Faculty Profiles - KAGAWA Shunsuke

Papers - KAGAWA Shunsuke

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悪性リンパ腫合併胸部食道癌症例の治療経験

横道直佑, 白川靖博, 野間和広, 田辺俊介, 森川達也, 近藤喜太, 櫻間教文, 岸本浩行, 宇野太, 永坂岳司, 西崎正彦, 香川俊輔, 藤原俊義

岡山医学会雑誌 123 ( 2 ) 166 - 166 2011.8

頭頸部癌・食道癌におけるPEGを用いた栄養管理の有用性の検討

田辺俊介, 白川靖博, 野間和広, 横道直佑, 森川達也, 近藤喜太, 櫻間教文, 岸本浩行, 宇野太, 永坂岳司, 西崎正彦, 香川俊輔, 藤原俊義

岡山医学会雑誌 123 ( 2 ) 166 - 166 2011.8

岡山大学病院における胃癌に対するダビンチS(da Vinci S surgical system)によるロボット支援腹腔鏡下手術の導入

香川俊輔, 西崎正彦, 宇野太, 岸本浩行, 白川靖博, 永坂岳司, 野間和広, 田辺俊介, 近藤喜太, 横道直佑, 森川達也, 佃和憲, 浅野博昭, 内藤稔, 藤原俊義

岡山医学会雑誌 123 ( 2 ) 167 - 167 2011.8

同時多発性胃癌術後の残胃癌に関する検討

香川俊輔, 宇野太, 岸本浩行, 西崎正彦, 白川靖博, 永坂岳司, 野間和広, 近藤喜太, 田辺俊介, 藤原俊義

日本消化器外科学会総会 66回 297 - 297 2011.7

岡山大学外科研修マネージメントセンター医局を超えた外科研修教育の取り組み

菊地覚次, 香川俊輔, 篠浦先, 野間和広, 松岡順治, 土井原博義, 八木孝仁, 佐野俊二, 三好新一郎, 藤原俊義

日本消化器外科学会総会 66回 185 - 185 2011.7

胃癌に対する腹腔鏡下手術の新たな考え方と工夫肝十二指腸間膜左側アプローチによるNo.12a郭清

西崎正彦, 香川俊輔, 宇野太, 岸本浩行, 合地明, 藤原俊義

日本消化器外科学会総会 66回 276 - 276 2011.7

食道GISTの切除例2例の経験

井筒将斗, 白川靖博, 田辺俊介, 近藤喜太, 野間和広, 櫻間教文, 宇野太, 永坂岳司, 香川俊輔, 繁光薫, 山辻知樹, 羽井佐実, 松岡順治, 猶本良夫, 藤原俊義

岡山医学会雑誌 123 ( 1 ) 74 - 74 2011.4

Stage IVa食道癌の治療方針の検討

田辺俊介, 白川靖博, 井筒将斗, 近藤喜太, 野間和広, 櫻間教文, 宇野太, 永坂岳司, 香川俊輔, 繁光薫, 山辻知樹, 羽井佐実, 松岡順治, 猶本良夫, 藤原俊義

岡山医学会雑誌 123 ( 1 ) 74 - 74 2011.4

MicroRNAs as potential target gene in cancer gene therapy of gastrointestinal tumors Reviewed

Hiroshi Tazawa, Shunsuke Kagawa, Toshiyoshi Fujiwara

EXPERT OPINION ON BIOLOGICAL THERAPY 11 ( 2 ) 145 - 155 2011.2

Language：English Publisher：INFORMA HEALTHCARE

Introduction: MicroRNA (miRNA) is a small non-coding RNA, which negatively regulates the expression of many target genes, thereby contributing to the modulation of diverse cell fates. Recent advances in molecular biology have revealed the potential role of miRNAs in tumor initiation, progression and metastasis. Aberrant regulation of miRNAs has been frequently reported in a variety of cancers, including gastrointestinal tumors, suggesting that cancer-related miRNAs are promising as novel biomarkers for tumor diagnosis and are potential target genes for cancer gene therapy against gastrointestinal tumors.
Areas covered: The review focuses on the role of specific miRNAs (miR-192/194/215 and miR-7) in the differentiation of gastrointestinal epithelium and on the role of tumor-suppressive (miR-34, miR-143, miR-145) and oncogenic miRNAs (miR-21, miR-17-92 cluster) in gastrointestinal tumors. Furthermore, the potential role of miRNAs as novel biomarkers and target genes for cancer gene therapy against gastrointestinal tumors are discussed. We will also outline the potential clinical application of miRNAs for tumor diagnosis and cancer gene therapy against gastrointestinal tumors.
Expert opinion: Exploration of tumor-related miRNAs would provide important opportunities for the development of novel cancer gene therapies aimed at normalizing the critical miRNAs that are deregulated in gastrointestinal tumors.

DOI： 10.1517/14712598.2011.542749

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Telomerase-specific oncolytic virotherapy for human gastrointestinal cancer.

Fujiwara T, Shirakawa Y, Kagawa S

Expert Rev Anticancer Ther 2011

Preclinical evaluation of telomerase-specific oncolytic virotherapy for human bone and soft tissue sarcomas. 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 : an official journal of the American Association for Cancer Research 17 ( 7 ) 1828 - 38 2011

Language：English Publishing type：Research paper (scientific journal)

PURPOSE: Tumor-specific replication-selective oncolytic virotherapy is a promising antitumor therapy for induction of cell death in tumor cells but not of normal cells. We previously developed an oncolytic adenovirus, OBP-301, that kills human epithelial malignant cells in a telomerase-dependent manner. Recent evidence suggests that nonepithelial malignant cells, which have low telomerase activity, maintain telomere length through alternative lengthening of telomeres (ALT). However, it remains unclear whether OBP-301 is cytopathic for nonepithelial malignant cells. Here, we evaluated the antitumor effect of OBP-301 on human bone and soft tissue sarcoma cells. EXPERIMENTAL DESIGN: The cytopathic activity of OBP-301, coxsackie and adenovirus receptor (CAR) expression, and telomerase activity were examined in 10 bone (OST, U2OS, HOS, HuO9, MNNG/HOS, SaOS-2, NOS-2, NOS-10, NDCS-1, and OUMS-27) and in 4 soft tissue (CCS, NMS-2, SYO-1, and NMFH-1) sarcoma cell lines. OBP-301 antitumor effects were assessed using orthotopic tumor xenograft models. The fiber-modified OBP-301 (termed OBP-405) was used to confirm an antitumor effect on OBP-301-resistant sarcomas. RESULTS: OBP-301 was cytopathic for 12 sarcoma cell lines but not for the non-CAR-expressing OUMS-27 and NMFH-1 cells. Sensitivity to OBP-301 was dependent on CAR expression and not on telomerase activity. ALT-type sarcomas were also sensitive to OBP-301 because of upregulation of human telomerase reverse transcriptase (hTERT) mRNA following virus infection. Intratumoral injection of OBP-301 significantly suppressed the growth of OST and SYO-1 tumors. Furthermore, fiber-modified OBP-405 showed antitumor effects on OBP-301-resistant OUMS-27 and NMFH-1 cells. CONCLUSIONS: A telomerase-specific oncolytic adenovirus is a promising antitumor reagent for the treatment of bone and soft tissue sarcomas.

DOI： 10.1158/1078-0432.CCR-10-2066

PubMed

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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

Language：Japanese Publisher：Okayama Medical Association

DNA修復機能阻害は放射線感受性を増強させるため，DNA修復に関与する因子の阻害剤は放射線増感剤となり得る．我々の開発したテロメラーゼ依存的腫瘍融解アデノウイルス製剤OBP-301（テロメライシン）は，アデノウイルスE1B55kDaタンパクを介して細胞のDNA修復に重要な役割を果たすMRN複合体（Mre11，Rad50，NBS1）を分解する機能を有する．このMRN複合体の分解によりATM（ataxia-telangiectasia mutated）の活性化が抑制され結果的にDNA修復機構が阻害される．我々はOBP-301と放射線との併用が強力な相乗効果を生み出すことをマウスの皮下腫瘍モデルおよび食道癌同所性モデルにおいて証明した．これらの結果はOBP-301が将来有望な放射線増感剤となり得ることだけでなく，E1B55kDaタンパクを産生する腫瘍融解アデノウイルス製剤と放射線との併用が悪性腫瘍に対する有力な治療戦略となり得ることを示す．

DOI： 10.4044/joma.123.103

CiNii Article

CiNii Books

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Synergistic Interaction of Telomerase-Specific Oncolytic Virotherapy and Chemotherapeutic Agents for Human Cancer.

Fujiwara T, Kagawa S, Tazawa H

Curr Pharm Biotechnol 2011

胃がん (新しい手術のモダリティ) -- (最新の外科治療総論 : アプローチを中心に)

西﨑正彦, 香川俊輔, 藤原俊義

がん治療レクチャー : チーム医療のための 2 ( 4 ) 788 - 792 2011

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

Telomerase-dependent oncolytic adenovirus sensitizes human cancer cells to ionizing radiation via inhibition of DNA repair machinery. Reviewed International journal

Kuroda S, Fujiwara T, Shirakawa Y, Yamasaki Y, Yano S, Uno F, Tazawa H, Hashimoto Y, Watanabe Y, Noma K, Urata Y, Kagawa S, Fujiwara T

Cancer research 70 ( 22 ) 9339 - 9348 2010.11

Language：English Publishing type：Research paper (scientific journal)

The inability to repair DNA double-strand breaks (DSB) leads to radiosensitization, such that ionizing radiation combined with molecular inhibition of cellular DSB processing may greatly affect treatment of human cancer. As a variety of viral products interact with the DNA repair machinery, oncolytic virotherapy may improve the therapeutic window of conventional radiotherapy. Here, we describe the mechanistic basis for synergy of irradiation and OBP-301 (Telomelysin), an attenuated type-5 adenovirus with oncolytic potency that contains the human telomerase reverse transcriptase promoter to regulate viral replication. OBP-301 infection led to E1B55kDa viral protein expression that degraded the complex formed by Mre11, Rad50, and NBS1, which senses DSBs. Subsequently, the phosphorylation of cellular ataxia-telangiectasia mutated protein was inhibited, disrupting the signaling pathway controlling DNA repair. Thus, tumor cells infected with OBP-301 could be rendered sensitive to ionizing radiation. Moreover, by using noninvasive whole-body imaging, we showed that intratumoral injection of OBP-301 followed by regional irradiation induces a substantial antitumor effect, resulting from tumor cell-specific radiosensitization, in an orthotopic human esophageal cancer xenograft model. These results illustrate the potential of combining oncolytic virotherapy and ionizing radiation as a promising strategy in the management of human cancer.

DOI： 10.1158/0008-5472.CAN-10-2333

PubMed

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Portal/splenic Vein Thrombosis Following Splenectomy in Gastric Cancer Surgery Reviewed

Shunsuke Kagawa, Futoshi Uno, Akira Gochi, Yoshio Naomoto, Toshiyoshi Fujiwara

ASIAN JOURNAL OF SURGERY 33 ( 4 ) 208 - 211 2010.10

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SINGAPORE PTE LTD

Although splenectomy is often performed along with en bloc node dissection in gastric cancer surgery, portal/splenic vein thrombosis (PSVT) has been rarely reported. We recently encountered a case of PSVT after a splenectomy was performed during gastric cancer surgery. A 53-year-old woman underwent total gastrectomy, splenectomy, and en bloc regional lymph node dissection for gastric cancer. An uneventful postoperative course ended with abrupt development of a fever and general fatigue. Laboratory tests showed elevated levels of liver transaminases and fibrinogen degenerative products. Contrast-enhanced computed tomography revealed splenic vein thrombosis and partial liver infarction. Immediate anticoagulant treatment resulted in clinical improvement and partial thrombolysis in 2 months. PSVT after splenectomy in haematological disorders has been recognized as a possibly lethal complication. However, it has been underappreciated in cases of splenectomy for gastric cancer. The present case demonstrates the importance of considering PSVT as a possible complication of splenectomy in gastric cancer surgery. [Asian J Surg 2010;33(4):208-11]

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腹腔鏡下胃切除術における穿刺法による肝外側域の挙上 Reviewed

香川俊輔, 宇野太, 重安邦俊, 合地明, 藤原俊義

日本内視鏡外科学会雑誌 15 ( 7 ) 456 - 456 2010.10

当科における食道憩室手術症例の報告

田辺俊介, 藤原裕子, 近藤喜太, 藤原康宏, 野間和広, 櫻間教文, 宇野太, 永坂岳司, 香川俊輔, 白川靖博, 山辻知樹, 小林直哉, 藤原俊義, 羽井佐実, 松岡順治, 猶本良夫

岡山医学会雑誌 122 ( 2 ) 180 - 180 2010.8

Preclinical Evaluation of Differentially Targeting Dual Virotherapy for Human Solid Cancer Reviewed

Ryo Sakai, Shunsuke Kagawa, Yasumoto Yamasaki, Toru Kojima, Futoshi Uno, Yuuri Hashimoto, Yuichi Watanabe, Yasuo Urata, Noriaki Tanaka, Toshiyoshi Fujiwara

MOLECULAR CANCER THERAPEUTICS 9 ( 6 ) 1884 - 1893 2010.6

Language：English Publishing type：Research paper (scientific journal) Publisher：AMER ASSOC CANCER RESEARCH

Multimodal approaches combining drugs that differentially function is the most popular regimen for treating human cancer. Understanding the molecular mechanisms underlying the synergistic, potentiative, and antagonistic effects of drug combinations could facilitate the discovery of novel efficacious combinations. We previously showed that telomerase-specific replication-competent adenovirus (Telomelysin, OBP-301), in which the human telomerase reverse transcriptase promoter controls the adenoviral E1 gene expression, induces a selective antitumor effect in human cancer cells. Here, using E1-deleted replication-deficient adenovirus expressing the p53 tumor suppressor gene (Advexin, Ad-p53) and OBP-301, we investigate how these adenoviruses that kill tumor cells with different mechanisms could work in combination on human cancer. We found that E1-deficient Ad-p53 could kill cancer cells more efficiently in the presence of OBP-301 than Ad-p53 alone or OBP-301 alone, because Ad-p53 could become replication-competent by being supplied adenoviral E1 from coinfected OBP-301 in trans. Ad-p53 plus OBP-301 induced high levels of p53 protein expression without p21 induction, resulting in apoptotic cell death documented by active caspase-3 expression with a cytometric bead array and an increased subdiploid apoptotic fraction of the cell cycle. For in vivo evaluation, nude mice xenografted with human lung tumors received intratumoral injection of OBP-301 and/or Ad-p53. Analysis of the growth of implanted tumors showed an enhanced antitumor effect in combination therapy. Our data show that Ad-p53 in combination with OBP-301 induces not only oncolytic but also apoptotic cancer cell death and enhances antitumor activity in vitro and in vivo, providing potential merits as a multimodal treatment for human cancer. Mol Cancer Ther; 9(6); 1884-93. (C)2010 AACR.

DOI： 10.1158/1535-7163.MCT-10-0205

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Papers - KAGAWA Shunsuke