2013

  • 腫瘍特異的制限増殖型アデノウイルスを用いた血液循環腫瘍細胞の遺伝子解析技術の開発(Development of genetic analysis of circulating tumor cells using a telomerase-specific replication-competent adenovirus)

    重安 邦俊, 橋本 悠里, 宇野 太, 永坂 岳司, 田澤 大, 香川 俊輔, 水口 裕之, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   71回   50 - 50   2012.8

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  • 癌関連線維芽細胞が食道癌の増殖に寄与する(Cancer-associated fibroblasts contribute to progression of esophageal cancer)

    渡邉 伸一郎, 野間 和広, 浦野 真一, 大原 利章, 橋本 悠里, 田澤 大, 藤原 俊義

    日本癌学会総会記事   71回   143 - 143   2012.8

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  • テロメラーゼ依存性増殖型アデノウイルス製剤を用いた早期大腸癌の低侵襲治療の開発(Less invasive therapeutic intervention for early colorectal cancers using telomerase-dependent replicating adenovirus)

    菊地 覚次, 岸本 浩行, 田澤 大, 橋本 悠里, 宇野 太, 西崎 正彦, 香川 俊輔, 浦田 泰生, ロバート・ホフマン, 藤原 俊義

    日本癌学会総会記事   71回   202 - 202   2012.8

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  • がん特異的増殖アデノウイルス製剤OBP-401を用いた生体内癌組織蛍光イメージング

    岸本 浩行, 菊地 覚次, 橋本 悠里, 宇野 太, 田澤 大, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本消化器外科学会総会   67回   1 - 1   2012.7

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  • Preclinical evaluation of cytotoxic effect of photosensitive fluorescent protein in human cancer cells

    Hiroshi Tazawa, Tsuyoshi Sasaki, Yuuri Hashimoto, Satoru Kikuchi, Hiroyuki Kishimoto, Hiroyuki Mizuguchi, Toshiyoshi Fujiwara

    CANCER RESEARCH   72   2012.4

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    DOI: 10.1158/1538-7445.AM2012-5656

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  • Inhibitory effect of oncolytic adenovirus on transforming growth factor-beta-induced epithelial-mesenchymal transition in human cancer cells

    Yuuri Hashimoto, Hiroshi Tazawa, Yasuo Urata, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   72   2012.4

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    DOI: 10.1158/1538-7445.AM2012-343

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  • A precise orthotopic rectal tumor model for evaluating therapeutic response of cancer treatment

    Satoru Kikuchi, Hiroyuki Kishimoto, Hiroshi Tazawa, Yuuri Hashimoto, Futoshi Uno, Masahiko Nishizaki, Shunsuke Kagawa, Yasuo Urata, Robert M. Hoffman, Toshiyoshi Fujiwara

    CANCER RESEARCH   72   2012.4

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    DOI: 10.1158/1538-7445.AM2012-2442

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  • Iron deficiency suppresses EMT through down-regulation of N-cadherin in esophageal cancer.

    Shinichiro Watanabe, Seishi Nishitani, Kazuhiro Noma, Toshiaki Ohara, Yasuko Tomono, Yuuri Hashimoto, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   72   2012.4

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    DOI: 10.1158/1538-7445.AM2012-2421

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  • A highly sensitive detection system of genetic alterations in circulating tumor cells using a telomerase-specific replication-competent adenovirus

    Kunitoshi Shigeyasu, Yuuri Hashimoto, Tatsuya Morikawa, Yoshiko Mori, Dong-Sheng Sun, Shunsuke Kagawa, Futoshi Uno, Hiroshi Tazawa, Takeshi Nagasaka, Satoru Kyo, Hiroyuki Mizuguchi, Yasuo Urata, Toshiyoshi Fujiwara

    CANCER RESEARCH   72   2012.4

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    DOI: 10.1158/1538-7445.AM2012-2385

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  • p53-mediated apoptotic signaling overcomes the resistance to oncolytic adenovirus in human osteosarcoma cells

    Joe Hasel, Tsuyoshi Sasaki, Hiroshi Tazawa, Yuuri Hashimoto, Toshiyuki Kunisada, Yasuo Urata, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   72   2012.4

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    DOI: 10.1158/1538-7445.AM2012-5651

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  • Iron chelator contributes to anti-angiogenic therapy via selective induction of VEGF-A

    Toshiaki Ohara, Kazuhiro Noma, Seishi Nishitani, Shinichiro Watanabe, Yasuko Tomono, Yuuri Hashimoto, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   72   2012.4

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    DOI: 10.1158/1538-7445.AM2012-2323

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  • Preclinical evaluation of telomerase-specific oncolytic virotherapy for human bone and soft tissue sarcomas

    124 ( 2 )   105 - 110   2012

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  • 鉄欠乏状態は食道がんにおいてNカドヘリンを低下させることでEMTを抑制する(Iron deficiency suppress EMT through downregulation of N-cadherin in esophageal cancer)

    西谷 正史, 野間 和広, 大原 利章, 長谷井 嬢, 佐々木 剛, 渡邊 伸一郎, 大西 哲平, 吉田 亮介, 橋本 悠里, 田澤 大, 宇野 太, 香川 俊輔, 藤原 俊義

    日本癌学会総会記事   70回   467 - 468   2011.9

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  • 胃癌幹細胞に対するテロメラーゼ特異的腫瘍融解ウイルス治療

    香川 俊輔, 矢野 修也, 田澤 大, 橋本 悠里, 宇野 太, 岸本 浩行, 西崎 正彦, 浦田 泰生, 藤原 俊義

    日本癌治療学会誌   46 ( 2 )   395 - 395   2011.9

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  • HER2陰性胃癌細胞におけるHER2細胞外ドメイン発現によるトラスツズマブへの感受性誘導

    吉田 亮介, 田澤 大, 橋本 悠里, 大西 哲平, 岸本 浩行, 宇野 太, 西崎 正彦, 香川 俊輔, 藤原 俊義

    日本癌治療学会誌   46 ( 2 )   655 - 655   2011.9

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  • IS-9-3 Mechanism of resistance to trastuzumab and molecular sensitization via ADCC activation by exogenous expression of HER2 extracellular domain in breast cancer cells(IS-9 Translational research in breast cancer treatment)

    Yoshida Ryosuke

    Journal of Japan Surgical Society   112 ( 1 )   202 - 202   2011.5

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  • 体内鉄コントロールを利用したBevacizumabの新規治療法

    大原 利章, 野間 和広, 友野 靖子, 西谷 正史, 田辺 俊介, 田澤 大, 白川 靖博, 藤原 俊義

    日本外科学会雑誌   112 ( 臨増1-2 )   771 - 771   2011.5

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  • Bioengineered oncolytic adenovirus induces autophagic cell death through an E2F1-microRNA-7-epidermal growth factor receptor axis

    Hiroshi Tazawa, Shuya Yano, Ryosuke Yoshida, Yasuo Urata, Toshiyoshi Fujiwara

    CANCER RESEARCH   71   2011.4

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    DOI: 10.1158/1538-7445.AM2011-2862

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  • Iron deficiency suppress EMT through downregulation of N-cadherin in esophageal cancer

    Seishi Nishitani, Kazuhiro Noma, Shinichiro Watanabe, Teppei Onishi, Toshiaki Ohara, Yasuko Tomono, Yuuri Hashimoto, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   71   2011.4

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    DOI: 10.1158/1538-7445.AM2011-3363

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  • Iron controlled treatment can be novel therapeutic agent and biomarker of Bevacizumab

    Toshiaki Ohara, Kazuhiro Noma, Shinichiro Watanabe, Teppei Ohnishi, Seishi Nishitani, Yasuko Tomono, Yuuri Hashimoto, Hiroshi Tazawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   71   2011.4

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    DOI: 10.1158/1538-7445.AM2011-4247

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  • Mechanism of resistance to trastuzumab and molecular sensitization via ADCC activation by exogenous expression of HER2 extracellular domain in human breast cancer cells

    Ryosuke Yoshida, Hiroshi Tazawa, Yuuri Hashimoto, Futoshi Uno, Shunsuke Kagawa, Toshiyoshi Fujiwara

    CANCER RESEARCH   71   2011.4

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    DOI: 10.1158/1538-7445.AM2011-720

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  • Preclinical evaluation of telomerase-specific oncolytic virotherapy for human bone and soft tissue sarcomas

    Tsuyoshi Sasaki, Hiroshi Tazawa, Jo Hasei, Toshiyuki Kunisada, Aki Yoshida, Yuki Morimoto, Yasuo Urata, Kazuhiro Nouso, Toshifumi Ozaki, Toshiyoshi Fujiwara

    CANCER RESEARCH   71   2011.4

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    DOI: 10.1158/1538-7445.AM2011-5415

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  • Radiosensitization by telomerase-dependent oncolytic adenovirus

    Kuroda Shinji, Noma Kazuhiro, Urata Yasuo, Kagawa Shunsuke, Fujiwara Toshiyoshi, Fujiwara Toshiya, Shirakawa Yasuhiro, Yamasaki Yasumoto, Yano Syuya, Uno Futoshi, Tazawa Hiroshi, Hashimoto Yuuri, Watanabe Yuichi

    Okayama Igakkai Zasshi (Journal of Okayama Medical Association)   123 ( 2 )   103 - 109   2011

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  • TELOMERASE-SPECIFIC ONCOLYTIC ADENOVIRUS ARMED WITH WILD-TYPE P53 GENE (CGCT-04) EFFICIENTLY INDUCES APOPTOSIS IN HUMAN CANCER CELLS

    Yasumoto Yamasaki, Hideki Onimatsu, Yuuri Hashimoto, Toru Kojima, Hiroshi Tazawa, Shunsuke Kagawa, Hiroyuki Mizuguchi, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    JOURNAL OF GENE MEDICINE   12 ( 12 )   1035 - 1035   2010.12

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  • PRECLINICAL STUDY OF TELOMERASE-SELECTIVE ONCOLYTIC ADENOVIRUS (OBP-301) IN COMBINATION WITH CHEMOTHERAPEUTIC AGENT AND RADIATION

    Hiroshi Tazawa, Yuuri Hashimoto, Shinji Kuroda, Yasuo Urata, Toshiyoshi Fujiwara

    JOURNAL OF GENE MEDICINE   12 ( 12 )   1035 - 1036   2010.12

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  • A NOVEL TELOMERASE-SPECIFIC ONCOLYTIC VIROTHERAPY TARGETING GASTRIC CANCER STEM CELLS

    Shuya Yano, Yuuri Hashimoto, Toru Kojima, Shinji Kuroda, Hiroshi Tazawa, Futoshi Uno, Shunsuke Kagawa, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    JOURNAL OF GENE MEDICINE   11 ( 12 )   1154 - 1154   2009.12

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  • ゲノム研究が切り開く肺がんの新たな予防・治療戦略 肺癌に対する遺伝子およびベクターを用いた分子治療(Novel therapeutic and preventive strategies blazed by genome research on lung cancer Gene and Vector-based Molecular Therapy for Lung Cancer)

    香川 俊輔, 黒田 新士, 宇野 太, 田澤 大, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   68回   56 - 56   2009.8

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  • Clinical Application of Telomerase-Specific Oncolytic Adenovirs to Ex Vivo Biological Imaging of Human Circulating Tumor Cells

    Futoshi Uno, Yuuri Hashimoto, Toru Kojima, Shunsuke Kagawa, Hiroshi Tazawa, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    MOLECULAR THERAPY   17   S237 - S237   2009.5

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  • Telomerase-specific oncolytic adenovirus armed with wild-type p53 gene (CGCT-04) efficiently induces apoptosis in human cancer cells

    Yasumoto Yamasaki, Hideki Onimatsu, Yuuri Hashimoto, Toru Kojima, Hiroshi Tazawa, Shunsuke Kagawa, Hiroyuki Mizuguchi, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    CANCER RESEARCH   69   2009.5

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  • Telomerase-specific oncolytic virotherapy purging cancer stem cells

    Shuya Yano, Yuuri Hashimoto, Shinji Kuroda, Tohru Kojima, Futoshi Uno, Hiroshi Tazawa, Shunsuke Kagawa, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    CANCER RESEARCH   69   2009.5

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  • Preclinical study of telomerase-selective oncolytic adenovirus (OBP-301) in combination with chemotherapeutic agents

    Hiroshi Tazawa, Yuuri Hashimoto, Shinji Kuroda, Yasuo Urata, Toshiyoshi Fujiwara

    CANCER RESEARCH   69   2009.5

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  • Telomerase-specific oncolytic adenovirus mediates molecular sensitization to ionizing radiation in human cancer cells through E1B55kDa expression

    Shinji Kuroda, Toshiya Fujiwara, Hiroshi Tazawa, Futoshi Uno, Shunsuke Kagawa, Yuuri Hashimoto, Masaaki Ouchi, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    CANCER RESEARCH   69   2009.5

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  • Biological purging of lymph node metastasis of gastrointestinal cancer by telomerase-specific virotherapy

    Toru Kojima, Yuuri Hashimoto, Shinji Kuroda, Yasumoto Yamasaki, Shuya Yano, Hiroshi Tazawa, Futoshi Uno, Shunsuke Kagawa, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

    CANCER RESEARCH   69   2009.5

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  • テロメラーゼ依存性腫瘍融解ウイルスの抗腫瘍活性における抗がん剤併用の相乗効果(Preclinical study of telomerase-selective oncolytic adenovirus in combination with chemotherapeutic agents)

    田澤 大, 橋本 悠里, 黒田 新士, 浦田 泰生, 藤原 俊義

    日本癌学会総会記事   67回   239 - 239   2008.9

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  • テロメラーゼ依存性腫瘍融解アデノウイルスによる放射線感受性増強 E1B55kDaによるATMリン酸化阻害(Radiosensitization by telomerase-specific oncolytic adenovirus via E1B 55kDa-mediated inhibition of ATM phosphorylation)

    黒田 新士, 藤原 俊哉, 矢野 修也, 山崎 泰源, 児島 亨, 宇野 太, 香川 俊輔, 田澤 大, 橋本 悠里, 大内 正明, 浦田 泰生, 田中 紀章, 藤原 俊義

    日本癌学会総会記事   67回   90 - 90   2008.9

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  • 胃癌幹細胞に対する新規治療 テロメラーゼ特異的腫瘍融解ウイルス治療(A Novel Telomerase-Specific Oncolytic Virotherapy Targeting Human Gastric Cancer Stem Cells)

    矢野 修也, 橋本 悠里, 山崎 泰源, 黒田 新士, 児島 亨, 田澤 大, 宇野 太, 香川 俊輔, 大内 正明, 浦田 泰生, 田中 紀章, 藤原 俊義

    日本癌学会総会記事   67回   73 - 74   2008.9

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  • スーパーオキシドジスムターゼの経口投与による炎症介在性腫瘍進行の予防(Prevention of inflammation-mediated tumor progression by orally available superoxide dismutase)

    小沼 邦重, 塩野谷 博, 田澤 大, 松原 範宜, 小林 正伸, 細川 眞澄男, 岡田 太

    日本癌学会総会記事   66回   295 - 295   2007.8

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  • 良性腫瘍の炎症介在性の転移能獲得における反応性一酸化窒素の関与(Involvement of reactive nitrogen oxides for acquisition of metastatic properties of benign tumors through inflammation)

    岡田 太, 田澤 大, 小沼 邦重, 小林 正伸, 細川 眞澄男

    日本癌学会総会記事   66回   295 - 295   2007.8

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  • The role of nitrative DNA damage in inflammation-associated carcinogenesis

    H. Ohshima, T. Sawa, H. Tazawa, S. Kawanishi

    NITRIC OXIDE-BIOLOGY AND CHEMISTRY   17   S10 - S10   2007

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    DOI: 10.1016/j.niox.2007.09.011

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  • 発癌・悪性化要因としての炎症細胞由来活性酸素の証明

    岡田太, 小沼邦重, 田中宏樹, 田澤大, 小林正伸, 細川眞澄男

    日本癌学会学術総会記事   65th   263   2006.8

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  • 炎症による大腸腺腫プログレッションに伴う蛋白質fascinの変化とその機能解析

    岡田太, 河口徳一, 田沢大, 小林正伸, 北川知行, 細川真澄男

    日本癌学会学術総会記事   64th   152 - 153   2005.8

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  • Possible association between tandem repeat number polymorphism of a (CCTTT) pentanucleotide in inducible nitric oxide synthase promoter region and gastric cancer in japanese women

    M Tatemichi, T Sawa, H Tazawa, S Wada, Gilibert, I, T Katoh, H Ohshima

    NITRIC OXIDE-BIOLOGY AND CHEMISTRY   11 ( 1 )   104 - 104   2004.8

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  • Quantitative analysis of 8-nitroguanine in biological fluids by HPLC-electrochemical detection coupled with immunoaffinity purification

    T Sawa, A Barbin, T Akaike, H Tazawa, S Ohnishi, H Ohshima

    NITRIC OXIDE-BIOLOGY AND CHEMISTRY   11 ( 1 )   105 - 105   2004.8

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  • The roles of inducible nitric oxide synthase and p53 on cyclooxygenase-2 expression in mice macrophages

    S Wada, M Tatemichi, H Tazawa, T Sawa, H Nishino, H Ohshima

    NITRIC OXIDE-BIOLOGY AND CHEMISTRY   11 ( 1 )   102 - 102   2004.8

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  • Suppression of thymic lymphoma and increased non-thymic lymphomagenesis in Trp53-deficient mice lacking inducible nitric oxide synthase gene

    M Tatemichi, H Tazawa, M Masuda, M Saleem, S Wada, P Cros, Gilibert, I, LA Donehower, H Ohgaki, H Ohshima

    NITRIC OXIDE-BIOLOGY AND CHEMISTRY   11 ( 1 )   105 - 105   2004.8

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  • 炎症によるヒト大腸腺腫細胞の癌化に伴う遺伝子発現変化

    岡田太, 田沢大, 小林正伸, 河口徳一, 北川知行, 細川真澄男

    日本癌学会総会記事   62nd   281 - 281   2003.8

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  • 慢性炎症によるヒト大腸腺腫細胞のがん化に伴うfascin蛋白の発現増加

    岡田太, HABELHAH H, 小林徳栄, 田沢大, DING W, 小林正伸, 河口徳一, 北川知行, 細川真澄男

    日本癌学会総会記事   61st   60   2002.8

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  • ヒト家族性大腸腺腫細胞の悪性化におけるNOの役割

    岡田太, 河口徳一, 小林徳栄, 田沢大, 守内哲也, 西野輔翼, 北川知行, 細川真澄男

    日本癌学会総会記事   60th   76 - 76   2001.9

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  • マウス線維肉腫細胞の転移能獲得に占める好中球の役割

    田沢大, 岡田太, 小林徳栄, 宇根良衛, 守内哲也, 仙道富士郎, 細川真澄男

    日本癌学会総会記事   60th   175 - 175   2001.9

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  • Conversion of human colonic adenoma cells to adenocarcinoma′ cells through inflammation in nude mice.

    Okada F., Kawaguchi T., Habelhah H., Kobayashi T., ′ Tazawa H., Takeichi N., Kitagawa T., Hosokawa M.

    Collected papers from Institute for Genetic Medicine Hokkaido University   2   208 - 219   2001

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  • ゼラチンスポンジ同時皮下移植によるマウス線維肉腫細胞の悪性化進展における好中球の役割

    田沢大, 岡田太, 小林徳栄, DING W, 宇根良衛, 守内哲也, 仙道富士郎, 細川真澄男

    Japanese Journal of Cancer Research   91 ( Supplement (Sept) )   289 - 289   2000.9

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  • サイモシンβ4発現調節によるマウス線維肉腫細胞の悪性化形質の転換

    小林徳栄, 藤井信之, 伊藤哲, 岡田太, 田沢大, 守内哲也, 細川真澄男

    Japanese Journal of Cancer Research   91 ( Supplement (Sept) )   517 - 517   2000.9

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  • 家族性大腸腺腫FPCK‐1‐1細胞のプログレッションにおける活性窒素の役割

    岡田太, 河口徳一, 小林徳栄, 田沢大, 波江野力, 守内哲也, 北川知行, 細川真澄男

    Japanese Journal of Cancer Research   91 ( Supplement (Sept) )   57 - 57   2000.9

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  • 家族性大腸腺腫FPCK‐1‐1細胞の悪性化における間質反応の役割

    岡田太, 河口徳一, 小林徳栄, 田沢大, 守内哲也, 北川知行, 細川真澄男

    日本癌学会総会記事   58th   590 - 590   1999.8

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  • マウス線維肉腫細胞の悪性化進展におけるE1AFの発現増強とその意義

    田沢大, HABELHAH H, 岡田太, 小林徳栄, 藤永恵, 吉田幸一, 守内哲也, 細川真澄男

    日本癌学会総会記事   58th   599 - 599   1999.8

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Awards

  • がん研究奨励賞

    2013.6   岡山医学会  

    田澤 大

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  • アンジェスMG賞

    2012.6   日本遺伝子治療学会  

    田澤 大

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  • とやま賞(医薬部門)

    2010.5   財団法人 富山県ひとづくり財団  

    田澤 大

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  • 優秀発表賞

    2007.9   日本疾患モデル学会  

    田澤 大

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Research Projects

  • 原発性脊椎腫瘍に対する腫瘍融解ウイルス療法の確立

    Grant number:24K12352  2024.04 - 2027.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    鷹取 亮, 吉田 晶, 小田 孔明, 魚谷 弘二, 篠原 健介, 藤原 智洋, 田澤 大

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

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  • 脊椎脊髄腫瘍に対する腫瘍融解ウイルス療法の確立

    Grant number:23K08589  2023.04 - 2026.03

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    魚谷 弘二, 吉田 晶, 尾崎 敏文, 藤原 智洋, 田澤 大, 三澤 治夫, 小田 孔明

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    Grant amount:\4810000 ( Direct expense: \3700000 、 Indirect expense:\1110000 )

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  • Immune molecular mechanism for enhancing antitumor potency of a next-generation oncolytic virus by pre-immunization

    Grant number:22H03148  2022.04 - 2025.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    藤原 俊義, 田澤 大, 黒田 新士

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    Grant amount:\17680000 ( Direct expense: \13600000 、 Indirect expense:\4080000 )

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  • Exploration of metabolic factors to inhibit tumor-specific p53 gene therapy in pancreatic cancer

    Grant number:21K07219  2021.04 - 2024.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    田澤 大

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    Grant amount:\4160000 ( Direct expense: \3200000 、 Indirect expense:\960000 )

    遺伝子変異に応じたゲノム医療は癌患者に最適な個別化治療を提供することが期待されている。しかし、KRAS/p53変異膵臓癌への治療法は未だ確立していない。申請者は癌特異的にp53を誘導するアデノウイルス製剤OBP-702を開発し、KRAS/p53変異膵臓癌細胞の腫瘍増殖を抑制することを明らかにし、臨床応用を進めている。しかし、膵臓癌細胞には解糖系と非解糖系の代謝サブタイプが存在し、アデノウイルスに対する感受性が代謝サブタイプによって異なることが示唆されている。
    本研究では、解糖系と非解糖系のヒト膵臓癌細胞を用いてOBP-702に対する感受性を阻害する代謝関連因子を網羅的に解析し、代謝調節剤を併用することでOBP-702抵抗性を改善する最適なOBP-702個別化治療の開発を行う。
    令和3年度は、解糖系のヒト膵臓癌細胞株2種類(MIAPaCa-2、PK-45H)と非解糖系のヒト膵臓癌細胞株2種類(PK-59、Capan-2)における代謝関連因子の発現をウェスタンブロット法で解析し、解糖系のヒト膵臓癌細胞は非解糖系に比べてLDHA、IDH1、GOT1の発現レベルが高いことを確認した。次に、OBP-702に対する感受性をXTTアッセイで解析し、解糖系のヒト膵臓癌細胞は非解糖系に比べてウイルス感受性が高いことを確認した。ウイルス感受性の違いはp53非搭載型のアデノウイルス製剤OBP-301でも同様の結果であった。ウイルス感受性の違いのメカニズムを明らかにするために、細胞表面のウイルス受容体やインテグリンの発現をFACS法で解析したが、大きな違いは認めなかった。一方、ウイルス感染後のE1Aの発現をウェスタンブロット法で解析し、解糖系のヒト膵臓癌細胞は非解糖系に比べてE1Aの発現レベルが高いことを確認した。以上より、代謝関連因子がウイルスの複製効率に大きく関与している可能性が示唆された。

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  • Development of a next-generation viral agent targeting immunosuppression by crosstalk in the pancreatic cancer microenvironment

    Grant number:19H03731  2019.04 - 2022.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    Fujiwara Toshiyoshi

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    Grant amount:\17550000 ( Direct expense: \13500000 、 Indirect expense:\4050000 )

    We examined the effect of OBP-702, a next-generation armed adenovirus OBP-702, which carries the multifunctional tumor suppressor p53 gene, on the immunosuppressive pancreatic cancer microenvironment. Pancreatic cancer stromal cells (human pancreatic stellate cells: hPSC) promoted tumor growth by coexisting with pancreatic cancer cells in the pancreatic cancer microenvironment, and OBP-702 produced strong p53 gene expression in hPSC. By inducing selective apoptosis, in addition to the antitumor effect on the pancreatic cancer cells, OBP-702 exhibited a profound antitumor activity through the control of the pancreatic cancer microenvironment.

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  • Imaging system for progression of gastrointestinal cancer and its application to anti-metastasis therapy

    Grant number:17K10589  2017.04 - 2020.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Nishizaki Masahiko

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    Grant amount:\4550000 ( Direct expense: \3500000 、 Indirect expense:\1050000 )

    Patients with metastatic and disseminated gastrointestinal cancers show poor prognosis and the development of anti-metastasis therapy to prevent cancer metastasis and dissemination is an important issue. Here, we developed a drug screening system using colorectal cancer (CRC) cells with fluorescence probe for epithelial-mesenchymal transition (EMT). Anti-inflammatory drug aspirin inhibited inflammatory cytokine-induced EMT and prevented peritoneal dissemination of CRC cells. In the future, we need to evaluate the therapeutic effect of aspirin in the metastasis and dissemination of non-CRC cells.

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  • Preclinical study of tumor-specific p53 gene therapy against refractory pancreatic cancer

    Grant number:16K10596  2016.04 - 2019.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    TAZAWA HIROSHI

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    Grant amount:\4680000 ( Direct expense: \3600000 、 Indirect expense:\1080000 )

    Pancreatic ductal adenocarcinoma (PDAC) frequently shows invasion and metastasis, leading to treatment resistance and poor prognosis. The development of novel antitumor strategy for PDAC is an urgent issue. Here, we show that a tumor-specific replication-competent oncolytic adenovirus expressing tumor suppressor p53, OBP-702, inhibits the migration and invasion abilities and tumor growth and induces the immunogenic cell death in human PDAC cells. In the future, the clinical application of a multiplidisciplinary therapy with OBP-702 is important.

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  • Development of the Dual fluorescent cytology with tumor-specific viruses for gastrointestinal cancer precision medicine

    Grant number:16H05416  2016.04 - 2019.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    FUJIWARA Toshiyoshi

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    Grant amount:\17680000 ( Direct expense: \13600000 、 Indirect expense:\4080000 )

    Peritoneal dissemination is the most common form of metastasis in gastrointestinal cancer, and is associated with an extremely poor prognosis. We developed a new approach to visualize floating tumor cells using a green fluorescent protein (GFP)-expressing attenuated adenovirus in which the telomerase promoter regulates viral replication (TelomeScan, OBP-401). Moreover, we used a unique TelomeScan derivative (TelomeScan-F45, OBP-1101) that have a strict replication control function by micro-RNA together with targeting properties through CD46; however, unfortunately, the combination strategy was not able to show the usefulness.

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  • Analysis for intraperitoneal cancer microenvironment to elucidate the biological mechanism of peritoneal metastasis of gastrointestinal cancer

    Grant number:15K15193  2015.04 - 2017.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Exploratory Research

    Shunsuke Kagawa, KURODA Shinji, NAGASAKA Takeshi, TAZAWA Hiroshi, FUJIWARA Toshiyoshi

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    Grant amount:\3770000 ( Direct expense: \2900000 、 Indirect expense:\870000 )

    Gastrointestinal cancer develops peritoneal dissemination, which is known to be refractory to current therapy. To overcome it, cancer microenvironment is need to be analyzed. For analysis of cells constituting the intraperitoneal microenvironment, we obtained peritoneal lavage fluid from patients with stomach cancer and pancreatic cancer and employed cancer-specific GFP expression virus TelomeScan to label cancer cell and immunostaining, which revealed the prevalence of tumor-associated macrophages (TAM) in the peritoneal cavity. Under the co-culture of stomach cancer or pancreatic cancer cells with TAM, the epithelial to mesenchymal transition of cancer cells, the enhancement of malignant phenotypes such as infiltration, migration, and acquired resistance to the chemotherapeutic agents were observed. These results suggested that intraperitoneal microenvironment, especially TAM, may contribute to the refractoriness of gastrointestinal tumor peritoneal dissemination.

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  • Development of anti-metastasis therapy in the inflammation-related gastric cancer progression

    Grant number:26461978  2014.04 - 2017.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    NISHIZAKI MASAHIKO

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    Grant amount:\4940000 ( Direct expense: \3800000 、 Indirect expense:\1140000 )

    Chronic inflammation-related inflammatory microenvironment is a risk factor in gastric cancer development. In this study, we showed the promoting effect of inflammatory microenvironment, such as stromal fibroblast and macrophage, in gastric cancer progression. Moreover, we confirmed that a tumor-specific replication-competent oncolytic adenovirus OBP-702 that induces tumor suppressor p53 gene had a therapeutic potential to induce profound anti-tumor effect against intraperitoneal metastasis of gastric cancer.

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  • Novel targeting therapy to cancer-associated fibroblasts for treatment-resistant carcinomas

    Grant number:26861077  2014.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)

    Noma Kazuhiro, KATSUBE Ryoichi, SHIRAKAWA Yasuhiro, OHARA Toshiaki, FUJIWARA Toshiyoshi, TAZAWA Hiroshi

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    Grant amount:\3770000 ( Direct expense: \2900000 、 Indirect expense:\870000 )

    CAF of fibroblast cells by esophageal cancer and the promoted malignancy of cancer cells by the CAF were verified. Fibroblasts turned into CAF in the interaction of the cancer cells, the cancer cells by stimulation of the CAF enhanced the malignancy. In addition, cancer cells which are stimulated by CAF had acquired a treatment-resistant phenotype to chemotherapy and radiation therapy. In animal studies it was observed a decreased anti-tumor effect of 5-FU in the group inoculated with CAF, showing treatment-resistant as well as in vitro. It has been predicted that controlling the CAF can suppress the acquisition of growth and therapy-resistant cancers. Subsequently, we have succeeded in developing selectively Photoimmunotherapy that target the CAF.

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  • Development of novel microRNA-based therapy against KRAS/BRAF-mutant colorectal cancer

    Grant number:25462057  2013.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    TAZAWA HIROSHI

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    Grant amount:\5070000 ( Direct expense: \3900000 、 Indirect expense:\1170000 )

    KRAS/BRAF-mutant colorectal cancer is an intractable disease that frequently shows the refractory to chemotherapy, recurrence and metastatic progression. Since EGFR signaling pathway is constitutively activated in KRAS/BRAF-mutant colorectal cancer, the development of novel therapy for strongly suppressing EGFR signaling pathway is important issue. Here we show that oncolytic adenoviruses have profound antitumor effect through activation of EGFR-suppressive microRNA and induction of apoptosis- and autophagy-related cell death against KRAS/BRAF-mutant colorectal cancer.

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  • Photoimmunotherapy for gastrointestinal cancer

    Grant number:25462021  2013.04 - 2016.03

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    Tanabe Shunsuke, KAGAWA Shunsuke, OYAMA Takanori, FUJIWARA Toshiyoshi, TAZAWA Hiroshi

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    Grant amount:\4940000 ( Direct expense: \3800000 、 Indirect expense:\1140000 )

    The lack of particular target antigens in gastric cancer other than HER2 has hampered the development of new treatments for gastric cancer.We hypothesized that HER2-extracellular domain (HER2-ECD) gene transduction combined with trastuzumab-based photoimmunotherapy (PIT) might provide excellent and selective antitumor effects for peritoneal dissemination of gastric cancer. Adenovirus/HER2-ECD(Ad/HER2-ECD) efficiently transduced HER2-ECD into HER2-negative gastric cancer cells. Trastuzumab-mediated PIT induced selective cell death of HER2-ECD-transduced tumor cells, even in heterogeneous gastric cancer cells.Anti-HER2 PIT integrated with adenoviral HER2-ECD gene transfer was applied in mice bearing peritoneal dissemination of HER2-negative gastric cancer. Intraperitoneal administration of Ad/HER2-ECD and Tra-IR700 with PIT inhibited peritoneal metastasis and prolonged the survival of mice. Molecular-targeted PIT integrated with gene transfer technology is a promising strategy.

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  • Fluorescence-guided detection and genetic analysis of circulating tumor cells

    Grant number:23591932  2011 - 2013

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    KAGAWA Shunsuke, FUJIWARA Toshiyoshi, TAZAWA Hiroshi, SHIGEYASU Kunitoshi

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    Grant amount:\5200000 ( Direct expense: \4000000 、 Indirect expense:\1200000 )

    In addition to the conventional clinical information, molecular information obtained from cancer tissue is being used for proper selection of cancer therapy. The circulating tumor cells in the blood of cancer patients, if available, might be valuable source for such molecular information. We tried and succeeded to capture and analyze the rare tumor cells in the blood using a virus that can detect cancer cells with a fluorescent dye. This technology must be a novel molecular diagnostic method for cancer.

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  • Tumor suppressor FHIT regulates tumor invasion of pancreatic cancer cells via inhibiting association of Ezrin and Actin cytoskeleton

    Grant number:23592009  2011 - 2013

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)

    NISHIZAKI Masahiko, FUJIWARA Toshiyoshi, KAGAWA Shunsuke, NAGASAKA Takeshi, TAZAWA Hiroshi

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    Grant amount:\5070000 ( Direct expense: \3900000 、 Indirect expense:\1170000 )

    Ezrin is recognized as a key component in tumor metastasis and regulated by PKC. Abnormalities of tumor suppressor FHIT, whitch shares homology with PKCI (PKC-interacting protein), have been found in pancreatic cancers. In this study, we showed that FHIT overexpression in S2-VP10 pancreatic adenocarcinoma cells by transfection of Ad- FHIT suppressed migratory/invasive capacities of tumor cells. We observed that overexpression of FHIT largely reduced threonine-phosphorylated Ezrin. Furthermore, FHIT overexpression interrupted not only Ezrin and Actin cytoskeleton interaction but also Ezrin and PKC alpha interaction. We also found Fhit and PKC alpha binding in the immunoprecipitation analysis. Ectopic activation of FHIT significantly reduced the invasive potential in S2-VP10 cells. These findings suggested that overexpression of FHIT protein might regulate tumor invasion via inhibiting Ezrin and Actin cytoskeleton interaction.

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  • Circulating Tumor Cell of Gastrointestinal Stromal Tumor

    Grant number:23659651  2011 - 2012

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Challenging Exploratory Research

    UNO Futoshi, FUJIWARA Toshiyoshi, KAGAWA Shunsuke, NISHIZAKI Masahiko, NAGASAKA Takeshi, TAZAWA Hiroshi, SHIGEYAU Kunitoshi, HASHIMOTO Yuuri

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    Grant amount:\3640000 ( Direct expense: \2800000 、 Indirect expense:\840000 )

    We detected circulating tumor cells (CTCs) in the peripheral blood of Gastrointestinal Stromal Tumor (GIST) patients after some fundamental research useing a green fluorescent protein (GFP)-expressing attenuated adenovirus-5 vector, in which the hTERT promoter regulates viral replication (TelomeScan). CTCs were identified in samples from 6 of 12 patients with GIST. These results suggest that CTSs detection with our method might be a new bio-marker for GIST which frequently accompanied liver metastases.

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  • Induction of autophagic cell death via microRNA-mediated gene regulatory network

    Grant number:22791310  2010 - 2012

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)

    TAZAWA Hiroshi

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    Grant amount:\3900000 ( Direct expense: \3000000 、 Indirect expense:\900000 )

    Tumor-specific replication-competent oncolytic adenovirus is a promising antitumor agent. However, the mechanism on the virus-mediated cell death remains unclear. Here we show that telomerase-specific replication-competent oncolytic adenovirus Telomelysin induces autophagic cell death through microRNA-mediated gene regulatory network.

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