2021/12/21 更新

写真a

オカ タカシ
岡 剛史
OKA Takashi
所属
医歯薬学域 講師(特任)
職名
講師(特任)
外部リンク

学位

  • 医学博士 ( 高知医科大学 )

  • 工学博士 ( 大阪大学 )

研究キーワード

  • Lymphoma

  • Leukemia

  • Epigenetics

  • Virus

  • リンパ腫

  • 白血病

  • エピジェネテイックス

  • ウィルス

研究分野

  • ライフサイエンス / ウイルス学

  • ライフサイエンス / 生物物理学

  • ライフサイエンス / 分子生物学

  • ライフサイエンス / 人体病理学

  • ライフサイエンス / 実験病理学

学歴

  • 大阪大学    

    - 1983年

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    国名: 日本国

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  • 大阪大学   Graduate School, Division of Engineering Science  

    - 1983年

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経歴

  • - 岡山大学医歯薬学総合研究科社会環境生命科学専攻病原ウイルス学分野 講師

    2017年

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  • - Senior Assistant Professor,Department of Virology,Social and Environmental Sciences,Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,Okayama University

    2017年

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  • 岡山大学医歯薬学総合研究科病態制御科学専攻腫瘍病理学分野 講師

    2016年 - 2017年

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  • Senior Assistant Professor,Department of Pathology and Oncology,Biopathological Sciences,Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,Okayama University

    2016年 - 2017年

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  • 岡山大学医歯薬学総合研究科 助教

    2004年 - 2016年

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

    2004年 - 2016年

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  • Research Associate,Medical School,Okayama University

    1996年 - 2004年

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  • 岡山大学医学部第二病理学教室 助手

    1996年 - 2004年

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  • アメリカ ハーバード大学・ハーバードAIDS研究所 細胞生物学部門 客員研究員

    1994年 - 1995年

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  • Visiting Scientist,Harvard University, AIDS Insititut, Department of Cell Biology

    1994年 - 1995年

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  • アメリカ テキサス大学M.D.アンダーソン癌センター、分子病理学部門 客員助教授

    1992年 - 1994年

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  • Visiting Assistant Professor,Texas University, MD. Anderson Cancer Center, Department of Molecular Pathology

    1992年 - 1994年

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  • 大阪大学微生物病研究所腫瘍ウイルス部門 研究員   Research Institute for Microbial Diseases

    1983年 - 1984年

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  • Researcher

    1983年 - 1984年

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所属学協会

  • 日本免疫学会

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  • The Society of Japanese Virologists.

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  • (International Retrovirology Association

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  • International association for comparative research on leukemia and Related Diseases

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  • American Association of Cancer Research

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  • International union of microbiological societies

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  • 日本癌学会

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  • 日本ウイルス学会

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  • 日本病理学会

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  • 国際HTLV学会(International Retrovirology Association)

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  • 国際比較白血病・関連疾患学会(International association for comparative research on leukemia and Related Disease)

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  • アメリカ癌学会(American Association of Cancer Research)

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  • エピジェネテイックス研究会

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  • 国際微生物学会連合(International Union of Microbiological Societies)

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  • 日本分子生物学会

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  • American Association for the Advancement of Science

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委員歴

  • 日本病理学会   評議員  

    2004年   

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    団体区分:学協会

    日本病理学会

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書籍等出版物

  • 成人T細胞白血病・リンパ腫におけるエピジェネテイック異常と発症・進展機構の解析

    2014年 

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  • Accumulation of Specific Epigenetic Abnormalities during Development and Progression of T cell Leukemia/Lymphoma.

    INTECH Open Access Publisher  2011年 

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  • jointly worked

    2011年 

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  • Gene silencing:New research

    Nova Science Publishers,Inc,New Yoek  2006年 

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  • Immunoelectron microscopic study of the expression of T-cell receptor(TCR) /CD3 complex in human T-Cymphotropic Virus(HTLV) - producing cells (共著)

    in "Cells and Diseases" Hematolymphoreticular Study Group, Seoul, Korea  1997年 

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  • Immunoelectron microscopic study of the expression of T-cell receptor(TCR) CD3 complex in human T-Cymphotropic Virus(HTLV) - producing cells "jointly worked"

    in "Cells and Diseases" Hematolymphoreticular Study Group, Seoul, Korea  1997年 

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  • Ultrastructural and immunoelectron microscopic comparisons of human T-lymphotropic virus type-(]G0001[) Japanese monkey derived type-C virus particles.(共著)

    in Approaches to cancer therapy research in France & Japan. Fukutani, R., et al., edited, Pergamon Press,  1987年 

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  • Ultrastructural and immunoelectron microscopic comparisons of human T-lymphotropic virus type-(]G0001[) Japanese monkey derived type-C virus particles."jointly worked"

    in Approaches to cancer therapy research in France & Japan. Fukutani, R., et al., edited, Pergamon Press,  1987年 

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  • Effects of magnetic fields on the growth of Ehrlich''s ascites tumor cells.(共著)

    in Symposium on Biomagnetics. edited by Nakagawa K., Sun Enterprise Press, Tokyo,  1980年 

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  • Effects of magnetic fields on the growth of cultured cells.

    in Symposium on Biomagnetics., edited by Nakagawa, K., Sun Enterprise Press, Tokyo,  1980年 

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  • Effects of homogeneous magnetic fields on the growth of tumor cells."jointly worked"

    in Symposium on Biomagnetics., edited by Nakagawa K., Sun Enterprise Press, Tokyo,  1980年 

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  • Effects of magnetic fields on the growth of Ehrlich''s ascites tumor cells."jointly worked"

    in Symposium on Biomagnetics. edited by Nakagawa K., Sun Enterprise Press, Tokyo,  1980年 

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  • Effects of magnetic fields on the growth of cultured cells.

    in Symposium on Biomagnetics., edited by Nakagawa, K., Sun Enterprise Press, Tokyo,  1980年 

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  • Effects of homogeneous magnetic fields on the growth of tumor cells.(共著)

    in Symposium on Biomagnetics., edited by Nakagawa K., Sun Enterprise Press, Tokyo,  1980年 

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MISC

  • Merkel cell polyomavirus and Langerhans cell neoplasm. 国際誌

    Ichiro Murakami, Noriko Wada, Junko Nakashima, Mitsuko Iguchi, Makoto Toi, Yumiko Hashida, Tomonori Higuchi, Masanori Daibata, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Yasushi Horie, Keiko Nagata, Kazuhiko Hayashi, Takashi Oka, Tadashi Yoshino, Toshihiko Imamura, Akira Morimoto, Shinsaku Imashuku, Jean Gogusev, Francis Jauber

    Cell Communication and Signaling   16 ( 1 )   49 - 61   2018年

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  • Merkel cell polyomavirus and Langerhans cell neoplasm. 国際誌

    Ichiro Murakami, Noriko Wada, Junko Nakashima, Mitsuko Iguchi, Makoto Toi, Yumiko Hashida, Tomonori Higuchi, Masanori Daibata, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Yasushi Horie, Keiko Nagata, Kazuhiko Hayashi, Takashi Oka, Tadashi Yoshino, Toshihiko Imamura, Akira Morimoto, Shinsaku Imashuku, Jean Gogusev, Francis Jauber

    Cell Communication and Signaling   16 ( 1 )   49 - 61   2018年

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    記述言語:英語  

    BACKGROUND: The relationship between various external agents such as pollen, food, and infectious agents and human sensitivity exists and is variable depending upon individual's health conditions. For example, we believe that the pathogenetic potential of the Merkel cell polyomavirus (MCPyV), the resident virus in skin, is variable and depends from the degree of individual's reactivity. MCPyV as well as Epstein-Barr virus, which are normally connected with humans under the form of subclinical infection, are thought to be involved at various degrees in several neoplastic and inflammatory diseases. In this review, we cover two types of Langerhans cell neoplasms, the Langerhans cell sarcoma (LCS) and Langerhans cell histiocytosis (LCH), represented as either neoplastic or inflammatory diseases caused by MCPyV. METHODS: We meta-analyzed both our previous analyses, composed of quantitative PCR for MCPyV-DNA, proteomics, immunohistochemistry which construct IL-17 endocrine model and interleukin-1 (IL-1) activation loop model, and other groups' data. RESULTS: We have shown that there were subgroups associated with the MCPyV as a causal agent in these two different neoplasms. Comparatively, LCS, distinct from the LCH, is a neoplastic lesion (or sarcoma) without presence of inflammatory granuloma frequently observed in the elderly. LCH is a proliferative disease of Langerhans-like abnormal cells which carry mutations of genes involved in the RAS/MAPK signaling pathway. We found that MCPyV may be involved in the development of LCH. CONCLUSION: We hypothesized that a subgroup of LCS developed according the same mechanism involved in Merkel cell carcinoma pathogenesis. We proposed LCH developed from an inflammatory process that was sustained due to gene mutations. We hypothesized that MCPyV infection triggered an IL-1 activation loop that lies beneath the pathogenesis of LCH and propose a new triple-factor model.

    DOI: 10.1186/s12964-018-0261-y

    PubMed

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  • Gene expression analysis of hypersensitivity to mosquito bite, chronic active EBV infection and NK/T-lymphoma/leukemia

    Kana Washio, Takashi Oka, Lamia Abdalkader, Michiko Muraoka, Akira Shimada, Megumi Oda, Hiaki Sato, Katsuyoshi Takata, Yoshitoyo Kagami, Norio Shimizu, Seiichi Kato, Hiroshi Kimura, Kazunori Nishizaki, Tadashi Yoshino, Hirokazu Tsukahara

    LEUKEMIA & LYMPHOMA   58 ( 11 )   2683 - 2694   2017年

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    記述言語:英語   出版者・発行元:TAYLOR & FRANCIS LTD  

    The human herpes virus, Epstein-Barr virus (EBV), is a known oncogenic virus and plays important roles in life-threatening T/NK-cell lymphoproliferative disorders (T/NK-cell LPD) such as hypersensitivity to mosquito bite (HMB), chronic active EBV infection (CAEBV), and NK/T-cell lymphoma/leukemia. During the clinical courses of HMB and CAEBV, patients frequently develop malignant lymphomas and the diseases passively progress sequentially. In the present study, gene expression of CD16((-))CD56((+))-, EBV(+) HMB, CAEBV, NK-lymphoma, and NK-leukemia cell lines, which were established from patients, was analyzed using oligonucleotide microarrays and compared to that of CD56(bright)CD16(dim/-) NK cells from healthy donors. Principal components analysis showed that CAEBV and NK-lymphoma cells were relatively closely located, indicating that they had similar expression profiles. Unsupervised hierarchal clustering analyses of microarray data and gene ontology analysis revealed specific gene clusters and identified several candidate genes responsible for disease that can be used to discriminate each category of NK-LPD and NK-cell lymphoma/leukemia.

    DOI: 10.1080/10428194.2017.1304762

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  • Gene expression analysis of hypersensitivity to mosquito bite, chronic active EBV infection and NK/T-lymphoma/leukemia

    Kana Washio, Takashi Oka, Lamia Abdalkader, Michiko Muraoka, Akira Shimada, Megumi Oda, Hiaki Sato, Katsuyoshi Takata, Yoshitoyo Kagami, Norio Shimizu, Seiichi Kato, Hiroshi Kimura, Kazunori Nishizaki, Tadashi Yoshino, Hirokazu Tsukahara

    LEUKEMIA & LYMPHOMA   58 ( 11 )   2683 - 2694   2017年

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    記述言語:英語   出版者・発行元:TAYLOR & FRANCIS LTD  

    The human herpes virus, Epstein-Barr virus (EBV), is a known oncogenic virus and plays important roles in life-threatening T/NK-cell lymphoproliferative disorders (T/NK-cell LPD) such as hypersensitivity to mosquito bite (HMB), chronic active EBV infection (CAEBV), and NK/T-cell lymphoma/leukemia. During the clinical courses of HMB and CAEBV, patients frequently develop malignant lymphomas and the diseases passively progress sequentially. In the present study, gene expression of CD16((-))CD56((+))-, EBV(+) HMB, CAEBV, NK-lymphoma, and NK-leukemia cell lines, which were established from patients, was analyzed using oligonucleotide microarrays and compared to that of CD56(bright)CD16(dim/-) NK cells from healthy donors. Principal components analysis showed that CAEBV and NK-lymphoma cells were relatively closely located, indicating that they had similar expression profiles. Unsupervised hierarchal clustering analyses of microarray data and gene ontology analysis revealed specific gene clusters and identified several candidate genes responsible for disease that can be used to discriminate each category of NK-LPD and NK-cell lymphoma/leukemia.

    DOI: 10.1080/10428194.2017.1304762

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  • Aberrant differential expression of EZH1 and EZH2 in Polycomb repressive complex 2 among B- and T/NK-cell neoplasms

    Lamia Abdalkader, Takashi Oka, Katsuyoshi Takata, Hiaki Sato, Ichiro Murakami, Arie P. Otte, Tadashi Yoshino

    PATHOLOGY   48 ( 5 )   467 - 482   2016年8月

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    記述言語:英語   出版者・発行元:ELSEVIER SCIENCE BV  

    The Polycomb repressive complex-2 members (EZH2, EED, SUZ12 and EZH1) are important regulators of haematopoiesis, cell cycle and differentiation. Over expression of EZH2 has been linked to cancer metastases and poor prognosis. Detailed information on the expression of other members in normal and neoplastic lymphoid tissue remains to be elucidated. Immunohistochemical and immunofluorescent analyses of 156 samples from haematopoietic neoplasms patients and 27 haematopoietic cell lines were used.
    B-cell neoplasms showed a significant over-expression of EZH2, EED and SUZ12 in the aggressive subtypes compared to the indolent subtypes and normal tissue (p = 0.000-0.046) while expression of EZH1 was decreased in mantle cell lymphoma compared to normal tissue (p = 0.011). T/NK-cell neoplasms also showed significant over expression of EZH2, EED and SUZ12 (p = 0.000-0.002) and decreased expression of EZH1 (p = 0.001) compared to normal cells. EZH2 and EZH1 have opposite expression patterns both in normal and neoplastic lymphoid tissues as well as an opposite relation to Ki-67. These results were supported by western blotting analyses. Immunofluorescent staining revealed a difference in the intracellular localisation of EZH1 compared to other members.
    These evidences suggest that EZH2 and EZH1 are important in the counter-balancing mechanisms controlling proliferation/resting of lymphoid cells. The disruption of the balanced EZH2/EZH1 ratio may play important roles in the pathogenesis of lymphomas.

    DOI: 10.1016/j.pathol.2016.05.002

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  • Acute-phase ITIH4 levels distinguish multi-system from single-system Langerhans cell histiocytosis via plasma peptidomics

    Ichiro Murakami, Yukiko Oh, Akira Morimoto, Hitoshi Sano, Susumu Kanzaki, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Keiko Nagata, Kazuhiko Hayashi, Shinsaku Imashuku, Jean Gogusev, Francis Jaubert, Takashi Oka, Tadashi Yoshino

    CLINICAL PROTEOMICS   12   16 - 23   2015年6月

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    記述言語:英語   出版者・発行元:BIOMED CENTRAL LTD  

    Background: Langerhans cell histiocytosis (LCH) is a proliferative disorder in which abnormal Langerhans cell (LC)-like cells (LCH cells) intermingle with inflammatory cells. Whether LCH is reactive or neoplastic remains a controversial matter. We recently described Merkel cell polyomavirus (MCPyV) as a possible causative agent of LCH and proposed interleukin-1 loop model: LCH is a reactive disorder with an underlying oncogenic potential and we now propose to test this theory by looking for acute markers of inflammation. We detected MCPyV-DNA in the peripheral blood cells of patients with high-risk organ-type (LCH-risk organ (RO) (+)) but not those with non-high-risk organ-type LCH (LCH-RO (-)); this difference was significant. LCH-RO (-) is further classified by its involvement of either a single organ system (SS-LCH) or multiple organ systems (MS-LCH). In patients with LCH-RO (-), MCPyV-DNA sequences were present in LCH tissues, and significant differences were observed between LCH tissues and control tissues associated with conditions such as dermatopathic lymphadenopathy and reactive lymphoid hyperplasia. Although MCPyV causes subclinical infection in nearly all people and 22 % of healthy adults will harbor MCPyV in their buffy coats, circulating monocytes could serve as MCPyV reservoirs and cause disseminated skin lesions.
    Methods: Plasma sample from 12 patients with LCH-RO (-) (5 MS-LCH and 7 SS-LCH) and 5 non-LCH patients were analyzed by peptidomics. Mass spectrometry (MS) spectra were acquired and peptides exhibiting quantitative differences between MS-LCH and SS-LCH patients were targeted.
    Results: One new candidate biomarker, m/z 3145 was selected and identified after obtaining a MS/MS fragmentation pattern using liquid chromatography-MS/MS. This peak was identified as a proteolytic fragment derived from interalpha- trypsin inhibitor heavy chain 4 (ITIH4, [PDB: Q14624]).
    Conclusions: Peptidomics of LCH have revealed that the level of acute-phase ITIH4 distinguishes MS-LCH-RO (-) from SS-LCH-RO (-). Acute-phase proteins serve non-specific, physiological immune functions within the innate immune system. LCH may be a reactive disorder with both underlying neoplastic potential of antigen presenting cells harboring BRAF mutations and hyper-immunity of other inflammatory cells against MCPyV infection. Among LCH-RO (-), MCPyV-DNA sequences were present in both MS-LCH tissues and SS-LCH tissues without significant differences. ITIH4 may show that LCH activity or LCH subtypes correlates with the systemic or localized reactions of MCPyV infection.

    DOI: 10.1186/s12014-015-9089-2

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  • Interleukin-1 loop model for pathogenesis of Langerhans cell histiocytosis

    Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Keiko Nagata, Yasushi Horie, Kazuhiko Hayashi, Toshihiko Imamura, Akira Morimoto, Shinsaku Imashuku, Jean Gogusev, Francis Jaubert, Katsuyoshi Takata, Takashi Oka, Tadashi Yoshino

    CELL COMMUNICATION AND SIGNALING   13   13   2015年2月

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    記述言語:英語   掲載種別:書評論文,書評,文献紹介等   出版者・発行元:BIOMED CENTRAL LTD  

    We propose Langerhans cell histiocytosis (LCH) is an inflammatory process that is prolonged by mutations. We hypothesize that Merkel cell polyomavirus (MCPyV) infection triggers an interleukin-1 (IL-1) activation loop that underlies the pathogenesis of LCH. Langerhans cells (LCs) are antigen presenting cells in the skin. When LCs encounter exogenous antigens, they migrate from the epidermis into draining lymphoid tissues to initiate T-cell activity. It has been proposed that LC migration-related factors, including E-cadherin, matrix metalloproteinase, and Notch ligand induce LCH activity. We found that the tyrosine phosphatase SHP-1, which binds IL-1 receptor-associated kinase 1, is expressed at a significantly higher level in LCH affecting multiple organ systems (MS-LCH) than in LCH affecting a single organ system (SS-LCH). IL-1 stimulates T helper 17 cells and their signature cytokine IL-17 had been a matter of controversy. We detected higher levels of IL-17A receptor expression in MS-LCH than in SS-LCH and proposed an IL-17 endocrine model that could settle the controversy. IL-1 is the first cytokine secreted in response to sensitizers and promotes LC migration from sentinel tissues. Myeloid differentiation primary response 88 (MyD88), downstream of the IL-1 receptor, has functions in both RAS signaling and inflammation, leading to human cell transformation. In 2010, an activating mutation in the B-rapidly accelerated fibrosarcoma gene (BRAF) V600E was found in LCH. This BRAF mutation induces phosphorylation of the extracellular signal-regulated kinase (ERK) that may play an important role with MyD88 in LCH pathogenesis. However, phosphorylated ERK (pERK) is rapidly dephosphorylated by dual specificity phosphatase 6 (DUSP6), and limited proliferation is predicted in BRAF mutant cells. MyD88 binds pERK via its D-domain, thereby preventing pERK-DUSP6 interaction and maintaining ERK in an active, phosphorylated state. We detected MCPyV-DNA in the peripheral blood cells of two out of three patients with LCH in high-risk organs but not in those of patients with LCH in non-high-risk organs (0/12; P = .029). MCPyV infection can trigger precursor LCH cells with BRAF mutation to produce IL-1; the IL-1 loop is amplified in all LCH subclasses. Our model indicates both BRAF mutation and IL-1 loop regulation as potential therapeutic targets.

    DOI: 10.1186/s12964-015-0092-z

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  • Establishment of a Langerhans cell histiocytosis lesion cell line with dermal dendritic cell characteristics

    Ichiro Murakami, Jean Gogusev, Francis Jaubert, Michiko Matsushita, Kazuhiko Hayashi, Ikuo Miura, Takehiro Tanaka, Takashi Oka, Tadashi Yoshino

    ONCOLOGY REPORTS   33 ( 1 )   171 - 178   2015年1月

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    記述言語:英語   出版者・発行元:SPANDIDOS PUBL LTD  

    A cell line named PRU-1, derived from a Langerhans cell (LC) histiocytosis (LCH) skull lesion of a 7-year-old boy, was established and characterized. PRU-1 is an adherent spindle-shaped cell line that shows no Birbeck granules on electron microscopy. Flow cytometric analysis of cells collected from the early seventh passage showed no LC phenotypes of CD1a and S100 protein. Immunostaining of PRU-1 cells also revealed no expression of LC markers but showed expression of CD11c, CD54 (ICAM-1) and CD68, which was also observed in some peripherally located cells of the original LCH lesion. The PRU-1 cells stained positive for factor XIIIa and negative for CD34, suggesting a dermal dendritic cell phenotype. Cytogenetic analyses revealed abnormalities such as 39, XY, -2, -4, -8, -12, -12, -14, add (18)(q21), 20, +mar and 44, XY, -11, -14, add(18)(q21). TCR rearrangement in the PRU-1 cells was not amplified by PCR. Tumorigenicity was not proven by xenografting into SCID mice. A conditioned medium from PRU-1 culture induced the proliferation of peripheral blood lymphocytes as well as the activation of monocytes from a healthy donor into CD1a-positive LC-like cells. Because the phenotypic characteristics of PRU-1 differed from those of CD1a-positive abnormal LC-like cells (LCH cells), it was likely that the PRU-1 cells were derived from peripherally located cells of the LCH lesion rather than LCH cells. LCH has been regarded as a type of granulomatous neoplasm with several intermingled inflammatory cells and influenced by stimuli such as Merkel cell polyomavirus (MCPyV) infection or cigarette smoking. However, in the PRU-1 cells, MCPyV-DNA was not detected by PCR. Stromal cell-like PRU-1 cells are likely to produce some growth or differentiation factors, which may play important roles in LCH lesion formation, cell maintenance and LC-like cell induction.

    DOI: 10.3892/or.2014.3567

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  • Establishment of a Langerhans cell histiocytosis lesion cell line with dermal dendritic cell characteristics

    Ichiro Murakami, Jean Gogusev, Francis Jaubert, Michiko Matsushita, Kazuhiko Hayashi, Ikuo Miura, Takehiro Tanaka, Takashi Oka, Tadashi Yoshino

    ONCOLOGY REPORTS   33 ( 1 )   171 - 178   2015年1月

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    記述言語:英語   出版者・発行元:SPANDIDOS PUBL LTD  

    A cell line named PRU-1, derived from a Langerhans cell (LC) histiocytosis (LCH) skull lesion of a 7-year-old boy, was established and characterized. PRU-1 is an adherent spindle-shaped cell line that shows no Birbeck granules on electron microscopy. Flow cytometric analysis of cells collected from the early seventh passage showed no LC phenotypes of CD1a and S100 protein. Immunostaining of PRU-1 cells also revealed no expression of LC markers but showed expression of CD11c, CD54 (ICAM-1) and CD68, which was also observed in some peripherally located cells of the original LCH lesion. The PRU-1 cells stained positive for factor XIIIa and negative for CD34, suggesting a dermal dendritic cell phenotype. Cytogenetic analyses revealed abnormalities such as 39, XY, -2, -4, -8, -12, -12, -14, add (18)(q21), 20, +mar and 44, XY, -11, -14, add(18)(q21). TCR rearrangement in the PRU-1 cells was not amplified by PCR. Tumorigenicity was not proven by xenografting into SCID mice. A conditioned medium from PRU-1 culture induced the proliferation of peripheral blood lymphocytes as well as the activation of monocytes from a healthy donor into CD1a-positive LC-like cells. Because the phenotypic characteristics of PRU-1 differed from those of CD1a-positive abnormal LC-like cells (LCH cells), it was likely that the PRU-1 cells were derived from peripherally located cells of the LCH lesion rather than LCH cells. LCH has been regarded as a type of granulomatous neoplasm with several intermingled inflammatory cells and influenced by stimuli such as Merkel cell polyomavirus (MCPyV) infection or cigarette smoking. However, in the PRU-1 cells, MCPyV-DNA was not detected by PCR. Stromal cell-like PRU-1 cells are likely to produce some growth or differentiation factors, which may play important roles in LCH lesion formation, cell maintenance and LC-like cell induction.

    DOI: 10.3892/or.2014.3567

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  • Detection of T-cell receptor γ gene rearrangement in paraffin-embedded T or natural killer/T-cell lymphoma samples using the BIOMED-2 protocol.

    Miyata-Takata T, Takata K, Yamanouchi S, Sato Y, Harada M, Oka T, Tanaka T, Maeda Y, Tanimoto M, Yoshino T

    Leuk Lymphoma.   55 ( 9 )   2161 - 2164   2014年9月

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  • Detection of T-cell receptor gamma gene rearrangement in paraffin-embedded T or natural killer/T-cell lymphoma samples using the BIOMED-2 protocol

    Tomoko Miyata-Takata, Katsuyoshi Takata, Sachiko Yamanouchi, Yasuharu Sato, Mai Harada, Takashi Oka, Takehiro Tanaka, Yoshinobu Maeda, Mitsune Tanimoto, Tadashi Yoshino

    LEUKEMIA & LYMPHOMA   55 ( 9 )   2161 - 2164   2014年9月

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    記述言語:英語   出版者・発行元:INFORMA HEALTHCARE  

    While the use of polymerase chain reaction (PCR)-based clonality analysis of formalin-fixed paraffin-embedded (FFPE) tissue has recently become widespread, the detection sensitivity for lymphoma subtypes using FFPE samples is not well known. Here, we analyzed T-cell receptor gamma chain (TCRG) gene rearrangement clonality in 100 cases of T-or natural killer (NK)/T-cell lymphoma and examined detection sensitivity according to lymphoma subtype. Clonality was detected in approximately 80% of the major T-cell lymphoma subtypes: peripheral T-cell lymphoma, not otherwise specified, 84% (21/25 cases); angioimmunoblastic T-cell lymphoma, 71% (15/21 cases); and adult T-cell leukemia/lymphoma, 80% (8/10 cases). The number of clonal peaks differed according to subtype. TCRG gene rearrangement was not detected in 63 cases of B-cell lymphoma or reactive lesions. Thus, clonality analysis can effectively and reliably detect TCRG gene rearrangement in T-cell lymphoma cases and could, therefore, be a useful diagnostic tool in routine practice.

    DOI: 10.3109/10428194.2013.871634

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  • High viral load of Merkel cell polyomavirus DNA sequences in Langerhans cell sarcoma tissues

    Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu Nakamoto, Mitsunori Yamakawa, Hirokazu Nakamine, Katsuyoshi Takata, Takashi Oka, Tadashi Yoshino

    INFECTIOUS AGENTS AND CANCER   9   15 - 18   2014年5月

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    記述言語:英語   出版者・発行元:BIOMED CENTRAL LTD  

    Background: Langerhans cell (LC) sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent.
    Findings: We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328-0.772 copies/cell (Merkel cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7).
    Conclusions: Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/cell) than low load of LCH (0.003, median of 12 cases) (P < 0.01) may suggest a virally induced tumorigenic process in some LCS. Although the absence of LT antigen expression may indicate a different role for MCPyV in this pathology, some subtypes of LCS may develop in the background of MCPyV-infected LC. To the best of our knowledge, this is the first report on the relationship between MCPyV and LCS. The recent discovery of MCPyV opened new therapeutic avenues for MCC. These data open novel possibilities for therapeutic interventions against LCS.

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  • High viral load of Merkel cell polyomavirus DNA sequences in Langerhans cell sarcoma tissues

    Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shu Nakamoto, Mitsunori Yamakawa, Hirokazu Nakamine, Katsuyoshi Takata, Takashi Oka, Tadashi Yoshino

    INFECTIOUS AGENTS AND CANCER   9   15 - 18   2014年5月

     詳細を見る

    記述言語:英語   出版者・発行元:BIOMED CENTRAL LTD  

    Background: Langerhans cell (LC) sarcoma (LCS) is a high-grade neoplasm with overtly malignant cytologic features and an LC phenotype. We very recently suggested that LC behaves as a reservoir for common dermotropic Merkel cell polyomavirus (MCPyV) and determined the relationship between LC histiocytosis (LCH), which has an underlining oncogenic capacity, and MCPyV as a trigger for a reactive process rather than a neoplastic process. We propose LC to be a reservoir for MCPyV and hypothesize that some LCS subtypes may be related to the MCPyV agent.
    Findings: We examined seven LCS tissues using multiplex quantitative PCR (Q-PCR) and immunohistochemistry with anti MCPyV large-T (LT) antigen antibody. High viral loads of MCPyV DNA sequences (viral load = relative levels of MCPyV) were detected (0.328-0.772 copies/cell (Merkel cell carcinoma (MCC) = 1.0)) using Q-PCR in 43% (3/7) tissues, but LT antigen expression was not observed (0/7).
    Conclusions: Frequent MCPyV-DNA amplification suggests that LCS in some patients may be related to MCPyV infection. Moreover, the higher viral load of LCS (median, 0.453 copies/cell) than low load of LCH (0.003, median of 12 cases) (P < 0.01) may suggest a virally induced tumorigenic process in some LCS. Although the absence of LT antigen expression may indicate a different role for MCPyV in this pathology, some subtypes of LCS may develop in the background of MCPyV-infected LC. To the best of our knowledge, this is the first report on the relationship between MCPyV and LCS. The recent discovery of MCPyV opened new therapeutic avenues for MCC. These data open novel possibilities for therapeutic interventions against LCS.

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  • Gene expression analysis in children with complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis

    Mitsuru Tsuge, Takashi Oka, Nobuko Yamashita, Yukie Saito, Yosuke Fujii, Yoshiharu Nagaoka, Masato Yashiro, Hirokazu Tsukahara, Tsuneo Morishima

    JOURNAL OF NEUROVIROLOGY   20 ( 1 )   73 - 84   2014年2月

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    記述言語:英語   出版者・発行元:SPRINGER  

    Viral infections have been implicated as a cause of complex seizures in children. The pathogenic differences in complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis remain unclear. This study analyzed the gene expression profiles in the peripheral whole blood from pediatric patients with complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis. The gene expression profiles of ten patients (five with seizures and five without) with influenza A(H1N1)pdm09 and six patients (three with seizures and three without) with rotavirus gastroenteritis were examined. Gene expression profiles in the whole blood were different in complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis. Transcripts related to the immune response were significantly differentially expressed in complex seizures with influenza A(H1N1)pdm09, and transcripts related to the stress response were significantly differentially expressed in complex seizures with rotavirus gastroenteritis. Pathway analysis showed that the mitogen-activated protein kinases in the T cell receptor signaling pathway were activated in complex seizures due to influenza A(H1N1)pdm09. Dysregulation of the genes related to immune response or stress response could contribute to the pathogenic differences of the complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis.

    DOI: 10.1007/s13365-013-0231-5

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  • Gene expression analysis in children with complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis

    Mitsuru Tsuge, Takashi Oka, Nobuko Yamashita, Yukie Saito, Yosuke Fujii, Yoshiharu Nagaoka, Masato Yashiro, Hirokazu Tsukahara, Tsuneo Morishima

    JOURNAL OF NEUROVIROLOGY   20 ( 1 )   73 - 84   2014年2月

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    記述言語:英語   出版者・発行元:SPRINGER  

    Viral infections have been implicated as a cause of complex seizures in children. The pathogenic differences in complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis remain unclear. This study analyzed the gene expression profiles in the peripheral whole blood from pediatric patients with complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis. The gene expression profiles of ten patients (five with seizures and five without) with influenza A(H1N1)pdm09 and six patients (three with seizures and three without) with rotavirus gastroenteritis were examined. Gene expression profiles in the whole blood were different in complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis. Transcripts related to the immune response were significantly differentially expressed in complex seizures with influenza A(H1N1)pdm09, and transcripts related to the stress response were significantly differentially expressed in complex seizures with rotavirus gastroenteritis. Pathway analysis showed that the mitogen-activated protein kinases in the T cell receptor signaling pathway were activated in complex seizures due to influenza A(H1N1)pdm09. Dysregulation of the genes related to immune response or stress response could contribute to the pathogenic differences of the complex seizures due to influenza A(H1N1)pdm09 or rotavirus gastroenteritis.

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  • Necrotic and apoptotic cells serve as nuclei for calcification on osteoblastic differentiation of human mesenchymal stem cells in vitro

    Hirofumi Fujita, Masanao Yamamoto, Tetsuya Ogino, Hirotsugu Kobuchi, Naoko Ohmoto, Eriko Aoyama, Takashi Oka, Tohru Nakanishi, Keiji Inoue, Junzo Sasaki

    CELL BIOCHEMISTRY AND FUNCTION   32 ( 1 )   77 - 86   2014年1月

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    記述言語:英語   出版者・発行元:WILEY-BLACKWELL  

    A close relationship between cell death and pathological calcification has recently been reported, such as vascular calcification in atherosclerosis. However, the roles of cell death in calcification by osteoblast lineage have not been elucidated in detail. In this study, we investigated whether cell death is involved in the calcification on osteoblastic differentiation of human bone marrow mesenchymal stem cells (hMSC) under osteogenic culture in vitro. Apoptosis and necrosis occurred in an osteogenic culture of hMSC, and cell death preceded calcification. The generation of intracellular reactive oxygen species, chromatin condensation and fragmentation, and caspase-3 activation increased in this culture. A pan-caspase inhibitor (Z-VAD-FMK) and anti-oxidants (Tiron and n-acetylcysteine) inhibited osteogenic culture-induced cell death and calcification. Furthermore, calcification was significantly promoted by the addition of necrotic dead cells or its membrane fraction. Spontaneously dead cells by osteogenic culture and exogenously added necrotic cells were surrounded by calcium deposits. Induction of localized cell death by photodynamic treatment in the osteogenic culture resulted in co-localized calcification. These findings show that necrotic and apoptotic cell deaths were induced in an osteogenic culture of hMSC and indicated that both necrotic and apoptotic cells of osteoblast lineage served as nuclei for calcification on osteoblastic differentiation of hMSC in vitro. Copyright (c) 2013 John Wiley & Sons, Ltd.

    DOI: 10.1002/cbf.2974

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  • Merkel cell polyomavirus DNA sequences in peripheral blood and tissues from patients with Langerhans cell histiocytosis

    Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Toshihiko Imamura, Akira Morimoto, Shinsaku Imashuku, Jean Gogusev, Francis Jaubert, Katsuyoshi Takata, Takashi Oka, Tadashi Yoshino

    HUMAN PATHOLOGY   45 ( 1 )   119 - 126   2014年1月

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    記述言語:英語   出版者・発行元:W B SAUNDERS CO-ELSEVIER INC  

    Langerhans cell histiocytosis (LCH) is a group of granulomatous disorders in which abnormal Langerhans cells proliferate as either a localized lesion in a single bone or disseminated disease involving two or more organs or systems. Because the different LCH forms exhibit significantly elevated levels of inflammatory molecules, including pro-inflammatory cytokines and tissue-degrading enzymes, we investigated for a possible viral trigger in LCH pathogenesis. We looked for Merkel cell polyomavirus (MCPyV) in peripheral blood cells and tissues using quantitative real-time PCR and immunohistochemistry staining with anti-MCPyV large T-antigen antibody. Our findings revealed elevated amounts of MCPyV DNA in the peripheral blood cells of 2 of 3 patients affected by LCH with high-risk organ involvement (RO+) and absence of MCPyV DNA in the blood cells in all 12 LCH-RO-patients (P = .029). With lower viral loads (0.002-0.033 copies/cell), an elevated number of MCPyV DNA sequences was detected in 12 LCH tissues in comparison with control tissues obtained from patients with reactive lymphoid hyperplasia (0/5; P = .0007), skin diseases not related to LCH in children younger than 2 years (0/11; P = .0007), or dermatopathic lymphadenopathy (5/20; P = .0002). The data, including frequent but lower viral loads and low large-T antigen expression rate (2/13 LCH tissues), suggest that development of LCH as a reactive rather than a neoplastic process may be related to MCPyV infection. (C) 2014 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.humpath.2013.05.028

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  • Merkel cell polyomavirus DNA sequences in peripheral blood and tissues from patients with Langerhans cell histiocytosis

    Ichiro Murakami, Michiko Matsushita, Takeshi Iwasaki, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Toshihiko Imamura, Akira Morimoto, Shinsaku Imashuku, Jean Gogusev, Francis Jaubert, Katsuyoshi Takata, Takashi Oka, Tadashi Yoshino

    HUMAN PATHOLOGY   45 ( 1 )   119 - 126   2014年1月

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    記述言語:英語   出版者・発行元:W B SAUNDERS CO-ELSEVIER INC  

    Langerhans cell histiocytosis (LCH) is a group of granulomatous disorders in which abnormal Langerhans cells proliferate as either a localized lesion in a single bone or disseminated disease involving two or more organs or systems. Because the different LCH forms exhibit significantly elevated levels of inflammatory molecules, including pro-inflammatory cytokines and tissue-degrading enzymes, we investigated for a possible viral trigger in LCH pathogenesis. We looked for Merkel cell polyomavirus (MCPyV) in peripheral blood cells and tissues using quantitative real-time PCR and immunohistochemistry staining with anti-MCPyV large T-antigen antibody. Our findings revealed elevated amounts of MCPyV DNA in the peripheral blood cells of 2 of 3 patients affected by LCH with high-risk organ involvement (RO+) and absence of MCPyV DNA in the blood cells in all 12 LCH-RO-patients (P = .029). With lower viral loads (0.002-0.033 copies/cell), an elevated number of MCPyV DNA sequences was detected in 12 LCH tissues in comparison with control tissues obtained from patients with reactive lymphoid hyperplasia (0/5; P = .0007), skin diseases not related to LCH in children younger than 2 years (0/11; P = .0007), or dermatopathic lymphadenopathy (5/20; P = .0002). The data, including frequent but lower viral loads and low large-T antigen expression rate (2/13 LCH tissues), suggest that development of LCH as a reactive rather than a neoplastic process may be related to MCPyV infection. (C) 2014 Elsevier Inc. All rights reserved.

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  • Necrotic and apoptotic cells serve as nuclei for calcification on osteoblastic differentiation of human mesenchymal stem cells in vitro

    Hirofumi Fujita, Masanao Yamamoto, Tetsuya Ogino, Hirotsugu Kobuchi, Naoko Ohmoto, Eriko Aoyama, Takashi Oka, Tohru Nakanishi, Keiji Inoue, Junzo Sasaki

    CELL BIOCHEMISTRY AND FUNCTION   32 ( 1 )   77 - 86   2014年1月

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    記述言語:英語   出版者・発行元:WILEY-BLACKWELL  

    A close relationship between cell death and pathological calcification has recently been reported, such as vascular calcification in atherosclerosis. However, the roles of cell death in calcification by osteoblast lineage have not been elucidated in detail. In this study, we investigated whether cell death is involved in the calcification on osteoblastic differentiation of human bone marrow mesenchymal stem cells (hMSC) under osteogenic culture in vitro. Apoptosis and necrosis occurred in an osteogenic culture of hMSC, and cell death preceded calcification. The generation of intracellular reactive oxygen species, chromatin condensation and fragmentation, and caspase-3 activation increased in this culture. A pan-caspase inhibitor (Z-VAD-FMK) and anti-oxidants (Tiron and n-acetylcysteine) inhibited osteogenic culture-induced cell death and calcification. Furthermore, calcification was significantly promoted by the addition of necrotic dead cells or its membrane fraction. Spontaneously dead cells by osteogenic culture and exogenously added necrotic cells were surrounded by calcium deposits. Induction of localized cell death by photodynamic treatment in the osteogenic culture resulted in co-localized calcification. These findings show that necrotic and apoptotic cell deaths were induced in an osteogenic culture of hMSC and indicated that both necrotic and apoptotic cells of osteoblast lineage served as nuclei for calcification on osteoblastic differentiation of hMSC in vitro. Copyright (c) 2013 John Wiley & Sons, Ltd.

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  • In aggressive variants of non-Hodgkin lymphomas, Ezh2 is strongly expressed and polycomb repressive complex PRC1.4 dominates over PRC1.2

    Lamia Abd Al Kader, Takashi Oka, Katsuyoshi Takata, Xu Sun, Hiaki Sato, Ichiro Murakami, Tomohiro Toji, Akihiro Manabe, Hiroshi Kimura, Tadashi Yoshino

    VIRCHOWS ARCHIV   463 ( 5 )   697 - 711   2013年11月

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    記述言語:英語   出版者・発行元:SPRINGER  

    Polycomb group (PcG) proteins are important for the regulation of hematopoiesis by regulating chromatin compaction and silencing genes related to differentiation and cell cycle. Overexpression of enhancer of zeste homologue 2 (Ezh2) and Bmi-1/PCGF4 has been implicated in solid organ cancers, while Mel-18/PCGF2 has been reported as a tumor suppressor. Detailed expression profiles of PcG proteins and their diagnostic significance in malignant lymphomas are still unknown. In this study, we analyzed the expression levels of Ezh2, Bmi-1, Mel-18, and Ki67 in 197 Hodgkin's and non-Hodgkin's lymphoma patient samples and in lymphoma cell lines using immunohistochemistry, fluorescent immunocytochemistry, and Western blotting. Immunohistochemical staining showed that Ezh2 expression was significantly increased in aggressive compared to indolent subtypes of B cell neoplasms (P = 0.000-0.030), while no significant differences in Bmi-1 expression were found between these subtypes. Compared to the normal counterpart, T cell lymphomas showed significant overexpression of Bmi-1 (P = 0.011) and Ezh2 (P = 0.000). The Ki67 labeling index showed a positive correlation with Ezh2 expression in B cell lymphomas (correlation coefficient (Co) = 0.983, P = 0.000) and T/NK cell lymphomas (Co = 0.629, P = 0.000). Fluorescent immunohistochemical staining showed coexpression of Ezh2 and Ki67 in the same tumor cells, indicating that Ezh2 expression correlates with cell proliferation. Both B and T/NK cell neoplasms showed low expression of Mel-18 and high expression of both Bmi-1 and Ezh2. In conclusion, in aggressive lymphoma variants, Ezh2 is strongly expressed and polycomb repressive complex PRC1.4 dominates over PRC1.2. Coexpression of Bmi-1 and Ezh2 is a characteristic of aggressive lymphomas. Ezh2 correlates with the proliferation and aggressive nature of non-Hodgkin's lymphomas.

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  • Pathogenic mechanisms of influenza A(H1N1)pdm09 infection elucidated on gene expression profiling

    Nobuko Yamashita, Hirokazu Tsukahara, Mitsuru Tsuge, Yoshiharu Nagaoka, Masato Yashiro, Yukie Saito, Yosuke Fujii, Takashi Oka, Tsuneo Morishima

    Pediatrics International   55 ( 5 )   572 - 577   2013年10月

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    記述言語:英語  

    Background: The pathogenic mechanisms underlying influenza A(H1N1)pdm09-associated central nervous system (CNS) manifestations and pneumonia remain unclear. This study examined A(H1N1)pdm09 host responses using gene expression profiles of patients' peripheral blood. Methods: Sixteen A(H1N1)pdm09-infected children in three groups were examined: a CNS group, with convulsion and altered consciousness (n = 6)
    a pneumonia (Pneu) group (n = 5)
    and a group of infected control patients (n = 5). The signal ratios of the acute to recovery phases in CNS or Pneu were analyzed versus those of the control. Results: The CNS (619 transcripts) and Pneu (656 transcripts) groups had significantly increased signal ratios compared to the control group. Regarding the increased ratios of transcripts shown by multiple probes, contactin-associated protein-like 3 transcripts, oleoyl-ACP hydrolase transcripts, and interleukin 1 type 1 receptor were observed in CNS and Pneu. Increased ratios of prostaglandin-endoperoxide synthase 2 and α-synuclein were characteristic of CNS. Alkaline phosphatase and the Fc fragment of IgA receptor were characteristic of Pneu. Regarding enriched gene ontology terms, 'response to lipopolysaccharide', 'innate immune response', and 'intrinsic to membrane' were observed commonly in CNS and Pneu. Enriched gene ontology terms related to 'hemoglobin' and 'hemostasis' were, respectively, characteristic of CNS and Pneu. Conclusion: These symptom-associated transcripts might be some clues to the pathogenesis of the A(H1N1)pdm09 infection. © 2013 Japan Pediatric Society.

    DOI: 10.1111/ped.12139

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  • IL-17A receptor expression differs between subclasses of Langerhans cell histiocytosis, which might settle the IL-17A controversy

    Ichiro Murakami, Akira Morimoto, Takashi Oka, Satoshi Kuwamoto, Masako Kato, Yasushi Horie, Kazuhiko Hayashi, Jean Gogusev, Francis Jaubert, Shinsaku Imashuku, Lamia Abd Al-Kadar, Katsuyoshi Takata, Tadashi Yoshino

    VIRCHOWS ARCHIV   462 ( 2 )   219 - 228   2013年2月

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    記述言語:英語   出版者・発行元:SPRINGER  

    Langerhans cell histiocytosis (LCH) is a lymphoproliferative disorder consisting of abnormal Langerhans cell-like cells and other lymphoid cells. LCH presents as either a multisystem LCH (LCH-MS) or a single-system LCH (LCH-SS). Currently, neither the pathogeneses nor the factors that define these disease subclasses have been elucidated. The interleukin (IL)-17A autocrine LCH model and IL-17A-targeted therapies have been proposed and have engendered much controversy. Those authors showed high serum IL-17A levels in LCH and argued that serum IL-17A-dependent fusion activities in vitro, rather than serum IL-17A levels, correlated with LCH severity (i.e. the IL-17A paradox). In contrast, others could not confirm the IL-17A autocrine model. So began the controversy on IL-17A, which still continues. We approached the IL-17A controversy and the IL-17A paradox from a new perspective in considering the expression levels of IL-17A receptor (IL-17RA). We detected higher levels of IL-17RA protein expression in LCH-MS (n = 10) as compared to LCH-SS (n = 9) (P = 0.041) by immunofluorescence. We reconfirmed these data by re-analyzing GSE16395 mRNA data. We found that serum levels of IL-17A were higher in LCH (n = 38) as compared to controls (n = 20) (P = 0.005) with no significant difference between LCH subclasses. We propose an IL-17A endocrine model and stress that changes in IL-17RA expression levels are important for defining LCH subclasses. We hypothesize that these IL-17RA data could clarify the IL-17A controversy and the IL-17A paradox. As a potential treatment of LCH-MS, we indicate the possibility of an IL-17RA-targeted therapy.

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  • Upregulation of Ezh2 expression correlates with higher tumor proliferation and grade in non-Hodgkin's B- and T-cell lymphoma.

    Lamia Abd Al-Kader, Takashi Oka, Katsuyoshi Takata, Xu Sun, Hiaki Sato, Ichiro Murakami, Hiroshi Kimura, Arie P. Otte, Tadashi Yoshino

    Cancer Research   72   1034 - 1034   2012年

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  • Tyrosine phosphatase SHP-1 is expressed higher in multisystem than in single-system Langerhans cell histiocytosis by immunohistochemistry

    Ichiro Murakami, Takashi Oka, Satoshi Kuwamoto, Masako Kato, Kazuhiko Hayashi, Jean Gogusev, Toshihiko Imamura, Akira Morimoto, Shinsaku Imashuku, Tadashi Yoshino

    VIRCHOWS ARCHIV   459 ( 2 )   227 - 234   2011年8月

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    記述言語:英語   出版者・発行元:SPRINGER  

    Langerhans cell histiocytosis (LCH) is a proliferative disorder of Langerhans cell (LC)-like CD1a-positive cell (LCH cell) with unknown causes. LCH consists of two subtypes: single-system LCH (LCH-SS) with favorable prognosis and multisystem LCH (LCH-MS) with poor prognosis. LCH has been indicated as a neoplastic disorder from monoclonal characteristics of LCH cells. This study aimed to investigate an expression of tyrosine phosphatase SHP-1 in LCH, since its expression levels were variously reported in many tumors, overexpression in ovarian cancers (a candidate oncoprotein), and downregulation by methylation in gastric cancers, prostate cancers, malignant lymphomas, and leukemias (a putative tumor suppressor). By immunohistochemistry (IHC), the SHP-1 expression in LCs and LCH cells was compared in LCH (two subtypes: LCH-SS = 21, LCH-MS = 12), dermatopathic lymphadenopathy (DLA) (n = 9) and normal epidermal LCs (n = 3) near LCH lesion. IHC results were analyzed semiquantitatively using a Photoshop software. The mean intensity score (IS) of DLA, LCH-SS, LCH-MS, and LCs were 47, 100, 139, and 167 (in arbitrary unit), respectively. The IS had significant differences among LCH-SS, LCH-MS, and DLA (p < 0.01). SHP-1 is expressed significantly higher in LCH-MS than in LCH-SS. SHP-1 can be a progression marker of LCH. SHP-1 is also useful for differential diagnosis between LCH in lymph nodes and DLA.

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  • Effect of Risedronate on Osteoblast Differentiation, Expression of Receptor Activator of NF-kappa B Ligand and Apoptosis in Mesenchymal Stem Cells

    Hirofumi Fujita, Kazuko Kurokawa, Tetsuya Ogino, Mio Ono, Masanao Yamamoto, Takashi Oka, Tohru Nakanishi, Naoya Kobayashi, Noriaki Tanaka, Tomohiro Ogawa, Etsuko Suzaki, Kozo Utsumi, Junzo Sasaki

    BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY   109 ( 2 )   78 - 84   2011年8月

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    記述言語:英語   出版者・発行元:WILEY-BLACKWELL  

    Nitrogen-containing bisphosphonates (BPs) are antiresorptive drugs used for the treatment of metabolic bone diseases. Bone marrow stromal cells such as mesenchymal stem cells (MSCs) and MSC-derived osteoblasts that originate from MSCs are known to regulate osteoclast differentiation and activation via the expression of receptor activator of NF-kappa B ligand (RANKL). Although the effects of nitrogen-containing BPs on osteoclasts and osteoblasts have been well investigated, their effects in MSCs have not been clarified. In this study, we investigated the effects of risedronate (RIS), a nitrogen-containing BP, on osteoblast differentiation, RANKL expression and apoptosis in human and rat MSCs. RIS suppressed the formation of mineralized nodules and mRNA expression of differentiation marker genes such as bone sialoprotein and osteocalcin in MSC-derived osteoblasts. The RANKL expression induced by 1,25-(OH)(2) vitamin D(3) was not affected by RIS in human MSC-derived osteoblasts. In addition, treatment with high-concentration RIS induced chromatin condensation, an apoptosis feature, in MSCs. RIS-induced chromatin condensation was suppressed by a pan-caspase inhibitor zVAD-FMK and a cell-permeable isoprenoid analogue geranylgeraniol. These results indicate that RIS suppressed osteoblast differentiation and induced caspase-and isoprenoid depletion-dependent apoptosis and suggest that the antiresorptive effect of RIS is not mediated by a decrease in the RANKL expression in MSC-derived osteoblasts.

    DOI: 10.1111/j.1742-7843.2011.00685.x

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  • Downregulation of the B-cell receptor signaling component CD79b in plasma cell myeloma: A possible post transcriptional regulation

    Xingang Huang, Katsuyoshi Takata, Yasuharu Sato, Takehiro Tanaka, Kouichi Ichimura, Maiko Tamura, Takashi Oka, Tadashi Yoshino

    PATHOLOGY INTERNATIONAL   61 ( 3 )   122 - 129   2011年3月

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    記述言語:英語   出版者・発行元:WILEY-BLACKWELL  

    The CD79 molecule, encoded by the CD79a and CD79b genes, is a signaling unit of the B-cell receptor complex, which transmits signals of B-cell activation, growth, and differentiation. They are B-cell-specific and expressed at most stages of B-cell development. Although plasma cells have been believed to lack these gene products, the regulation of CD79 expression in plasma cells is still controversial. In particular, the regulation of CD79b expression remains unclear. We sought to examine CD79b expression in normal and neoplastic plasma cells by immunohistochemical analysis. Out of the 23 clinical samples and 11 cell lines of plasma cell myeloma (PCM), none of the clinical samples and only 1 of 11 cell lines expressed CD79b immunohistologically, whereas non-neoplastic plasma cells in reactive hyperplastic lymph nodes exhibited loss of CD79b protein expression. This finding is quite different from our previous report on CD79a. Not only immunocytochemistry, but also RT-PCR and Western blot analysis of PCM cell lines gave identical results. Interestingly, we detected mRNA transcripts of CD79b in PCM cell lines, although protein translation was lacking. These findings suggest that expression of CD79b is downregulated in both plasma cells and plasma cell myeloma, and this process is possibly under post transcriptional regulation.

    DOI: 10.1111/j.1440-1827.2010.02634.x

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  • Cumulative epigenetic abnormalities in host genes with viral and microbial infection during initiation and progression of malignant lymphoma/leukemia

    Takashi Oka, Hiaki Sato, Mamoru Ouchida, Atae Utsunomiya, Tadashi Yoshino

    Cancers   3 ( 1 )   568 - 581   2011年3月

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    記述言語:英語   掲載種別:書評論文,書評,文献紹介等  

    Although cancers have been thought to be predominantly driven by acquired genetic changes, it is becoming clear that microenvironment-mediated epigenetic alterations play important roles. Aberrant promoter hypermethylation is a prevalent phenomenon in human cancers as well as malignant lymphoma/leukemia. Tumor suppressor genes become frequent targets of aberrant hypermethylation in the course of gene-silencing due to the increased and deregulated DNA methyltransferases (DNMTs). The purpose of this article is to review the current status of knowledge about the contribution of cumulative epigenetic abnormalities of the host genes after microbial and virus infection to the crisis and progression of malignant lymphoma/leukemia. In addition, the relevance of this knowledge to malignant lymphoma/leukemia assessment, prevention and early detection will be discussed. © 2011 by the authors
    licensee MDPI, Basel, Switzerland.

    DOI: 10.3390/cancers3010568

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  • Multi-step aberrant CpG island hyper-methylation is associated with the progression of adult T–cell leukemia/lymphoma (ATLL).

    Hiaki Sato, Takashi Oka, Yoko Shinnou, Takami Kondo, Kana Washio, Masayuki Takano, Katsuyoshi Takata, Toshiaki Morito, Xingang_Huang, Maiko Tamura, Yuta Kitamura, Nobuya Ohara, Mamoru Ouchida, Koichi Ohshima, Kenji Shimizu, Mitsune Tanimoto, Kiyoshi Takahashi¶, Masao Matsuoka, Atae Utsunomiya, Tadashi Yoshino

    Ame. J Pathol   176 ( 1 )   402 - 415   2010年1月

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  • Multi-step accumulation of aberrant CpG island hypermethylation during progression of lymphoma/leukemia

    Takashi Oka, Takami Kondo, Hiaki Sato, Yoko Nakatani, Kana Washio, Ichiro Murakami, Nobuya Ohara, Kiyoshi Takahashi, Mamoru Ouchida, Mitsune Tanimoto, Tadashi Yoshino

    International Journal of Molecular Medicine   26 ( Sup1 )   S44   2010年

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  • Methylation of the thyrosine phosphatase SHP1 gene and loss of its protein in thyroid B-cell lymphoma.

    Saito N, Nakatani Y, Oka T, Ohshima K, Takashita M, Iwasaki H, Ikeda S

    Med.Bull.Fukuoka Univ.   37 ( 1 )   31 - 37   2010年

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  • Helicobacter pylori infection induce accumulation of aberrant CpG hypermethylation to promote development and progression of gastric MALT lymphoma

    Takashi Oka, Takami Kondo, Hiaki Sat, Yoko Shinnou, Kana Washio, Toshiaki Morit, Katsuyoshi Takat, Nobuya Ohara, Mamoru Ouchida, Kenji Shimizu, Tadashi Yoshin

    Proceedings of The 3rd International Symposium for Future Technology Creating Better Human Health and Society Comprehensive Approach to Cancer and Infectious Diseases   1 ( 1 )   105 - 105   2010年

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  • Methylation of the thyrosine phosphatase SHP1 gene and loss of its protein in thyroid B-cell lymphoma.

    Saito N, Nakatani Y, Oka T, Ohshima K, Takashita M, Iwasaki H, Ikeda S

    Med.Bull.Fukuoka Univ.   37 ( 1 )   31 - 37   2010年

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  • Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

    Daisuke Ekuni, James D. Firth, Tarun Nayer, Takaaki Tomofuji, Toshihiro Sanbe, Koichiro Irie, Tatsuo Yamamoto, Takashi Oka, Zhenzi Liu, Juergen Vielkind, Edward E. Putnins

    AMERICAN JOURNAL OF PATHOLOGY   175 ( 4 )   1398 - 1409   2009年10月

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    記述言語:英語   出版者・発行元:AMER SOC INVESTIGATIVE PATHOLOGY, INC  

    Reactive oxygen species (ROS) production is an antimicrobial response to pathogenic challenge that may, in the case of persistent infection, have deleterious effects on the tissue of origin. A rat periodontal disease model was used to study ROS-induced chronic epithelial inflammation and bone loss. Lipopolysaccharide (LPS) was applied for 8 weeks into the gingival sulcus, and histological analysis confirmed the onset of chronic disease. junctional epithelium was collected from healthy and diseased animals using laser-capture microdissection, and expression microarray analysis was performed. Of 19,730 genes changed in disease, 42 were up-regulated >= 4-fold. Three of the top 10 LPS-induced genes, monoamine oxidase B (MAO/B) and flavin-containing monooxygenase 1 and 2, are implicated in ROS signaling. LPS-associated induction of the ROS mediator H(2)O(2) as well as MAO/B and tumor necrosis factor (TNF)-alpha levels were validated in the rat histological sections and a porcine junctional epithelial cell culture model. Topical MAO inhibitors significantly counteracted LPS-associated elevation of H(2)O(2) production and TNF-alpha expression in vivo and in vitro, inhibited disease-associated apical migration and proliferation of junctional epithelium and inhibited induced systemic H(2)O(2) levels and alveolar bone loss in vivo. These results suggest that LPS induces chronic wounds via elevated MAO/B-mediated increases in H(2)O(2) and TNF-alpha activity by epithelial cells and is further associated with more distant effects on systemic oxidative stress and alveolar bone loss. (Am J Pathol 2009,175:1398-1409; DOI: 10.2353/ajpath.2009.090108)

    DOI: 10.2353/ajpath.2009.090108

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  • Lipopolysaccharide-Induced Epithelial Monoamine Oxidase Mediates Alveolar Bone Loss in a Rat Chronic Wound Model

    Daisuke Ekuni, James D. Firth, Tarun Nayer, Takaaki Tomofuji, Toshihiro Sanbe, Koichiro Irie, Tatsuo Yamamoto, Takashi Oka, Zhenzi Liu, Juergen Vielkind, Edward E. Putnins

    AMERICAN JOURNAL OF PATHOLOGY   175 ( 4 )   1398 - 1409   2009年10月

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    記述言語:英語   出版者・発行元:AMER SOC INVESTIGATIVE PATHOLOGY, INC  

    Reactive oxygen species (ROS) production is an antimicrobial response to pathogenic challenge that may, in the case of persistent infection, have deleterious effects on the tissue of origin. A rat periodontal disease model was used to study ROS-induced chronic epithelial inflammation and bone loss. Lipopolysaccharide (LPS) was applied for 8 weeks into the gingival sulcus, and histological analysis confirmed the onset of chronic disease. junctional epithelium was collected from healthy and diseased animals using laser-capture microdissection, and expression microarray analysis was performed. Of 19,730 genes changed in disease, 42 were up-regulated >= 4-fold. Three of the top 10 LPS-induced genes, monoamine oxidase B (MAO/B) and flavin-containing monooxygenase 1 and 2, are implicated in ROS signaling. LPS-associated induction of the ROS mediator H(2)O(2) as well as MAO/B and tumor necrosis factor (TNF)-alpha levels were validated in the rat histological sections and a porcine junctional epithelial cell culture model. Topical MAO inhibitors significantly counteracted LPS-associated elevation of H(2)O(2) production and TNF-alpha expression in vivo and in vitro, inhibited disease-associated apical migration and proliferation of junctional epithelium and inhibited induced systemic H(2)O(2) levels and alveolar bone loss in vivo. These results suggest that LPS induces chronic wounds via elevated MAO/B-mediated increases in H(2)O(2) and TNF-alpha activity by epithelial cells and is further associated with more distant effects on systemic oxidative stress and alveolar bone loss. (Am J Pathol 2009,175:1398-1409; DOI: 10.2353/ajpath.2009.090108)

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  • Accumulation of aberrant CpG hypermethylation by Helicobacter pylori infection promotes development and progression of gastric MALT lymphoma

    Takami Kondo, Takashi Oka, Hiaki Sato, Yoko Shinnou, Kana Washio, Masayuki Takano, Toshiaki Morito, Katsuyoshi Takata, Nobuya Ohara, Mamoru Ouchida, Kenji Shimizu, Tadashi Yoshino

    INTERNATIONAL JOURNAL OF ONCOLOGY   35 ( 3 )   547 - 557   2009年9月

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    記述言語:英語   出版者・発行元:SPANDIDOS PUBL LTD  

    Aberrant DNA hypermethylation is an important mechanism for the inactivation of tumor-related genes in human tumors. Gastric mucosa-associated lymphoid tissue (MALT) lymphomas arise from Helicobacter pylori-associated chronic gastritis: most patients are H. pylori-positive and eradication therapy is highly effective. In the present study, we used methylation-specific PCR to analyze the DNA methylation status of 11 tumor-related genes (Kip2, p16, hMLH-1, p15, p73, MGMT, DAPK, MINT1, MINT2, MINT31 and HCAD) in 21 specimens of MALT lymphoma, 5 specimens of MALT lymphoma with large cell component (high-grade MALT lymphoma), 15 specimens of diffuse large B-cell lymphoma (DLBCL), 8 specimens of complete remission of MALT lymphoma after eradication therapy, 5 specimens with no evidence of malignancy and PBMCs from 10 healthy donors. The average number of methylated genes was significantly greater in gastric lymphomas as compared to normal controls (P<0.001). The CpG island methylator phenotype (CIMP) was observed in 93.3% (14/15) of DLBCLs, 100% (5/5) of high-grade MALT lymphomas and 61.9% (13/21) of MALT lymphomas; in contrast, CIMP was not found in the control group (0%). The average number of methylated genes and the CIMP incidence significantly increased with H. pylori infection. Furthermore, aberrant CpG methylation of specific genes, such as p16, MGMT and MINT31, was consistently associated with H. pylori infection. These findings strongly suggest that H. pylori infection causes the aberrant DNA hypermethylation of specific genes and induces CIMP, which is an important epigenetic mechanism for the development and progression of gastric MALT lymphoma; additionally, our findings provide new epigenetic markers.

    DOI: 10.3892/ijo_00000366

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  • Accumulation of aberrant CpG hypermethylation by Helicobacter pylori infection promotes development and progression of gastric MALT lymphoma

    Takami Kondo, Takashi Oka, Hiaki Sato, Yoko Shinnou, Kana Washio, Masayuki Takano, Toshiaki Morito, Katsuyoshi Takata, Nobuya Ohara, Mamoru Ouchida, Kenji Shimizu, Tadashi Yoshino

    INTERNATIONAL JOURNAL OF ONCOLOGY   35 ( 3 )   547 - 557   2009年9月

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    記述言語:英語   出版者・発行元:SPANDIDOS PUBL LTD  

    Aberrant DNA hypermethylation is an important mechanism for the inactivation of tumor-related genes in human tumors. Gastric mucosa-associated lymphoid tissue (MALT) lymphomas arise from Helicobacter pylori-associated chronic gastritis: most patients are H. pylori-positive and eradication therapy is highly effective. In the present study, we used methylation-specific PCR to analyze the DNA methylation status of 11 tumor-related genes (Kip2, p16, hMLH-1, p15, p73, MGMT, DAPK, MINT1, MINT2, MINT31 and HCAD) in 21 specimens of MALT lymphoma, 5 specimens of MALT lymphoma with large cell component (high-grade MALT lymphoma), 15 specimens of diffuse large B-cell lymphoma (DLBCL), 8 specimens of complete remission of MALT lymphoma after eradication therapy, 5 specimens with no evidence of malignancy and PBMCs from 10 healthy donors. The average number of methylated genes was significantly greater in gastric lymphomas as compared to normal controls (P<0.001). The CpG island methylator phenotype (CIMP) was observed in 93.3% (14/15) of DLBCLs, 100% (5/5) of high-grade MALT lymphomas and 61.9% (13/21) of MALT lymphomas; in contrast, CIMP was not found in the control group (0%). The average number of methylated genes and the CIMP incidence significantly increased with H. pylori infection. Furthermore, aberrant CpG methylation of specific genes, such as p16, MGMT and MINT31, was consistently associated with H. pylori infection. These findings strongly suggest that H. pylori infection causes the aberrant DNA hypermethylation of specific genes and induces CIMP, which is an important epigenetic mechanism for the development and progression of gastric MALT lymphoma; additionally, our findings provide new epigenetic markers.

    DOI: 10.3892/ijo_00000366

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  • Duodenal and nodal follicular lymphomas are distinct: the former lacks activation-induced cytidine deaminase and follicular dendritic cells despite ongoing somatic hypermutations. 国際誌

    Katsuyoshi Takata, Yasuharu Sato, Naoya Nakamura, Yara Yukie Kikuti, Koichi Ichimura, Takehiro Tanaka, Toshiaki Morito, Maiko Tamura, Takashi Oka, Eisaku Kondo, Hiroyuki Okada, Akira Tari, Tadashi Yoshino

    Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc   22 ( 7 )   940 - 9   2009年7月

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    記述言語:英語  

    Although most follicular lymphomas are believed to be of nodal origin, they sometimes originate from the duodenum. We have reported that the latter differ from nodal follicular lymphomas in having lower clinical stages and uniformly low histological grades, along with variable region of immunoglobulin heavy chain gene (VH) usage that is more similar to mucosa-associated lymphoid tissue (MALT) lymphomas. Little is known, however, about whether they possess other characteristics of nodal follicular lymphomas, particularly ongoing mutations with follicular dendritic cells. We examined 17 cases for which PCR identified the monoclonal bands of the immunoglobulin gene. The duodenal cases showed ongoing mutations, but they lacked activation-induced cytidine deaminase (AID) expression, a statistically significant difference from the nodal cases (P<0.001), and their follicular dendritic cell networks were disrupted. Moreover, not only were VH deviations observed but also they used very restricted VH genes. Although the mechanisms of ongoing mutation without AID and follicular dendritic cell were not clarified, restricted VH usage strongly suggested that antigen stimulation was involved, and that was similar to MALT lymphomas. In conclusion, duodenal follicular lymphomas were shown to be unique, in that they had ongoing hypermutations such as nodal cases, but the mechanisms involved in the hypermutation were quite different; furthermore, restricted VH usage suggested a strong similarity to the antigen-dependent origin of MALT lymphomas.

    DOI: 10.1038/modpathol.2009.51

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  • Duodenal and nodal follicular lymphomas are distinct: the former lacks activation-induced cytidine deaminase and follicular dendritic cells despite ongoing somatic hypermutations. 国際誌

    Katsuyoshi Takata, Yasuharu Sato, Naoya Nakamura, Yara Yukie Kikuti, Koichi Ichimura, Takehiro Tanaka, Toshiaki Morito, Maiko Tamura, Takashi Oka, Eisaku Kondo, Hiroyuki Okada, Akira Tari, Tadashi Yoshino

    Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc   22 ( 7 )   940 - 9   2009年7月

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    記述言語:英語  

    Although most follicular lymphomas are believed to be of nodal origin, they sometimes originate from the duodenum. We have reported that the latter differ from nodal follicular lymphomas in having lower clinical stages and uniformly low histological grades, along with variable region of immunoglobulin heavy chain gene (VH) usage that is more similar to mucosa-associated lymphoid tissue (MALT) lymphomas. Little is known, however, about whether they possess other characteristics of nodal follicular lymphomas, particularly ongoing mutations with follicular dendritic cells. We examined 17 cases for which PCR identified the monoclonal bands of the immunoglobulin gene. The duodenal cases showed ongoing mutations, but they lacked activation-induced cytidine deaminase (AID) expression, a statistically significant difference from the nodal cases (P<0.001), and their follicular dendritic cell networks were disrupted. Moreover, not only were VH deviations observed but also they used very restricted VH genes. Although the mechanisms of ongoing mutation without AID and follicular dendritic cell were not clarified, restricted VH usage strongly suggested that antigen stimulation was involved, and that was similar to MALT lymphomas. In conclusion, duodenal follicular lymphomas were shown to be unique, in that they had ongoing hypermutations such as nodal cases, but the mechanisms involved in the hypermutation were quite different; furthermore, restricted VH usage suggested a strong similarity to the antigen-dependent origin of MALT lymphomas.

    DOI: 10.1038/modpathol.2009.51

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  • Immunohistochemical discrimination of plasmacytoid dendritic cells from myeloid dendritic cells in human pathological tissues.

    Nishikawa Y, Sato H, Oka T, Yoshino T, Takahashi

    J Clin Exp Hematop   49 ( 1 )   23 - 31   2009年

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  • Immunohistochemical discrimination of plasmacytoid dendritic cells from myeloid dendritic cells in human pathological tissues.

    Nishikawa Y, Sato H, Oka T, Yoshino T, Takahashi

    J Clin Exp Hematop   49 ( 1 )   23 - 31   2009年

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  • Duodenal follicular lymphomas share common characteristics with mucosa-associated lymphoid tissue lymphomas

    Y. Sato, K. Ichimura, T. Tanaka, K. Takata, T. Morito, H. Sato, Y. Sato, E. Kondo, H. Yanai, N. Ohara, T. Oka, T. Yoshino

    JOURNAL OF CLINICAL PATHOLOGY   61 ( 3 )   377 - 381   2008年3月

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    記述言語:英語   出版者・発行元:B M J PUBLISHING GROUP  

    Background: Follicular lymphomas occasionally arise in the extra-nodal organs and are frequently found in the duodenum. They are often localised tumours with multiple polyps around the ampulla of Vater.
    Aims: To examine a IgH/bcl-2 hybrid gene and VH gene to investigate the nature of the lymphoma cells and how they differ from nodal follicular lymphomas and MALT lymphomas.
    Methods: Of 40 patients reported previously, 35 with duodenal follicular lymphoma were studied in detail with respect to clinicopathological characteristics.
    Results: 37/40 patients were in clinical stage I (n= 30) or stage II (n= 7). Clonal immunoglobulin gene rearrangement was detected in 53.3% of examined cases, and rearrangement of IgH/bcl-2 gene at the major break point was detected in 27% of cases. Three of 8 examined cases were VH4 (38%); 2 out of them were VH4-34. As VH4 deviation is one of the common characteristics of MALT lymphomas and 2/3 were identical, duodenal follicular lymphomas have a similar aetiology to MALT lymphomas. Clinical course was also similar to that of MALT lymphomas.
    Conclusions: Results suggest that duodenal follicular lymphomas have intermediate characteristics of MALT lymphomas and nodal follicular lymphomas.

    DOI: 10.1136/jcp.2007.049825

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  • Duodenal follicular lymphomas share common characteristics with mucosa-associated lymphoid tissue lymphomas

    Y. Sato, K. Ichimura, T. Tanaka, K. Takata, T. Morito, H. Sato, Y. Sato, E. Kondo, H. Yanai, N. Ohara, T. Oka, T. Yoshino

    JOURNAL OF CLINICAL PATHOLOGY   61 ( 3 )   377 - 381   2008年3月

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    記述言語:英語   出版者・発行元:B M J PUBLISHING GROUP  

    Background: Follicular lymphomas occasionally arise in the extra-nodal organs and are frequently found in the duodenum. They are often localised tumours with multiple polyps around the ampulla of Vater.
    Aims: To examine a IgH/bcl-2 hybrid gene and VH gene to investigate the nature of the lymphoma cells and how they differ from nodal follicular lymphomas and MALT lymphomas.
    Methods: Of 40 patients reported previously, 35 with duodenal follicular lymphoma were studied in detail with respect to clinicopathological characteristics.
    Results: 37/40 patients were in clinical stage I (n= 30) or stage II (n= 7). Clonal immunoglobulin gene rearrangement was detected in 53.3% of examined cases, and rearrangement of IgH/bcl-2 gene at the major break point was detected in 27% of cases. Three of 8 examined cases were VH4 (38%); 2 out of them were VH4-34. As VH4 deviation is one of the common characteristics of MALT lymphomas and 2/3 were identical, duodenal follicular lymphomas have a similar aetiology to MALT lymphomas. Clinical course was also similar to that of MALT lymphomas.
    Conclusions: Results suggest that duodenal follicular lymphomas have intermediate characteristics of MALT lymphomas and nodal follicular lymphomas.

    DOI: 10.1136/jcp.2007.049825

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  • Duodenal follicular lymphomas share common characteristics with mucosa-associated lymphoid tissue lymphomas

    Y. Sato, K. Ichimura, T. Tanaka, K. Takata, T. Morito, H. Sato, Y. Sato, E. Kondo, H. Yanai, N. Ohara, T. Oka, T. Yoshino

    JOURNAL OF CLINICAL PATHOLOGY   61 ( 3 )   377 - 381   2008年3月

     詳細を見る

    記述言語:英語   出版者・発行元:B M J PUBLISHING GROUP  

    Background: Follicular lymphomas occasionally arise in the extra-nodal organs and are frequently found in the duodenum. They are often localised tumours with multiple polyps around the ampulla of Vater.
    Aims: To examine a IgH/bcl-2 hybrid gene and VH gene to investigate the nature of the lymphoma cells and how they differ from nodal follicular lymphomas and MALT lymphomas.
    Methods: Of 40 patients reported previously, 35 with duodenal follicular lymphoma were studied in detail with respect to clinicopathological characteristics.
    Results: 37/40 patients were in clinical stage I (n= 30) or stage II (n= 7). Clonal immunoglobulin gene rearrangement was detected in 53.3% of examined cases, and rearrangement of IgH/bcl-2 gene at the major break point was detected in 27% of cases. Three of 8 examined cases were VH4 (38%); 2 out of them were VH4-34. As VH4 deviation is one of the common characteristics of MALT lymphomas and 2/3 were identical, duodenal follicular lymphomas have a similar aetiology to MALT lymphomas. Clinical course was also similar to that of MALT lymphomas.
    Conclusions: Results suggest that duodenal follicular lymphomas have intermediate characteristics of MALT lymphomas and nodal follicular lymphomas.

    DOI: 10.1136/jcp.2007.049825

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  • リンパ系腫瘍におけるDNAメチル化異常.

    岡 剛史, 吉野正

    血液フロンテイア   18 ( 11 )   1 - 9   2008年

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  • リンパ系腫瘍におけるDNAメチル化異常.

    岡 剛史, 吉野正

    血液フロンテイア   18 ( 11 )   1 - 9   2008年

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  • IMMUNOHISTOCHEMICAL ANALYSES OF PTPN6 (SHP1) ON LANGERHANS CELL HISTIOCYTOSIS

    Ichiro Murakami, Takashi Oka, Hiaki Sato, Yuta Kitamura, Toshiaki Morito, Katsuyoshi Takata, Yoko Shinno, Masayuki Takano, Kana Washio, Xingang Huang, Maiko Tamura, Naoko Ohnishi, Koichi Ichimura, Yasuharu Sato, Hiroyuki Yanai, Nobuya Ohara, Eisaku Kondo, Kiyoshi Takahashi, Takehiro Tanaka, Jean Gogusev, Francis Jaubert, Akira Morimoto, Shinsaku Imashuku, Tadaatsu Akagi, Tadashi Yoshino

    Proceedings of XXIV Annual Meeting of the Histiocyte Society   2008年

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  • High Frequent Gene Silencing of Hemetopoietic Cell Specific Protein Tyrosinephosphatase SHP1 in Hemetopoietic Cell Malignancies.

    Oka T, Ouchida M, Tanimoto M, Shimizu K, Yoshino T

    International Journal of Medical and Biological Frontiers   11 ( 1 )   11 - 42   2007年

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  • Immunoelectron-microscopic study of CD4- and CD8- positive lymphocytes from healthy donors seropositive for human T-lymphotropic virus typeⅠ.

    Ohtsuki Y, Oka T, Manabe Y, Takeuchi T, Lee GH, Furihata M, Yoshino T, Taguchi H, Miyoshi I

    Biomedical Research   18 ( 2 )   83 - 88   2007年

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  • Downregulation of drs mRNA expression is associated with the progression of adult T-cell leukemia/lymphoma.

    Shimakage M, Inoue N, Ohshima K, Kawahara K, Yamamoto N, Oka T, Tambe Y, Yasui K, Matsumoto K, Yutsudo M, Inoue H

    Int J Oncol   30 ( 6 )   1343 - 1348   2007年

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  • Down-regulation of ASY/Nogo transcription associated with progression of adult T-cell leukemia/lymphoma

    Misuzu Shimakage, Nobumasa Inoue, Kohichi Ohshima, Kunimitsu Kawahara, Takashi Oka, Kazuta Yasui, Kayoko Matsumoto, Hirokazu Inoue, Akihiro Watari, Shinji Higashiyama, Masuo Yutsudo

    INTERNATIONAL JOURNAL OF CANCER   119 ( 7 )   1648 - 1653   2006年10月

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    記述言語:英語   出版者・発行元:WILEY-LISS  

    Adult T-cell leukemia/lymphoma (ATLL) is an aggressive form of human leukemia/lymphoma. Although this disease is initiated by infection with human T-lymphotropic virus type 1 (HTLV-1), many HTLV-1 carriers survive for a long period without aggressive illness, suggesting that other factors may play roles in the progression of ATLL to an aggressive state. However, the mechanism involved in this progression still remains unclear. Previously, we have reported that ASY/Nogo mRNA was markedly down-regulated in human small-cell lung carcinomas, whereas it was expressed in normal tissues and other lung carcinomas, such as adenocarcinoma and squamous cell carcinoma. To understand whether or not ASY/Nogo gene is involved in the progression of ATLL, we examined the expression of ASY/Nogo mRNA in smoldering, chronic and aggressive ATLL, and found that the expression level of ASY/Nogo mRNA was markedly reduced in clinically aggressive ATLL. HTLV-1 Tax expression was not affected by the down-regulation of ASY/Nogo mRNA. These results indicate that the ASY/Nogo gene may act as a suppressor against ATLL progression, independent of Tax expression. (c) 2006 Wiley-Liss, Inc.

    DOI: 10.1002/ijc.22011

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  • Dendritic cells interacting mainly with B cells in the lymphoepithelial symbiosis of the human palatine tonsil

    K Takahashi, Y Nishikawa, H Sato, T Oka, T Yoshino, K Miyatani

    VIRCHOWS ARCHIV   448 ( 5 )   623 - 629   2006年5月

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    記述言語:英語   出版者・発行元:SPRINGER  

    The lymphoepithelial symbiosis (LES) of the human palatine tonsil is composed of spindle- or starshaped epithelial cells forming a loose meshwork, containing numerous lymphocytes and dendritic cells (DCs). In the present study, we immunohistochemically characterized DCs in the LES (LES-DCs). LES-DCs were phenotypically immature DCs that were S100 beta+, fascin-, HLA-DR+, CD1a-, CD80-, CD83-, CD86-, and CD123-. The most characteristic feature of LES-DCs was that they contacted many B cells, which were mostly IgM+ IgD+ resting naive B cells. Langerhans cells (LCs) located in the nonsymbiotic squamous epithelium were immature DCs that were S100 beta+, fascin-, and CD1a+ and did not contact lymphocytes. In contrast to LES-DCs, interdigitating dendritic cells (IDCs) in the T zone were mature DCs that were HLA-DR+, CD1a-, fascin+, CD80+, CD83+, and CD86+ and contacted numerous CD4+ T cells. Two subsets of IDC, S100 beta+ fascin+ IDC (IDC-1) and S100 beta- fascin+ IDC (IDC-2), were identified, and the majority of IDCs are IDC-2. In contrast to IDCs, which were distributed in the T-cell area in groups, LES-DCs were distributed along the crypt as if forming a barrier. These findings suggest that LES-DCs are a novel type of DC playing an important role in the induction of humoral immune response against incoming air- or food-borne pathogenic antigens.

    DOI: 10.1007/s00428-005-0085-1

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  • Deviated VH4 immunoglobulin gene usage is found among thyroid mucosa-associated lymphoid tissue lymphomas, similar to the usage at other sites, but is not found in thyroid diffuse large B-cell lymphomas.

    Sato Y, Nakamura N, Nakamura S, Sakugawa S, Ichimura K, Tanaka T, Ohara N, Oka T, Kondo E, Yoshino T

    Mod Pathol   2006年

  • p27Kip1 is Detected on Most Gastric MALT Lymphomas, but not Large Cell Lymphomas.

    Sato H, Sato Y, Ichimura K, Oka T, Kondo E, Tanaka T, Kondo T, Ohara N, Takahashi K, Yoshino T

    J Clin Exp Hematopathol   2006年

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  • Expression of phosphorylated ser70 of bcl-2 correlates with malignancy in human colorectal neoplasms.

    Kondo E, Miyake T, Shibata M, Kimura T, Iwagaki H, Nakamura S, Tanaka T, Ohara N, Ichimura K, Oka T, Yanai H, Shibasaki F, Yoshino T

    Clin Cancer Res   2005年

  • Analysis of genomic homology of murine gammaherpesvirus (MHV)-72 to MHV-68 and impact of MHV-72 on the survival and tumorigenesis in the MHV-72-infected CB17 scid/scid and CB17+/+ mice.

    Oda W, Mistrikova J, Stancekova M, Dutia BM, Nash AA, Takahata H, Jin Z, Oka T, Hayashi K

    Pathol Int   2005年

  • Thymic myoid cells as a myasthenogenic antigen and antigen-presenting cells

    MY Matsumoto, H Matsuo, T Oka, T Fukudome, K Hayashi, H Shiraishi, M Motomura, N Shibuya, H Ayabe

    JOURNAL OF NEUROIMMUNOLOGY   150 ( 1-2 )   80 - 87   2004年5月

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    記述言語:英語   出版者・発行元:ELSEVIER SCIENCE BV  

    We investigated immune property of a myoid cell line, established from Fisher rat thymus. Immunization of syngeneic rats with the myoid cells induced anti-rat acetylcholine receptor (AChR). Implantation of them into the thymus failed to induce typical thymic pathology of human myasthenia gravis (MG) or anti-AChR responses. We also demonstrated that the myoid cells were able to present exogenous antigens to T cells and induce antigen-specific T cell proliferation. These results suggest that myoid cells have the potential antigenicity to induce anti-AChR and the functions of antigen-presenting cells, but their expansion in the thymus may not directly cause MG. (C) 2004 Elsevier B.V. All rights reserved.

    DOI: 10.1016/j.jneuroim.2004.01.022

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  • CD40iigand stimulation inhibits the proliferation of mantle cell lymphoma lines.

    Jin Z, Teramoto N, Hayashi K, Liu YX, Jin GS, Oka T, Takahashi K, Yoshino T, Akagi T

    Anticancer Res   2004年

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  • CD40 ligand stimulation inhibits the proliferation of mantle cell lymphoma lines.

    Jin Z, Tereamoto N, Hayashi K, Liu Y.X, Jin G, Oka T, Takahashi K, Yoshino T, Akagi T

    Anticancer Res.   2004年

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  • Induction and prevention of virus-associated malignant lymphoma by serial transmission of EBV-related virus from cynomolgus by blood transfusion in rabbits.

    Koirala T.R, Hayashi K, Jin Z, Onoda S, Tanaka T, Oda W, chimura K, Ohara N, Oka T, Yamada M, Yoshino T

    Acta. Med. Okayama   2004年

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  • Induction and prevention of virus-associated malignant lymphoma by serial transmission of EBV-related virus from cynomolgus by blood transfusion in rabbits.

    Koirala TR, Hayashi K, Z Jin, Onoda S, Tanaka T, Oda W, Ichimura K, Ohara N, Oka T, Yamada M, Yoshino T

    Acta Med Okayama   2004年

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  • Activated proliferation of B-cell lymphomas/leukemias with the SHP1 gene silencing by aberrant CpG methylation

    M Koyama, T Oka, M Ouchida, Y Nakatani, R Nishiuchi, T Yoshino, K Hayashi, T Akagi, Y Seino

    LABORATORY INVESTIGATION   83 ( 12 )   1849 - 1858   2003年12月

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    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Previously we showed reduced protein and mRNA expression of the SHP1 gene in lymphoma/leukemia cell lines and patient specimens by Northern blot, RT-PCR, Western blot, and immunohistochemical analyses. In this study, aberrant methylation in the SHP1 gene promoter was detected in many B-cell leukemia/lymphoma cell lines as well as in patient specimens, including diffuse large B-cell lymphoma (methylation frequency 93%), MALT lymphoma (82%), mantle cell lymphoma (75%), plasmacytoma (100%) and follicular lymphoma (96%) by methylation-specific PCR, bisulfite sequencing, and restriction enzyme-mediated PCR analyses. The methylation frequency was significantly higher in high-grade MALT lymphoma cases (100%) than in low-grade MALT lymphoma cases (70%), which correlated well with the frequency of no expression of SHP1 protein in high-grade (80%) and low-grade MALT lymphoma (54%). It suggests that the SHP1 gene silencing with aberrant CpG methylation relates to the lymphoma progression. SHP1 protein expression was recovered in B-cell lines after the treatment of the demethylating reagent: 5-aza-2'-deoxycytidine. Transfection of the intact SHP1 gene to the hematopoietic cultured cells, which show no expression of the SHP1 gene, induced growth inhibition, indicating that gene silencing of the SHP1 gene by aberrant methylation plays an important role to get the growth advantage of the malignant lymphoma/leukemia cells. The extraordinarily high frequency (75 to 100%) of CpG methylation of the SHP1 gene in B-cell lymphoma/leukemia patient specimens indicates that the SHP1 gene silencing is one of the critical events to the onset of malignant lymphomas/leukemias as well as important implications for the diagnostic or prognostic markers and the target of gene therapy. These data support the possibility that the SHP1 gene is one of the tumor suppressor genes.

    DOI: 10.1097/01.LAB.0000106503.65258.2B

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  • Activated proliferation of B-cell lymphomas/leukemias with the SHP1 gene silencing by aberrant CpG methylation

    M Koyama, T Oka, M Ouchida, Y Nakatani, R Nishiuchi, T Yoshino, K Hayashi, T Akagi, Y Seino

    LABORATORY INVESTIGATION   83 ( 12 )   1849 - 1858   2003年12月

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    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Previously we showed reduced protein and mRNA expression of the SHP1 gene in lymphoma/leukemia cell lines and patient specimens by Northern blot, RT-PCR, Western blot, and immunohistochemical analyses. In this study, aberrant methylation in the SHP1 gene promoter was detected in many B-cell leukemia/lymphoma cell lines as well as in patient specimens, including diffuse large B-cell lymphoma (methylation frequency 93%), MALT lymphoma (82%), mantle cell lymphoma (75%), plasmacytoma (100%) and follicular lymphoma (96%) by methylation-specific PCR, bisulfite sequencing, and restriction enzyme-mediated PCR analyses. The methylation frequency was significantly higher in high-grade MALT lymphoma cases (100%) than in low-grade MALT lymphoma cases (70%), which correlated well with the frequency of no expression of SHP1 protein in high-grade (80%) and low-grade MALT lymphoma (54%). It suggests that the SHP1 gene silencing with aberrant CpG methylation relates to the lymphoma progression. SHP1 protein expression was recovered in B-cell lines after the treatment of the demethylating reagent: 5-aza-2'-deoxycytidine. Transfection of the intact SHP1 gene to the hematopoietic cultured cells, which show no expression of the SHP1 gene, induced growth inhibition, indicating that gene silencing of the SHP1 gene by aberrant methylation plays an important role to get the growth advantage of the malignant lymphoma/leukemia cells. The extraordinarily high frequency (75 to 100%) of CpG methylation of the SHP1 gene in B-cell lymphoma/leukemia patient specimens indicates that the SHP1 gene silencing is one of the critical events to the onset of malignant lymphomas/leukemias as well as important implications for the diagnostic or prognostic markers and the target of gene therapy. These data support the possibility that the SHP1 gene is one of the tumor suppressor genes.

    DOI: 10.1097/01.LAB.0000106503.65258.2B

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  • Activated proliferation of B-cell lymphomas/leukemias with the SHP1 gene silencing by aberrant CpG methylation

    M Koyama, T Oka, M Ouchida, Y Nakatani, R Nishiuchi, T Yoshino, K Hayashi, T Akagi, Y Seino

    LABORATORY INVESTIGATION   83 ( 12 )   1849 - 1858   2003年12月

     詳細を見る

    記述言語:英語   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Previously we showed reduced protein and mRNA expression of the SHP1 gene in lymphoma/leukemia cell lines and patient specimens by Northern blot, RT-PCR, Western blot, and immunohistochemical analyses. In this study, aberrant methylation in the SHP1 gene promoter was detected in many B-cell leukemia/lymphoma cell lines as well as in patient specimens, including diffuse large B-cell lymphoma (methylation frequency 93%), MALT lymphoma (82%), mantle cell lymphoma (75%), plasmacytoma (100%) and follicular lymphoma (96%) by methylation-specific PCR, bisulfite sequencing, and restriction enzyme-mediated PCR analyses. The methylation frequency was significantly higher in high-grade MALT lymphoma cases (100%) than in low-grade MALT lymphoma cases (70%), which correlated well with the frequency of no expression of SHP1 protein in high-grade (80%) and low-grade MALT lymphoma (54%). It suggests that the SHP1 gene silencing with aberrant CpG methylation relates to the lymphoma progression. SHP1 protein expression was recovered in B-cell lines after the treatment of the demethylating reagent: 5-aza-2'-deoxycytidine. Transfection of the intact SHP1 gene to the hematopoietic cultured cells, which show no expression of the SHP1 gene, induced growth inhibition, indicating that gene silencing of the SHP1 gene by aberrant methylation plays an important role to get the growth advantage of the malignant lymphoma/leukemia cells. The extraordinarily high frequency (75 to 100%) of CpG methylation of the SHP1 gene in B-cell lymphoma/leukemia patient specimens indicates that the SHP1 gene silencing is one of the critical events to the onset of malignant lymphomas/leukemias as well as important implications for the diagnostic or prognostic markers and the target of gene therapy. These data support the possibility that the SHP1 gene is one of the tumor suppressor genes.

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  • 難治性リンパ腫発症関連遺伝子SHP1に関する最新知見

    岡 剛史, 大内田守

    日本臨床   61(11): 2025-2032   2003年

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  • Rabbit model for human EBV-associated hemophagocytic syndrome (HPS)--Sequential autopsy analysis and characterization of IL-2-dependent cell lines established from Herpesvirus papio-Induced fatal rabbit lymphoproliferative diseases with HPS--.

    Hayashi K, Jin ZS, Onoda S, Joko H, Teramoto N, Ohara N, Oda W, Tanaka T, Liu Y-X, Koirala TR, Oka T, Kondo E, Yoshino T, Takahashi K, Akagi T

    Am J Pathol   2003年

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  • Therapeutic trials for a rabbit model of EBV-associated Hemophagocytic Syndrome (HPS)--Effects of vidarabine or CHOP, and development of Herpesvirus papio (HVP)-negative lymphomas surrounded by HVP-infected lymphoproliferative disease--.

    Hayashi K, Joko H, Koirala TR, Onoda S, Jin ZS, Munemasa M, Ohara N, Oda W, Tanaka T, Oka T, Kondo E, Yoshino T, Takahashi K, Yamada M, Akagi T

    Histol Histopathol   2003年

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  • Rabbit model for human EBV-associated hemophagocytic syndrome (HPS).

    Hayashi K, Jin Z, Onoda S, Joko H, Teramoto N, Ohara N, Oda W, Tanaka T, Liu YX, Koirala R, Oka T, Kondo E, Yoshino T, Takahashi K, Akagi T

    Amer. J. Pathol   2003年

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  • Therapeutic trial for a rabbit model of EBV-associated hemophagocytic syndrome (HPS): Effects of vidarabine or CHOP, and development of Herpersvirus papio (HVP)-negative lymphomas surrounded by HVP-infected lymphoproliferative disease.

    Hayashi K, Joko H, Koirala T.R, Onoda S, Jin S.J, Munemasa M, Ohara N, Oda W, Tanaka T, Oka T, Kondo E, Yoshino T, Takahashi K, Yamada M, Akagi T

    Histol Histopathol   2003年

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  • 悪性リンパ腫・白血病におけるプロテイン チロシンフォスファターゼSHP1遺伝子の発現異常.

    岡 剛史, 吉野 正, 林 一彦, 赤木忠厚

    癌の臨床   48,10,561-568   2002年

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  • Gene silencing of the tyrosine phosphatase SHP1 gene by aberrant methylation in leukemias/lymphomas.

    Oka T, Ouchida M, Koyama M, Ogama Y, Takada S, Nakatani Y, Tanaka T, Yoshino T, Hayashi K, Ohara N, Kondo E, Takahashi K, Tsuchiyama J, Tanimoto M, Shimizu K, Akagi T

    Cancer Res   2002年

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  • Expression of heat shock protein 60 in normal and neoplastic human lymphoid tissues.

    Jin HS, Yoshino T, Jin Z, Oka T, Kobayashi K, Yamasaki R, Liu YX, Yokota K, Oguma K, Akagi T

    J Clin Exp Hematopathol   2002年

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  • On recent advances in DNA microarrays.

    Nakanishi T, Oka T, Akagi T

    Acta Med Okayama   55,6,319-328   2001年

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  • An animal model for human EBV-associated hemophagocytic syndrome-- Herpesvirus papio frequently induces fatal lymphoproliferative disorders with hemophagocytic syndrome in rabbits--.

    Hayashi K, Ohara N, Teramoto N, Onoda S, Chen HL, Oka T, Kondo E, Yoshino T, Takahashi K, Yates J, Akagi T

    Am J Pathol   2001年

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  • Morphological interactions of interdigitating dendritic cells with B and T cells in human mesenteric lymph nodes.

    Takahashi K, Asagoe K, Teramoto N, Kondo E, Oka T, Hayashi K, Yoshino T, Akagi T

    Am J Pathol   2001年

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  • Reduction of hematopoietic cell-specific tyroshine phosphatase SHP-1 gene expression in natural killer cell lymphoma and various types of lymphomas/leukemias: Combination analysis with cDNA expression array and tissue microarray.

    Oka T, Yoshino T, Hayashi K, Ohara N, Nakanishi T, Yamaai Y, Hiraki A, Sogawa CA, Kondo E, Teramoto N, Takahashi K, Tsuchiyama J, Akagi T

    Am J Pathol   2001年

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  • Loss of expression of α4β7 integrin and L-selectin is associated with high-grade progression of low-grade MALT lymphoma.

    Liu Y X, Yoshino T, Ohara N, Oka T, Jin Z S, Hayashi K, Akagi T

    Mod Pathol   2001年

  • Myasthenogenisity of thymic myoid cell.

    Yoshinaga M, Matsuo H, Oka T, Motomura M, Shibuya N, Ayabe H

    J. Neuroimmunol   2001年

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  • Differentiation of rat thymic myoid progenitor cell line established by coculture with human T-lymphotropic virus type-I-producing human T cells

    Takashi Oka, Kazuhiko Hayashi, Yasuo Nakaoka, Yuji Ohtsuki, Tadaatsu Akagi

    Cell and Tissue Research   300 ( 1 )   119 - 127   2000年

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    記述言語:英語  

    A thymus-derived myoid precursor cell line (ST1), which differentiates to myoid cells in the growth arrest condition, was established by the cocultivation of F344 rat thymic cells with human T-lymphotropic virus type-I (HTLV-I)-producing human lymphoid cells. No integration of HTLV-I was detected in ST1 cells by Southern blot hybridization. In a differentiation culture condition such as confluent culture or serum starvation, ST1 cells began to fuse, creating multinuclear giant cells, with the induced expression of MyoD1 and various muscle-specific antigens, including α-sarcomeric actin, skeletal muscle myosin, myoglobin, desmin, and acetylcholine receptor. Ultrastructural investigation revealed that differentiated ST1B cells created aggregates of thick and thin filaments with Z-band-like composition, then formed sarcomeric structures and tubular honeycomb arrays. Finally, these cells spontaneously contracted with a frequency of 0.5-2.0 Hz and synchronized with adjoining cells. Transplantation of ST1B cells into nude mice produced a small tumor nodule, showing clear differentiation to skeletal muscle cells. ST1B cells did not indicate any colony-forming activities in soft agar, demonstrating that ST1B cells retain some of the physiologically normal phenotypes. This rare cell line is promising for use in various physiological and pathological investigations including functional research of thymic myoid cells and the pathological role in autoimmune diseases, as well as animal model experiments of cell therapy related to muscular degenerative disorders or regeneration of injured muscles.

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  • Sequence analysis and variation of EBNA-1 in Epstein-Barr virus-related herpesvirus of cynomolgus monkey

    Nobuya Ohara, Kazuhiko Hayashi, Norihiro Teramoto, Takashi Oka, Koji Fujimoto, Yasuhiro Yoshikawa, Esmeralda Castanos-Velez, Peter Biberfeld, Tadaatsu Akagi

    Intervirology   43 ( 2 )   102 - 106   2000年

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    記述言語:英語   出版者・発行元:S. Karger AG  

    Objectives: The Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA-1) is an important protein for immortalization and tumorigenesis of infected cells. EBNA-1 gene variants may play a role in tumorigenesis. We determined the nucleotide and amino acid (aa) sequences of EBNA-1 in EBV-related herpesviruses from cynomolgus monkeys (cynomolgus-EBV) which induced malignant lymphomas in its natural host and in rabbits, and compared them with sequences of EBV and other lymphocryptoviruses (LCVs). Methods: Polymerase chain reaction and direct sequencing methods were performed using extracted DNA from cynomolgus-EBV-infected cell lines. Results: The amino acid sequences of cynomolgus-EBV EBNA-1 from two cell lines (Si-IIA: 588 aa
    Ts-B6: 619 aa) which are antigenically cross-reactive to human EBV EBNA-1 showed homology with human EBV (Si-IIA: 53%
    Ts-B6: 58%) and other LCVs from baboons (54 and 52%) and rhesus monkeys (60 and 58%), especially in the C- terminal unique domain. Homology of the EBNA-1 sequence between Si-IIA and Ts-B6 was 92%. The sequence difference between EBV and the related LCVs was manifested mainly in the length of the internal repeat 3-corresponding region, which contains serine in the glycine/alanine repeat region of nonhuman LCVs. Conclusion: Sequence variation of cynomolgus-EBV EBNA-1 from different cell lines was observed. However, their sequences show a relatively high homology with human EBV and share the common features of EBNA-1 of EBV and other LCVs. Copyright (C) 2000 S. Karger AG, Basel.

    DOI: 10.1159/000025031

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  • Sequence analysis and variation of EBNA-1 in Epstein-Barr virus-related herpesvirus of cynomolgus monkey

    Ohara N, Hayashi K, Teramoto N, Oka T, Fujimoto K, Yoshikawa Y, Castanos-Velez E, Biberfeld P, Akagi T

    Intervirology   2000年

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  • Sequence analysis and variation of EBNA-1 in Epstein-Barr virus-related herpesvirus of cynomolgus monkey

    Nobuya Ohara, Kazuhiko Hayashi, Norihiro Teramoto, Takashi Oka, Koji Fujimoto, Yasuhiro Yoshikawa, Esmeralda Castanos-Velez, Peter Biberfeld, Tadaatsu Akagi

    Intervirology   43 ( 2 )   102 - 106   2000年

     詳細を見る

    記述言語:英語   出版者・発行元:S. Karger AG  

    Objectives: The Epstein-Barr virus (EBV) nuclear antigen 1 (EBNA-1) is an important protein for immortalization and tumorigenesis of infected cells. EBNA-1 gene variants may play a role in tumorigenesis. We determined the nucleotide and amino acid (aa) sequences of EBNA-1 in EBV-related herpesviruses from cynomolgus monkeys (cynomolgus-EBV) which induced malignant lymphomas in its natural host and in rabbits, and compared them with sequences of EBV and other lymphocryptoviruses (LCVs). Methods: Polymerase chain reaction and direct sequencing methods were performed using extracted DNA from cynomolgus-EBV-infected cell lines. Results: The amino acid sequences of cynomolgus-EBV EBNA-1 from two cell lines (Si-IIA: 588 aa
    Ts-B6: 619 aa) which are antigenically cross-reactive to human EBV EBNA-1 showed homology with human EBV (Si-IIA: 53%
    Ts-B6: 58%) and other LCVs from baboons (54 and 52%) and rhesus monkeys (60 and 58%), especially in the C- terminal unique domain. Homology of the EBNA-1 sequence between Si-IIA and Ts-B6 was 92%. The sequence difference between EBV and the related LCVs was manifested mainly in the length of the internal repeat 3-corresponding region, which contains serine in the glycine/alanine repeat region of nonhuman LCVs. Conclusion: Sequence variation of cynomolgus-EBV EBNA-1 from different cell lines was observed. However, their sequences show a relatively high homology with human EBV and share the common features of EBNA-1 of EBV and other LCVs. Copyright (C) 2000 S. Karger AG, Basel.

    DOI: 10.1159/000025031

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  • Charactereization of Epstein-Barr virus-infected mantle cell lymphoma lines

    Z. Jin, N. Teramoto, T. Yoshino, K. Takada, T. Oka, K. Hayashi, T. Akagi

    Acta Med. Okayama   2000年

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  • Epstein-Barr virus (EBV)-negative nasophatyngeal carcinoma cell line TW03 enhaces its tumorigenicity.

    Teramoto N, Maeda A, Kobayashi K, Hayashi K, Oka T, Takahashi K, Takada K, Klein G, Akagi T

    Labo.Investigation   2000年

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  • Differentiation of rat thymic myoid progenitor cell line established by coculture with human T-lymphotropic virus type-I-producing human T cells

    Takashi Oka, Kazuhiko Hayashi, Yasuo Nakaoka, Yuji Ohtsuki, Tadaatsu Akagi

    Cell and Tissue Research   300 ( 1 )   119 - 127   2000年

     詳細を見る

    記述言語:英語  

    A thymus-derived myoid precursor cell line (ST1), which differentiates to myoid cells in the growth arrest condition, was established by the cocultivation of F344 rat thymic cells with human T-lymphotropic virus type-I (HTLV-I)-producing human lymphoid cells. No integration of HTLV-I was detected in ST1 cells by Southern blot hybridization. In a differentiation culture condition such as confluent culture or serum starvation, ST1 cells began to fuse, creating multinuclear giant cells, with the induced expression of MyoD1 and various muscle-specific antigens, including α-sarcomeric actin, skeletal muscle myosin, myoglobin, desmin, and acetylcholine receptor. Ultrastructural investigation revealed that differentiated ST1B cells created aggregates of thick and thin filaments with Z-band-like composition, then formed sarcomeric structures and tubular honeycomb arrays. Finally, these cells spontaneously contracted with a frequency of 0.5-2.0 Hz and synchronized with adjoining cells. Transplantation of ST1B cells into nude mice produced a small tumor nodule, showing clear differentiation to skeletal muscle cells. ST1B cells did not indicate any colony-forming activities in soft agar, demonstrating that ST1B cells retain some of the physiologically normal phenotypes. This rare cell line is promising for use in various physiological and pathological investigations including functional research of thymic myoid cells and the pathological role in autoimmune diseases, as well as animal model experiments of cell therapy related to muscular degenerative disorders or regeneration of injured muscles.

    DOI: 10.1007/s004410050053

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  • Differentiation of rat thymic myoid progenitor cell line established by coculture with HTLV-I-producing human T-cells.

    Oka T, Hayashi K, Nakaoka Y, Ohtsuki Y, Akagi T

    Cell & Tissue Res   2000年

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  • Myoid cell differentiation of rat thymus-derived progenitor cell line established by coculture with HTLV-I-producing human -T-cells

    Oka T, Hayashi K, Nakaoka Y, Ohtsuki Y, Akagi T

    J. AIDS and Human Retrovirol   1999年

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  • Cyno-EBV(EBV-related Herpesvirus from Cynomolgus Macaques) induces rabbit malignant lymphomas and their tumor cell lines frequently show specific chromosomal abnormalities

    Hayashi K, Chen H.L, Yanai H, Koirala T.R, Ohara N, Teramoto N, Oka T, Yoshino T, Takahashi K, Miyamoto K, Fujimoto K, Yoshikawa Y, Akagi T

    Labo. Investigation   1999年

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  • Evidence for specific immune response against P210 BCR-ABL in long-term remission CML patients treated with interferon

    T. Oka, K. J. Sastry, P. Nehete, S. J. Schapiro, J. Q. Guo, M. Talpaz, R. B. Arlinghaus

    Leukemia   12 ( 2 )   155 - 163   1998年

     詳細を見る

    記述言語:英語   出版者・発行元:Nature Publishing Group  

    Interferon-alpha treatment induces complete cytogenetic remission in 25% of Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CML) patients. These remissions are durable unlike remissions induced with other therapies and yet residual leukemia is detectable in most of these patients. Total peripheral blood mononuclear cells (PBMCs) from CML patients in long-term remission following interferon treatment exhibited significantly higher proliferative responses (four- to 15-fold over background) than normals directed against P210 BCR-ABL in extracts of transfected monkey fibroblast cells. Surprisingly, similar enhanced levels of specific proliferative responses were observed with extracts from cells expressing Bcr and/or Abl proteins. In contrast, extracts from vector only or v-Mos-expressing cells had background level responses. Control monkey fibroblast cells lacking BCR-ABL expression failed to induce proliferation over background levels. Normal individuals had no significant responses to Bcr/Abl extracts. On the other hand, peripheral blood mononuclear cells from allogeneic bone marrow transplant CML patients had proliferative responses to cell extracts independent of Bcr-Abl. These data indicate that patients in remission due to alpha-interferon treatment have significantly higher levels of specific cellular immunoreactivity against Bcr/Abl sequences than normal controls, which could play a role in maintaining cytogenetic remission in Ph-positive CML patients.

    DOI: 10.1038/sj.leu.2400919

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  • Evidence for specific immune response against P210 BCR-ABL in long-term remission CML patients treated with interferon

    T. Oka, K. J. Sastry, P. Nehete, S. J. Schapiro, J. Q. Guo, M. Talpaz, R. B. Arlinghaus

    Leukemia   12 ( 2 )   155 - 163   1998年

     詳細を見る

    記述言語:英語   出版者・発行元:Nature Publishing Group  

    Interferon-alpha treatment induces complete cytogenetic remission in 25% of Philadelphia chromosome (Ph)-positive chronic myelogenous leukemia (CML) patients. These remissions are durable unlike remissions induced with other therapies and yet residual leukemia is detectable in most of these patients. Total peripheral blood mononuclear cells (PBMCs) from CML patients in long-term remission following interferon treatment exhibited significantly higher proliferative responses (four- to 15-fold over background) than normals directed against P210 BCR-ABL in extracts of transfected monkey fibroblast cells. Surprisingly, similar enhanced levels of specific proliferative responses were observed with extracts from cells expressing Bcr and/or Abl proteins. In contrast, extracts from vector only or v-Mos-expressing cells had background level responses. Control monkey fibroblast cells lacking BCR-ABL expression failed to induce proliferation over background levels. Normal individuals had no significant responses to Bcr/Abl extracts. On the other hand, peripheral blood mononuclear cells from allogeneic bone marrow transplant CML patients had proliferative responses to cell extracts independent of Bcr-Abl. These data indicate that patients in remission due to alpha-interferon treatment have significantly higher levels of specific cellular immunoreactivity against Bcr/Abl sequences than normal controls, which could play a role in maintaining cytogenetic remission in Ph-positive CML patients.

    DOI: 10.1038/sj.leu.2400919

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  • Metastatic potential of lymphoma/leukemia cell lines in SCID mice is closely related to expression of CD44

    Nobuhiro Kawasaki, Yoshinobu Matsuo, Tadashi Yoshino, Hiroyuki Yanai, Takashi Oka, Norihiro Teramoto, Cao Liu, Eisaku Kondo, Jun Minowada, Tadaatsu Akagi

    Japanese Journal of Cancer Research   87 ( 10 )   1070 - 1077   1996年

     詳細を見る

    記述言語:英語   出版者・発行元:Japanese Cancer Association  

    To investigate whether the lymphocyte homing receptors, adhesion molecules regulating normal lymphocyte traffic, influence the dissemination of lymphoma cells, 24 lymphoma/leukemia cell lines were inoculated into SCID mice subcutaneously, and the correlation between the expression of the adhesion molecules and the metastatic potential of the cell lines was examined. Among the six adhesion molecules examined (LFA-1, ICAM-1, CLA, VLA-4, L-selectin and CD44), L-selectin increased the incidence of lymph node metastasis, and CD44 expression was related to both lymph node and organ (hematogenous) metastasis. A monoclonal antibody to the standard form of CD44 (CD44s), Hermes-3, inhibited the local growth and remote metastasis of CD44+ cell lines. Thus, it is concluded that at least CD44s expression is important in both lymphatic and hematogenous metastasis.

    DOI: 10.1111/j.1349-7006.1996.tb03112.x

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  • Metastatic potential of lymphoma/leukemia cell lines in SCID mice is closely related to expression of CD44

    Nobuhiro Kawasaki, Yoshinobu Matsuo, Tadashi Yoshino, Hiroyuki Yanai, Takashi Oka, Norihiro Teramoto, Cao Liu, Eisaku Kondo, Jun Minowada, Tadaatsu Akagi

    Japanese Journal of Cancer Research   87 ( 10 )   1070 - 1077   1996年

     詳細を見る

    記述言語:英語   出版者・発行元:Japanese Cancer Association  

    To investigate whether the lymphocyte homing receptors, adhesion molecules regulating normal lymphocyte traffic, influence the dissemination of lymphoma cells, 24 lymphoma/leukemia cell lines were inoculated into SCID mice subcutaneously, and the correlation between the expression of the adhesion molecules and the metastatic potential of the cell lines was examined. Among the six adhesion molecules examined (LFA-1, ICAM-1, CLA, VLA-4, L-selectin and CD44), L-selectin increased the incidence of lymph node metastasis, and CD44 expression was related to both lymph node and organ (hematogenous) metastasis. A monoclonal antibody to the standard form of CD44 (CD44s), Hermes-3, inhibited the local growth and remote metastasis of CD44+ cell lines. Thus, it is concluded that at least CD44s expression is important in both lymphatic and hematogenous metastasis.

    DOI: 10.1111/j.1349-7006.1996.tb03112.x

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  • Characterization of flat revertants isolated from cells transformed by Abelson murine leukemia virus (Ab-MuLV).(共著)

    J. Cellular Physiol.   145 ( 3 )   428 - 433   1990年

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  • Characterization of flat revertants isolated from cells transformed by Abelson murine leukemia virus (Ab‐MuLV)

    Takashi Oka, Masuo Yutsudo, Hirokazu Inoue, Fujito Higuchi, Akira Hakura

    Journal of Cellular Physiology   145 ( 3 )   428 - 433   1990年

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    記述言語:英語  

    Transformed Fisher rat fibroblast cell lines by Abelson murine leukemia virus frequently revert to the normal phenotype in usual culture conditions. Molecular Biological analysis of thre revertant clones isolated from the transformants showed that their morphological reversions were due to inactivation of the v‐abl oncogene at multiple steps including transcription, translation or v‐abl protein kinase activity itself without any change in structural gene expression of helper virus. These findings suggest the existence of a specific mechanism(s) for elimination of the v‐abl oncogene by segregation, mutation, or gene rearrangement in these cells. Copyright © 1990 Wiley‐Liss, Inc.

    DOI: 10.1002/jcp.1041450306

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  • Inactivation and activation of inward current during adaptation to potassium ions in Paramecium caudatum.(共著)

    Cell Struct. Funct.   14 ( 2 )   209 - 216   1989年

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    記述言語:英語  

    DOI: 10.1247/csf.14.209

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  • Inactivation and Activation of Inward Current During Adaptation to Potassium Ions in Paramecium Caudatum

    Takashi Oka, Yasuo Nakaoka

    Cell Structure and Function   14 ( 2 )   209 - 216   1989年

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    記述言語:英語  

    Paramecium cells adapted to 2 mM K+ were voltage clamped and transient inward currents induced by step-depolarizations were studied. When the external K+ concentration was increased to 8 mM, the inward current was largely suppressed. Similar suppression of the inward current was induced by positive shifts of the holding potential above the resting level. The suppression of inward current is, therefore, primarily caused by depolarizing changes in the membrane potential. During adaptation to 8 mM K+, the inward current recovered to about 70% of that in the cells adapted to 2 mM K+, the resting membrane repolarized, and the steady state inactivation of the inward current was shifted to a more positive level than the cells adapted to 2 mM K+. When mutant cells which lack depolarization-sensitive Ca-current were adapted to 8 mM K+, a step-depolarization induced a fast activation of outward current, which would subtract from the inward current in the wild-type cells, suggesting that the transient inward current of cells adapted to 8 mM K+ is partially reduced by the fast activation of outward current. © 1989, Japan Society for Cell Biology. All rights reserved.

    DOI: 10.1247/csf.14.209

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  • Transformation of hamster spleen lymphocytes by human T-cell leukemia virus type-(]G0001[).(共著)

    Int. J. Cancer   37 ( 5 )   775 - 779   1986年

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  • Transformation of hamster spleen lymphocytes by human T‐cell leukemia virus type I

    T. Akagi, H. Takata, Y. Ohtsuki, K. Takahashi, T. Oka, S. Yano, I. Miyoshi

    International Journal of Cancer   37 ( 5 )   775 - 779   1986年

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    記述言語:英語  

    Co‐cultivation of spleen cells of Syrian golden hamsters with lethally irradiated MT‐2 cells harboring human T‐cell leukemia virus type I (HTLV‐I) resulted in the establishment of lymphoid cell lines, HCT‐1 and HCT‐2, which exhibited the normal karyotype of golden hamsters. Cells of both the HCT‐1 and HCT‐2 lines lacked surface immunoglobulins and reacted with a monoclonal antibody (MAb) specific for hamster T cells. Some were positive for OKIal. None of them expressed HTLV structural antigens (p19 and p24) or virus particles, but they contained HTLV‐1 proviral DNA monoclonally. By immunochemical analysis of the labelled cell antigens, sera from adult T‐cell leukemia (ATL) patients reacted with the two polypeptides, p37 and p40, which may not be viral structural proteins and still remain to be characterized. HCT‐1 and HCT‐2 cells were transplantable into newborn hamsters, pre‐treated with anti‐hamster thymocyte serum and non‐treated, respectively, producing diffuse malignant lymphoma. These findings indicated that HTLV‐1 not only immortalized but also transformed hamster T cells non‐productively. Copyright © 1986 Wiley‐Liss, Inc., A Wiley Company

    DOI: 10.1002/ijc.2910370520

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  • T cell growth factors from adult T cell leukemia virus-transformed cell lines.(共著)

    FEBS LETTERS   177 ( 2 )   200 - 204   1984年11月

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  • T cell growth factors from adult T cell leukemia virus-transformed cell lines

    Yasuji Okai, Takashi Oka, Tadaatsu Akagi, Sayuri Kurata, Nobuo Fujiyoshi

    FEBS Letters   177 ( 2 )   200 - 204   1984年11月

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    記述言語:英語  

    Some characteristics of T cell growth factors derived from adult T cell leukemia virus (ATLV)-transformed cell lines, MT 1 and MT 2 were analyzed. MT 1 cells release significant interleukin 2 (IL 2) activity into the culture medium, which showed the same elution pattern of gel filtration and isoelectric focusing of IL 2 from lectin-stimulated normal human lymphocytes. This activity was also detected in the cell extract of MT 1. In contrast, MT 2 cell line did not produce IL 2 activity, but non-IL 2 type growth factor was observed. The significance of these factors from MT cell lines is discussed from the viewpoint of 'autokine' in ATLV-transformed cells. ALTV-transformed cell T cell growth factor. © 1984.

    DOI: 10.1016/0014-5793(84)81283-1

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▼全件表示

講演・口頭発表等

  • HTLV-1キャリアにおける異常DNAメチル化と成人T細胞白血病/リンパ腫(ATL)発症との関連について

    第4回日本HTLV-1学会学術集会  2017年 

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  • Sensitive detection of dynamic changes of metabolic abnormalities during onset and progression of adult T-cell leukemia/lymphoma (ATL) and induction of specific leukemic cell death by photodynamic action

    The18th International Conference on Human Retrovirology: HTLV and Related Viruses HTLV  2017年 

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  • Aberrant DNA methylation is associated with the clinical course in the same patients with ATL

    The18th International Conference on Human Retrovirology: HTLV and Related Viruses HTLV  2017年 

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  • Proteomic analysis on Langerhans cell histiocytosis patients and a new triple-risk factor model

    2017年 

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  • Sensitive detection of dynamic changes of metabolic abnormalities during onset and progression of adult T-cell leukemia/lymphoma (ATL) and induction of specific leukemic cell death by photodynamic action

    The18th International Conference on Human Retrovirology: HTLV and Related Viruses HTLV  2017年 

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  • Aberrant DNA methylation is associated with the clinical course in the same patients with ATL

    The18th International Conference on Human Retrovirology: HTLV and Related Viruses HTLV  2017年 

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  • Proteomic analysis on Langerhans cell histiocytosis patients and a new triple-risk factor model

    第106回日本病理学会総会  2017年 

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態の変動との関連

    第106回日本病理学会総会  2017年 

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  • 成人T細胞白血病/リンパ腫(ATL)を発症したHTLV-1キャリアにおける異常DNAメチル化の解析

    H29第57回日本リンパ網内系学会  2017年 

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  • ECOLOGY OF MERKEL CELL POLYOMAVIRUS IN HEALTHY SKIN SHOWS A CLOSE AGREEMENT WITH INTERLEUKIN-1 LOOP MODEL IN LANGERHANS CELL HISTIOCYTOSIS

    32nd Annual Meeting of the Histiocyte Society  2016年 

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  • ECOLOGY OF MERKEL CELL POLYOMAVIRUS IN HEALTHY SKIN SHOWS A CLOSE AGREEMENT WITH INTERLEUKIN-1 LOOP MODEL IN LANGERHANS CELL HISTIOCYTOSIS

    32nd Annual Meeting of the Histiocyte Society  2016年 

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  • Single cell dynamics of DNA methylation induced by the Tax gene expression of HTLV-I in adult T-cell leukemia/lymphoma

    The 9th International Symposium for Future Technology Creating Better Human Health and Society.New Horizons in Interdisciplinary Cancer Research  2016年 

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  • Single cell dynamics of DNA methylation perturbated by Tax gene expression of HTLV-I in adult T cell leukemia/lymphoma (ATL)

    The 74rd Annual Meeting of the Japanese Cancer Association, 2015  2015年 

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  • 成人T細胞白血病/リンパ腫(ATL)における特異的DNAメチル化と病態との関連

    第104回日本病理学会  2015年 

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  • ランゲルハンス細胞組織球症患者血清の質量分析器による解析

    第104回日本病理学会  2015年 

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  • 成人T細胞白血病リンパ腫に於ける一細胞DNAメチル化の変動解析

    第104回日本病理学会  2015年 

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態との関連

    第55回リンパ網内系学会学術集会  2015年 

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  • 成人T細胞白血病/リンパ腫(ATL)発症・進展特異的な代謝異常に関するメタボローム解析

    第55回リンパ網内系学会学術集会  2015年 

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  • 成人T細胞白血病/リンパ腫(ATL)におけるDNA異常メチル化と病態との関連

    第2回日本HTLV-1学会学術集会  2015年 

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  • Dynamic changes of DNA methylation in adult T cell leukemia/lymphoma (ATL)

    The 73rd Annual Meeting of the Japanese Cancer Association  2014年 

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  • Aberrant expression of Polycomb complex1 (PRC1) from balanced to Bmi-1/PCGF4 dominant over Mel-18/PCGF2 in malignant lymphoma

    2014年 

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  • Dynamic changes of DNA methylation in adult T cell leukemia/lymphoma (ATL)

    The 73rd Annual Meeting of the Japanese Cancer Association  2014年 

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  • Sensitive detection and specific induction of cell death in adult T-cell leukemia/lymphoma cells by photodynamic reactions

    The 7th International Symposium for Future Technology Creating Better Human Health and Society  2014年 

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  • B細胞腫瘍及びT/NK腫瘍におけるポリコーム抑制性複合体2(PRC2)のEzh1 と Ezh2の特異的発現

    第103回日本病理学会  2014年 

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  • 成人T細胞白血病/リンパ腫(ATL)細胞株における特異的DNAメチル化の解析

    第103回日本病理学会  2014年 

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  • メルケル細胞ポリオーマウイルス解析に依るランゲルハンス細胞肉腫の疾患モデル

    第103回日本病理学会  2014年 

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  • 成人T細胞白血病/リンパ腫(ATL)関連細胞株における特異的DNAメチル化の解析

    第53回リンパ網内系学会  2014年 

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  • Aberrant expression of Polycomb complex1 (PRC1) from balanced to Bmi-1/PCGF4 dominant over Mel-18/PCGF2 in malignant lymphoma

    第53回リンパ網内系学会  2014年 

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  • 成人T細胞白血病・リンパ腫(ATL)発症・進展に於ける代謝異常に関するメタボローム解析

    第1回日本HTLV−1学会  2014年 

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  • 成人T細胞白血病/リンパ腫(ATL)関連細胞株におけるDNA異常メチル化の解析

    第1回日本HTLV−1学会  2014年 

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  • High expression of Ezh2, Eed and Suz-12 in the aggressive variants of non-Hodgkin lymphoma

    The 72st Annual Meeting of the Japanese Cancer Association,  2013年 

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  • Sensitive detection and apoptotic cell death induction of adult T-cell leukemia/lymphoma (ATL) cells with photodynamic actions

    The16th International Conference on Human Retrovirology: HTLV and Related Viruses HTLV 2013  2013年 

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  • 成人T細胞白血病・リンパ腫(ATL)細胞の光動力学的反応による特異的細胞死の誘導

    HTLV-I 研究会  2013年 

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  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と予後との相関

    HTLV-I 研究会  2013年 

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  • Sensitive detection and cell death induced by ALA-mediated photodynamic actions in adult T-cell leukemia/lymphoma cells

    The 72st Annual Meeting of the Japanese Cancer Association,  2013年 

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  • ポリコーム群(PcG)蛋白の異常発現とnon-Hodgkin lymphomaの増殖性と悪性度

    「抗感受性悪性腫瘍に対する標準治療確率のための他施設共同研究」班 (飛内班)の「難治性リンパ腫小班」(木下班)平成24年度班会議,  2012年 

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  • Identification and profiling of aberrantly expressed microRNAs during progression of adult T-cell leukemia/lymphoma (ATLL)

    The 5th International Symposium for Future Technology Creating Better Human Health and Society Comprehensive Approach to Cancer and Infectious Diseases,  2012年 

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  • Upregulation of Ezh2 expression Correlates with Higher Tumor Proliferation and Grade in Non Hodgkin B and T Cell Lymphoma,

    American Association of Cancer Research (AACR) Annual Meeting  2012年 

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  • Dynamic changes of epigenetic abnormalities during initiation and progression of adult T-cell leukemia/lymphoma (ATLL)

    American Association of Cancer Research (AACR) Annual Meeting  2012年 

     詳細を見る

  • 成人T細胞白血病・リンパ腫(ATTL)の発症・進展におけるエビジェネティックス異常の動態解析

    第101回日本病理学会  2012年 

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  • ランゲルハンス細胞組織球症(LCH)におけるIL-17Rの検討

    第101回日本病理学会  2012年 

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  • Upregulation of Ezh2 expression Correlates with Grade in Non Hodgkin Lymphoma

    第101回日本病理学会  2012年 

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  • 十二指腸濾胞性リンパ腫の発症機構とエビジェネティクス解析

    第101回日本病理学会  2012年 

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  • Aberrant expression of Ezh2 correlates with tumor proliferation and signals a more aggressive nature in non Hodgkin lymphoma

    リンパ網内系学会2012  2012年 

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  • Aberrant expression of hsa-miR34a in leukemic cells of adult T-cell leukemia/lymphoma (ATL)

    リンパ網内系学会2012  2012年 

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常のダイナミックス

    HTLV-1研究会2012  2012年 

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  • Tumor proliferation index Ki67 correlates with PcG2 protein Ezh2 expression in non-Hodgkin lymphoma,

    第71回日本癌学会学術総会  2012年 

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  • 十二指腸濾胞性リンパ腫のメチル化解析と発症機構の解析,

    第71回日本癌学会学術総会  2012年 

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  • ANALYSES OF PTPN6 (SHP-1) TRANSFECTANT BY EXPRESSION ARRAY - COMPARED WITH OPEN DATA OF LCH SUBTYPE (GSE16395)-

    27th Annual Meeting of the Histiocyte Society  2011年 

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  • "Cumulative aberrant methylation in specific genes during progression of Adult T-cell Leukemia/Lymphoma (ATLL) "

    "The 4th International Symposium for Future Technology Creating Better Human Health and Society Comprehensive Approach to Cancer and Infectious Diseases "  2011年 

     詳細を見る

  • HTLV-1キャリアにおけるDNA メチル化の解析

    日本病理学会2011  2011年 

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  • PTPN6(SHP-1)遺伝子導入Langerhans cell 様細胞株(ELD-1)に関する検討

    日本病理学会2011  2011年 

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  • EZH2 is up-regulated in aggressive subtypes of non Hodgkin B and T cell lymphoma

    日本病理学会2011  2011年 

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  • 消化管follicular lymphomaの病理組織学的検索(十二指腸下行脚での特異性)

    日本病理学会2011  2011年 

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  • 成人T細胞白血病/リンパ腫(ATLL)におけるDNAメチル化と病態との関連

    日本病理学会2011  2011年 

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  • Cumulative kinetics of epigenetic abnormalities during initiation and progression of Adult T-cell Leukemia/Lymphoma (ATLL)

    15th International Conference on Human Retrovirology: HTLV and Related Retroviruses  2011年 

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  • Multi-step accumulation of aberrant CpG island hypermethylation in specific genes promotes development and progression of lymphomas/leukemias

    Invited Lecture at University of Amsterdam  2011年 

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるエピジェネテイックス異常

    日本リンパ網内系学会  2011年 

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  • Clonal Epigenetic Changes in Specific Genes during Progression of Adult T-cell Leukemia/Lymphoma (ATLL)

    XV International Congress of Virology,  2011年 

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  • Aberrant expression of PcG proteins in Non-Hodgkin B- and T-Cell Lymphoma: A relation to aggressive sub-types

    The XXV Symposium of the International Association for Comparative Research on Leukemia and Related Diseases  2011年 

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  • 成人T細胞白血病(ATLL)の進展に於けるエピジェネティック状態の動的変化

    第70回日本癌学会学術総会  2011年 

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  • 悪性リンパ腫に於けるEzh2の異常発現;aggressivenessとの関連

    第70回日本癌学会学術総会  2011年 

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  • B細胞リンパ腫におけるCD79b発現の検討

    第70回日本癌学会学術総会  2011年 

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  • 超微量検体による悪性リンパ腫・白血病の早期発見・診断・高感度病態モニタリング技術の開発

    Bio Japan 2011  2011年 

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  • 間葉系肝細胞の骨芽細胞分化に伴う石灰化における細胞死の関与

    第33回日本分子生物学会年会・第83回日本生化学会大会 合同大会  2010年 

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  • Helicobacter pylori infection induce accumulation of aberrant CpG hypermethylation to promote development and progression of gastric MALT lymphoma

    The 3rd International Symposium for Future Technology Creating Better Human Health and Society  2010年 

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  • Identification of novel direct target of miR-19a in MCF-7 breast cancer cell

    Annual Meeting of the American Association for Cancer Research  2010年 

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  • Langerhans cell histiocytosisにおける活性化型PTPN6(SHP-1)pY536の発現

    第99回日本病理学会総会  2010年 

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  • Development and progression of gastric MALT lymphoma are associated with accumulation of specific aberrant CpG hypermethylation by Helicobacter pylori infection

    Epigenetics研究会  2010年 

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  • HTLV-1キャリアにおけるDNA異常メチル化と病態との関連

    第3回HTLV研究会  2010年 

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  • 間葉系幹細胞の特異的分化に関与するエピジェネティック制御遺伝子の網羅的解析

    硬組織再生生物学会  2010年 

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  • Accumulation of aberrant CpG hypermethylation in specific genes induce development and progression of MALT lymphoma

    日本癌学会  2010年 

     詳細を見る

  • Down -regulation of BCR signaling component CD79b in plasm cell myeloma: potential post-transcriptionl mechanism

    日本癌学会  2010年 

     詳細を見る

  • Aberrant expression of Polycomb Group (PcG) gene:Bmi-1 in malignant lymphoma

    日本癌学会  2010年 

     詳細を見る

  • Multi-step accumulation of aberrant CpG island hypermethylation during progression of lymphoma/leukemia

    13th International Symposium on Molecular Medicine,15th World Congress on Advances in Oncology  2010年 

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  • 成人T細胞白血病・リンパ腫(ATLL)の発症・進展におけるEpigenetics異常の解析

    第二回木下班会議  2010年 

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  • TNF−アルファによるは骨細胞分化に対するヒト間養鶏肝細胞とリセドロナートの影響

    第33回日本分子生物学会年会・第83回日本生化学会大会 合同大会  2010年 

     詳細を見る

  • Association of specific DNA hypermethylation with the clinicopahthologic characteristics in Adult T cell leukemia/lymphoma

    日本癌学会  2009年 

     詳細を見る

  • Association of specific DNA hypermethylation with the clinicopahthologic characteristics in Adult T cell leukemia/lymphoma

    2009年 

     詳細を見る

  • 超微量検体による悪性リンパ腫・白血病の早期発見・診断・予後推定法の開発

    Innovation Japan 2009  2009年 

     詳細を見る

  • Immunohistochemical analyses of PTPN6(SHP1) on Langerhnas cell histiocytosis

    H20癌学会  2008年 

     詳細を見る

  • Association of aberrant DNA methylation with a poor prognosis in Adult T cell leukemia / lymphoma.

    H20癌学会  2008年 

     詳細を見る

  • Identification of the specific genes regulated by epigenetic mechanism during osteoblastic/adipocytic differentiations in human mesenchymal stem cells

    第31回日本分子生物学会、第81回日本生化学会合同大会  2008年 

     詳細を見る

  • Effect of nitrogen containing bisphosphonate on osteoblast differentiation of rat mesenchymal stem cell

    第31回日本分子生物学会、第81回日本生化学会合同大会  2008年 

     詳細を見る

  • Immunohistochemical analysis of PTPN6 (SHP-1) on Langerhans cell histiocytosis

    第97回日本病理学会  2008年 

     詳細を見る

  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNA メチル化と予後との相関について

    第97回日本病理学会  2008年 

     詳細を見る

  • T cellリンパ腫におけるSHP1の発現低下と、脱メチル化処理による発現回復がSignal pathwayに及ぼす変化

    第97回日本病理学会  2008年 

     詳細を見る

  • 樹状細胞と樹状マクロファージから視た胸腺腫のWHO 分類

    第97回日本病理学会  2008年 

     詳細を見る

  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態との関連

    H20リンパ網内系学会  2008年 

     詳細を見る

  • IMMUNOHISTOCHEMICAL ANALYSES OF PTPN6 (SHP1) ON LANGERHANS CELL HISTIOCYTOSIS

    International conference of LCH  2008年 

     詳細を見る

  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNA メチル化と病態・予後との相関

    第1回HTLV1研究会  2008年 

     詳細を見る

  • 悪性腫瘍とエピジェネティックス; 造血器腫瘍発症・進展におけるエピジェネティック異常

    臨床分子形態学会  2008年 

     詳細を見る

  • Molecular Pathological examination on aberrant expression of cyclinD1 and CD79a in multiple myeloma cell lines

    66thAnnual meeeting of the Japanese Cancer association  2007年 

     詳細を見る

  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype(CIMP)の解析

    第96回日本病理学会  2007年 

     詳細を見る

  • " Langerhans cell histiocytosisにおけるPTPN6(SHP-1)の発現

    第96回日本病理学会  2007年 

     詳細を見る

  • 胃原発悪性リンパ腫におけるmethylator phenotypeとH.pylori感染に関する検討

    第96回日本病理学会  2007年 

     詳細を見る

  • 間葉系幹細胞の脂肪細胞/骨芽細胞分化におけるエビジェネティックな制御機構の解析

    第96回日本病理学会  2007年 

     詳細を見る

  • 悪性リンパ腫・白血病におけるエピジェネティックな異常の解析

    第96回日本病理学会  2007年 

     詳細を見る

  • 成人T細胞性白血病/リンパ腫・関連疾患のエピジェネティック

    第22回悪性リンパ腫治療研究会  2007年 

     詳細を見る

  • Epigenetic abnormalities associated with Gene Silencing induce onset and progression of lymphomas/leukemias

    Annual Meeting of the American Association for Cancer Research, 2007,LA, USA  2007年 

     詳細を見る

  • CPG ISLAND METHYLATOR PHENOTYPE (CIMP) PROMOTES THE PROGRESSION OF ADULT T-CELL LEUKEMIA/LYMPHOMA (ATLL).

    Annual Meeting of the American Association for Cancer Research, 2007,LA, USA  2007年 

     詳細を見る

  • EPIGENETICALLY DISTINST MALIGNANT CELL POLULATION FORMS LYMPHOMA-INVOLVING LESION IN ACUTE TYPE ADULT T-CELL LEUKEMIA/LYMPHOMA (ATLL).

    13th International Conference on Human Retrovirology HTLV and Related Viruses  2007年 

     詳細を見る

  • ABERRANT DNA METHYLATION IS ASSOCIATED WITH THE CLINICOPATHOLOGIC CHARACTERISTICS IN PATIENTS WITH ADULT T-CELL LEUKEMIA/LYMPHOMA (ATLL).

    13th International Conference on Human Retrovirology HTLV and Related Viruses  2007年 

     詳細を見る

  • CPG ISLAND METHYLATOR PHENOTYPE (CIMP) PROMOTES THE PROGRESSION OF ADULT T-CELL LEUKEMIA/LYMPHOMA (ATLL).

    13th International Conference on Human Retrovirology HTLV and Related Viruses  2007年 

     詳細を見る

  • 成人T細胞白血病/リンパ腫(ATLL)における特異的DNAメチル化と病態・臨床症状との相関

    第47回日本リンパ網内系学会総会  2007年 

     詳細を見る

  • 胃原発悪性リンパ腫の発症・進展と特異的遺伝子のepigeneticな変化に関する検討

    第47回日本リンパ網内系学会総会  2007年 

     詳細を見る

  • Immunohistochemical analyses of PTPN6(SHP1) on Langerhans cell histiocytosis.

    66thAnnual meeeting of the Japanese Cancer association  2007年 

     詳細を見る

  • Genes specifically changing DNA methylation during osteoblastic/adipocytic differentiations in mesenchymal stem cells

    66thAnnual meeeting of the Japanese Cancer association  2007年 

     詳細を見る

  • 胃原発悪性リンパ腫におけるHelicobacter pylori感染とmethylator phenotype

    第65回癌学会総会  2006年 

     詳細を見る

  • MOLECULAR PATHOLOGICAL ANALYSIS OF THE PROTEIN TYROSINE PHOSPHATASE: SHP1 GENE IN THE PATHOGENESIS OF LYMPHOMAS AND LEUKEMIA

    97th Annual Meeting of American Association for Cancer Research 2006  2006年 

     詳細を見る

  • Abberant DNA metylation in the progression of adult T cell leukemia/lymphoma (ATLL).

    97th Annual Meeting of American Association for Cancer Research 2006  2006年 

     詳細を見る

  • 成人T細胞白血病/リンパ腫(ATLL)における病期の進行とDNAメチル化の関連

    第95回日本病理学会総会  2006年 

     詳細を見る

  • SHP1遺伝子発現抑制と悪性リンパ腫・白血病発症機構の解析

    第95回日本病理学会総会  2006年 

     詳細を見る

  • Langerhans cell histiocytosisにおけるkeratin及びVMAT2の発現

    第95回日本病理学会総会  2006年 

     詳細を見る

  • T細胞性リンパ腫における、SHP1発現とSTATsの活性化プロファイルとの関連

    第95回日本病理学会総会  2006年 

     詳細を見る

  • リンパ節胚中心におけるEpigeneticな遺伝子発現制御の解析

    第95回日本病理学会総会  2006年 

     詳細を見る

  • Aberrant DNA methylation during the progression of adult T cell leukemia/lymphoma (ATLL).

    20th IUBMB International Congress of Biochemistry and Molecular Biology and FAOBMB Congress  2006年 

     詳細を見る

  • Identification of the genes specifically changing DNA methylation status during osteoblastic/adipocytic differentiations in human mesenchymal stem cells

    20th IUBMB International Congress of Biochemistry and Molecular Biology and FAOBMB Congress  2006年 

     詳細を見る

  • High sensitive and high fidelity detection of hematopoietic malignancies with CpG methylation

    20th IUBMB International Congress of Biochemistry and Molecular Biology and FAOBMB Congress  2006年 

     詳細を見る

  • Helicobacter pylori infection induces the aberrant CpG island methylation in gastric MALT lymphoma

    20th IUBMB International Congress of Biochemistry and Molecular Biology and FAOBMB Congress  2006年 

     詳細を見る

  • The Aberrant DNA Hypermethylation Induced by Helicobacter Pylori Infection Develops the Progression of Gastric MALT Lymphoma

    The 9th Korean-Japanese Hematolymphoreticular workshop,  2006年 

     詳細を見る

  • CPG Island Methylator Phenotype (CIMP) Promotes the Progression of Adult T-Cell Leukemia/Lymphoma (ATLL)

    The 9th Korean-Japanese Hematolymphoreticular workshop,  2006年 

     詳細を見る

  • Gene Silencing Associated with Epigenetic Abnormalities Induce Onset and Progression of Lymphomas/Leukemias

    The 9th Korean-Japanese Hematolymphoreticular workshop,  2006年 

     詳細を見る

  • 異常メチル化によるSHP1 gene silencing と悪性リンパ腫・白血病発症機構

    第65回癌学会総会  2006年 

     詳細を見る

  • 成人T細胞白血病/リンパ腫(ATLL)におけるCpG island methylater phenotype (CIMP)の解析

    第65回癌学会総会  2006年 

     詳細を見る

  • 骨ランゲルハンス細胞組織球症病変から樹立された細胞株(PRU-1)の解析

    第64回日本癌学会学術総会  2005年 

     詳細を見る

  • 悪性リンパ腫・白血病の発症機構に関する分子病理学的解析

    第6回癌と免疫セミナー  2005年 

     詳細を見る

  • 造血器腫瘍の高感度・高精度検出技術の開発

    第94回日本病理学会総会  2005年 

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  • 胃MALTリンパ腫におけるp27Kip1,Ki67抗原,p53の発現

    第94回日本病理学会総会  2005年 

     詳細を見る

  • 骨ランゲルハンス細胞組織球症病変から樹立された細胞株(PRU-1)の解析

    第94回日本病理学会総会  2005年 

     詳細を見る

  • 悪性リンパ腫/白血病の発症機構におけるSHP-1 gene silencingの果たす役割についての解析

    第94回日本病理学会総会  2005年 

     詳細を見る

  • MHV-72とMHV-68の遺伝子比較並びにMHV-72感染マウスの病理と腫瘍発生への影響

    第94回日本病理学会総会  2005年 

     詳細を見る

  • T細胞性悪性リンパ腫における、SHP1 gene silencingの解析

    第64回日本癌学会学術総会  2005年 

     詳細を見る

  • 成人T細胞性白血病(ATL)におけるDNA異常メチル化の解析

    第64回日本癌学会学術総会  2005年 

     詳細を見る

  • MHV-72とMHV-68の遺伝子比較並びにMHV-72感染マウスの病理と腫瘍発生への影響

    第64回日本癌学会学術総会  2005年 

     詳細を見る

  • 悪性リンパ腫・白血病における異常メチル化によるSHP1 gene silencingの解析

    第64回日本癌学会学術総会  2005年 

     詳細を見る

  • Molecular Pathological Analyses of the Genes Related to the Pathogenesis of Lymphomas/leukemias with Complementary DNA and Tissue Microarray

    AACR speial conference in cancer research,“Chromatin,Chromosomes and cancer Epigenetics  2004年 

     詳細を見る

  • Hematopoitic cell specific thyrosine phosphatase: SHP1 as a Novel Biomarker of hematopoietic malignancies

    7th International Symposium on the molecular basis of predictive oncology & intervention strategies  2004年 

     詳細を見る

  • Regulatory role of Epstein-Barr virus-infection and CD40 ligand stimulation on the proliferation of Mantle cell lymphoma lines

    7th International Symposium on the molecular basis of predictive oncology & intervention strategies  2004年 

     詳細を見る

  • ヒト不死化間葉系幹細胞の全遺伝子発現プロファイル及びエピジェネテイック解析と再生医療への応用

    第3回日本再生医療学会総会  2004年 

     詳細を見る

  • EBV関連血球貪食症候群の家兎モデルを用いた治療法の検討及びリンパ腫の発生

    第93回日本病理学会総会  2004年 

     詳細を見る

  • High frequent inhibition of the SHP1 gene expression in T-cell lymphoma by CpG island methylation

    第93回日本病理学会総会  2004年 

     詳細を見る

  • Murine gammaherpesvirus 72 (MHV72) 感染マウスの急性期変化並びに長期観察により発生する腫瘍病変の解析

    v第93回日本病理学会総会  2004年 

     詳細を見る

  • 新規高感度・高精度悪性リンパ腫・白血病biomarker:チロシンフォスファターゼSHP1

    第1回日本病理学会カンファレンス、日本病理学会カンファレンス2004広島「ガンの発生と病態を巡るトピックス」  2004年 

     詳細を見る

  • SHP1遺伝子CpG islandメチル化によるB細胞リンパ腫の異常増殖

    第63回日本癌学会学術総会  2004年 

     詳細を見る

  • ヒト間葉系幹細胞の全遺伝子発現プロファイルとエピジェネテイック解析 - その再生医療への応用

    第26回日本分子生物学会年会  2003年 

     詳細を見る

  • Regulatory role of Epstein-Barr virus-infection and CD40 ligand stimulation on the proliferation of Mantle cell lymphoma lines

    7th International Symposium on the molecular basis of predictive oncology & intervention strategies  2003年 

     詳細を見る

  • cDNA microarray及び病理組織microarrayのNK/Tリンパ腫の発症機構の解析

    悪性リンパ腫治療研究会  2003年 

     詳細を見る

  • Transdifferentiation of thymic myoid progenitor cells and possible role of thymic myoid cells in myasthenia gravis

    The 15th annual meeting of Japanese soxiety for neuroimmunology in conjunction with COE international symposium  2003年 

     詳細を見る

  • Transdifferentiation of thymic myoid progenitor cells and possible role of thymic myoid cells in myasthenia gravis

    The 15th Annual Meeting of Japanese Society for Neuroimmunology in conjunction with COE International Symposium  2003年 

     詳細を見る

  • cDNA microarray及び病理組織microarrayのNK/Tリンパ腫の発症機構の解析

    悪性リンパ腫治療研究会  2003年 

     詳細を見る

  • EBV関連血球貪食症候群の家兎モデルを用いた治療法の検討

    第92回日本病理学会総会  2003年 

     詳細を見る

  • B細胞系悪性リンパ腫におけるSHP1遺伝子の発現抑制とCpG islandのメチル化の解析

    第92回日本病理学会総会  2003年 

     詳細を見る

  • Murine gammaherpesvirus 72 (MHV72) によるマウスの急性及び潜伏感染後の悪生リンパ腫誘発モデルの解析

    第92回日本病理学会総会  2003年 

     詳細を見る

  • 悪性リンパ腫・白血病におけるSHP1遺伝子の発現抑制機構の解析

    第92回日本病理学会総会  2003年 

     詳細を見る

  • リン酸化型Bcl-2の生体組織における発現ー大腸良・悪性腫瘍における解析

    第92回日本病理学会総会  2003年 

     詳細を見る

  • EBV-like virus (HVP)によるEBV関連血球貪食症候群家兎モデルを用いた治療法の検討およびリンパ腫の発生

    第62回日本癌学会総会  2003年 

     詳細を見る

  • EBV-like virus (HVP)の経口感染により誘発される血球貪食症候群とリンパ増殖性疾患を伴うウサギモデルの解析

    第62回日本癌学会総会  2003年 

     詳細を見る

  • 胃MALTリンパ腫の臨床病理:除菌後判定、発症及び除菌有効性因子

    第62回日本癌学会総会  2003年 

     詳細を見る

  • 悪性リンパ腫・白血病におけるチロシンフォスファターゼSHP1遺伝子発現抑制機構

    第62回日本癌学会総会  2003年 

     詳細を見る

  • Molecular Pathological analysis of the genes related to the pathogenesis of lymphomas and leukemias with cDNA and tissue maicroarray methods

    8th World Congress on Advances in Oncology and 6th International Symposium on Molecular Medicine  2003年 

     詳細を見る

  • Reduced expression of the SHP1 gene in B-cell lmalignancies detected by the aberrant methylation

    8th World Congress on Advances in Oncology and 6th International Symposium on Molecular Medicine  2003年 

     詳細を見る

  • High frequent gene scilencing of the SHP1 gene in T-cell lymphomas and leukemias by abberant methylation

    8th World Congress on Advances in Oncology and 6th International Symposium on Molecular Medicine  2003年 

     詳細を見る

  • cDNA microarray及び病理組織microarrayのNK/Tリンパ腫の発症機構の解析

    厚生省がん助成金「難治性リンパ腫様の分子生物学的特徴の解明と疾患特異的治療法の開発に関する研究」班会議  2002年 

     詳細を見る

  • 悪性リンパ腫・白血病におけるチロシンフォスファターゼSHP1遺伝子発現抑制

    第91回日本病理学会総会  2002年 

     詳細を見る

  • EBV関連血球貪食症候群の家兎モデル:EBV-like virusによる血球貪食症とリンパ球増殖異常由来細胞株の性状

    第91回日本病理学会総会  2002年 

     詳細を見る

  • ヒト口蓋扁桃のinterdigitating DCとPlasmacytoid DCの組織分布、形態、フェノタイプの違いについて

    第91回日本病理学会総会  2002年 

     詳細を見る

  • 悪性リンパ腫・白血病におけるチロシンフォスファターゼSHP1遺伝子発現抑制

    第91回日本病理学会総会  2002年 

     詳細を見る

  • Murine gammaherpesvirus 72 (MHV-72)の感染によるマウスの急性感染及び潜伏感染後の悪性リンパ腫誘発モデルの解析

    第42回日本リンパ網内系学会  2002年 

     詳細を見る

  • EBV関連血球貪食症候群の家兎モデル:Herpesvirus papioによる血球貪食症を伴う致死的ウサギリンパ球増殖異常症の病態解析

    2002年 

     詳細を見る

  • cDNA microarray及び病理組織microarrayのNK/Tリンパ腫の分子病態解明への応用

    日本病理学会秋期特別総会  2002年 

     詳細を見る

  • NK細胞腫瘍細胞株におけるgene expression profiling解析

    厚生省がん助成金「難治性リンパ腫様の分子生物学的特徴の解明と疾患特異的治療法の開発に関する研究」班会議  2001年 

     詳細を見る

  • Molecular Pathological Analysis of the Genes Related to the Pathogenesis of Adult T-cell Leukemia/Lymphoma with cDNA Expression Array and Tissue Microarray

    10th International Conference on Human Retrovirology:HTLV and Related Viruses  2001年 

     詳細を見る

  • Down reguration of Drs mRNA expression in lymphomas of adult T cell leukemia

    10th International Conference on Human Retrovirology:HTLV and Related Viruses  2001年 

     詳細を見る

  • Animal model of EBV-related lymphomagenesis: EBV-related herpesviruses from cynomorgus frequently induced rabbit T-cell lymphomas

    21th International Cancer Symposium in Sapporo: EBV and human cancer  2001年 

     詳細を見る

  • 悪性リンパ腫のgene expression profiling及び病理組織maisroarrayを用いた発症機構の解析

    厚生省がん助成金「難治性リンパ腫様の分子生物学的特徴の解明と疾患特異的治療法の開発に関する研究」班会議  2001年 

     詳細を見る

  • Myasthenogenisity of thymic myoid cells

    6th International Congress, International Society of Neuroimmunology  2001年 

     詳細を見る

  • 突然の精神症状にて発症し、脳生検にて生前診断しえたangiotropic lymphoma の一例

    日本病理学会  2000年 

     詳細を見る

  • EBV陰性Nasopharyngeal carcinoma cell line:TW03へのEBV再感染は腫瘍形成能をたかめる

    日本病理学会  2000年 

     詳細を見る

  • MALTリンパ腫における接着分子α4β7インテグリン、Lセレクチンの発現と高悪性度化に伴う発現減弱

    日本リンパ網内系学会  2000年 

     詳細を見る

  • Depressed expression of hematopoietic cell specific tyrosine phosphatase SHP1 in NK/T lymphoma revealed by complementary DNA and tissue microarrays

    日本癌学会  2000年 

     詳細を見る

  • Cyno-EBV(カニクイザル由来EBV関連ウイルス)のin vivo感染により不死化したウサギリンパ球株の性状解析

    日本癌学会  2000年 

     詳細を見る

  • 自己T細胞による単球由来樹状細胞の指状咬合細胞への成熟

    日本癌学会  2000年 

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  • 胸腺由来前駆細胞より分化したthymic myoid cellsのCD4+/8+胸腺細胞との特異的接着とアポトーシスCD4+/8+胸腺細胞の捕捉

    日本組織培養学会  2000年 

     詳細を見る

  • EBV-related herpesviruses from cynomolgus induce a high rate of rabbit T-cell lymphoma

    89th Annual meeting of US & Canadian Acad. of Pathol.  2000年 

     詳細を見る

  • Molecular Pathological analysis of the genes related to the pathogenesis of NK/T-lymphoma with complementary DNA and tissue maicroarray methods

    23th International Congress of the International Academy of Pathology  2000年 

     詳細を見る

  • Molecular analysis of ocular adenexal lymphoproliferative interdigitating cells

    23th International Congress of the International Academy of Pathology  2000年 

     詳細を見る

  • Loss of expression of α4β7 integrin and L-selectin is associated with high-grade progression of MALT lymphoma

    23th International Congress of the International Academy of Pathology  2000年 

     詳細を見る

  • Antigen-nonspecific T-cells mediate the maturation of immature monocyte-derived dendritic cells into interdigitating cells

    23th International Congress of the International Academy of Pathology  2000年 

     詳細を見る

  • 病理組織micro-array法によるNK/Tリンパ腫発症に関与する遺伝子群の分子病理学的解析

    日本病理学会  2000年 

     詳細を見る

  • Mantle cell lymphoma line(SP53)へのEBVの感染

    日本病理学会  2000年 

     詳細を見る

  • カニクイザル由来EBV関連ウイルスによるウサギ悪性リンパ腫誘発モデル:ウイルス亜系(3種類の細胞株)によるウサギモデルの比較

    日本病理学会  2000年 

     詳細を見る

  • カニクイザル由来EBV関連ヘルペスウイルスのEBNA1遺伝子構造

    日本癌学会  1999年 

     詳細を見る

  • サル由来EBV関連ヘルペスウイルス(Si-IIA-EBV)感染細胞におけるEBNA1の発現とEBNA1 遺伝子構造

    日本病理学会  1999年 

     詳細を見る

  • HTLV-I産生細胞との混合培養により樹立された前駆細胞より分化したthymic myoid cells とCD4+/CD8+胸腺細胞との特異的接着

    日本病理学会  1999年 

     詳細を見る

  • サルEBV関連ウイルスの輸血感染によるウサギ悪性リンパ腫発生とその予防

    日本病理学会  1999年 

     詳細を見る

  • Myoid cell differentiation of rat thymus-derived progenitor cell line established by co-culture with HTLV-I-producing human T cells

    9th International Conference on Human Retrovirology  1999年 

     詳細を見る

  • 病理組織micro-arrayの作成とlymphoma解析への応用

    日本癌学会  1999年 

     詳細を見る

  • 眼窩リンパ増殖性疾患の単クローン性の検討

    日本癌学会  1999年 

     詳細を見る

  • Apoptosis of CD4+/CD8+thymocytes by specific adhesionto thymic myoid cells differenciated from a rat thymus-derived myoid precursor cell line

    日本免疫学会  1999年 

     詳細を見る

  • 成熟樹状細胞に分化しうるヒト白血球のサブセットについて

    日本癌学会  1999年 

     詳細を見る

  • サルEBV関連ウイルスの輸血感染によるウサギ悪性リンパ腫発生とその予防

    日本癌学会  1999年 

     詳細を見る

▼全件表示

Works(作品等)

  • 第33回「バイオシーズ公開会」NPO法人 近畿バイオインダストリー振興会議主催

    2015年

     詳細を見る

  • 「中央西日本メディカルイノベーション2015」

    2015年

     詳細を見る

  • 岡山大学知恵の見本市2012

    2012年

     詳細を見る

  • Bio Japan 2011

    2011年

     詳細を見る

  • Innovation JAPAN2004

    2004年

     詳細を見る

  • Innovation JAPAN2004

    2004年

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  • 第3回国際バイオEXPO JAPAN

    2004年

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受賞

  • 日本白血病研究基金助成事業一般研究賞

    2012年  

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    受賞国:日本国

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  • Best presentation Award,9th Korean-Japanese Lymphoretucular Workshop (KJLW 2006)

    2006年  

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  • Best presentation Award,9th Korean-Japanese Lymphoretucular Workshop (KJLW 2006)

    2006年  

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  • Award for an Outstanding Achievement,"8th World Congress on Advances in Oncology and 6th International Symposium on Molecular Medicine

    2003年  

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    受賞国:日本国

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