田中 宏樹

最終更新日時: 2019/07/08 17:00:41

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氏名(漢字/フリガナ/アルファベット表記)
田中 宏樹/タナカ ヒロキ/Tanaka, Hiroki
所属部署・職名(部局/所属/講座等/職名)
医学研究科/メディカルイノベーションセンター/特定助教
全学電子メールアドレス
tanaka.hiroki.2x @ kyoto-u.ac.jp
電子メールアドレス
メールアドレス
htanaka @ dsk.med.kyoto-u.ac.jp
所属学会(国内)
学会名(日本語) 学会名(英語)
日本癌学会 The Japanese Cancer Association
日本癌治療学会 Japan Society of Clinical Oncology
所属学会(海外)
学会名(英語) 国名
American Society for Biochemistry and Molecular Biology
取得学位
学位名(日本語) 学位名(英語) 大学(日本語) 大学(英語) 取得区分
博士(医学) 京都大学
出身大学院・研究科等
大学名(日本語) 大学名(英語) 研究科名(日本語) 研究科名(英語) 専攻名(日本語) 専攻名(英語) 修了区分
京都大学 大学院医学研究科博士課程病理系専攻 修了
ORCID ID
https://orcid.org/https://orcid.org/0000-0003-3469-6555
researchmap URL
https://researchmap.jp/7000015399
研究テーマ
(日本語)
免疫系を含むがん微小環境によるがん制御機構の解明
(英語)
To elucidate the crosstalk between cancer cells and their microenvironment including immune system.
研究概要
(日本語)
がんの発症やその進展は、がん細胞のみならずその周囲のがん微小環境が関与していると考えられている。我々は、独自の腫瘍モデルを用いて、がん微小環境の免疫系や間葉系幹細胞とがん細胞との相互作用を分子レベルでの解明を目指している。
(英語)
Bidirectional communication between cancer cells and their microenvironment influences tumor initiation and progression, and patient prognosis. We focus on understanding how cancer cells are controlled by their microenvironment, and how hosts effectively remove cancer cells. We found a unique tumor-resistant mouse. Using our original mouse model, we try to uncover the crosstalk between malignant cells and their microenvironment, especially immune system and mesenchymal stem/stroma cells. Our ultimate goal is to utilize our knowledge in a rational design of effective microenvironment-targeted drugs for the treatment of cancers.
研究分野(キーワード)
キーワード(日本語) キーワード(英語)
免疫系 Immune System
がん微小環境 Tumor Microenvironment
がん免疫監視機構 Cancer Immunosurveillance
骨髄 Bone Marrow
間葉系幹細胞 Mesenchymal Stem/Stroma Cell
論文
著者 著者(日本語) 著者(英語) タイトル タイトル(日本語) タイトル(英語) 書誌情報等 書誌情報等(日本語) 書誌情報等(英語) 出版年月 査読の有無 記述言語 掲載種別 公開
Yamamoto R, Xu Y, Ikeda S, Sumida K, Tanaka H, Hozumi K, Takaori-Kondo A, Minato N Yamamoto R, Xu Y, Ikeda S, Sumida K, Tanaka H, Hozumi K, Takaori-Kondo A, Minato N Yamamoto R, Xu Y, Ikeda S, Sumida K, Tanaka H, Hozumi K, Takaori-Kondo A, Minato N Thymic Development of a Unique Bone Marrow-Resident Innate-like T Cell Subset with a Potent Innate Immune Function. Thymic Development of a Unique Bone Marrow-Resident Innate-like T Cell Subset with a Potent Innate Immune Function. Thymic Development of a Unique Bone Marrow-Resident Innate-like T Cell Subset with a Potent Innate Immune Function. Journal of immunology (Baltimore, Md. : 1950) Journal of immunology (Baltimore, Md. : 1950) Journal of immunology (Baltimore, Md. : 1950) 2019/05 公開
Imai T, Tanaka H, Hamazaki Y, Minato N Imai T, Tanaka H, Hamazaki Y, Minato N Imai T, Tanaka H, Hamazaki Y, Minato N Rap1 signal modulators control the maintenance of hematopoietic progenitors in bone marrow and adult long-term hematopoiesis. Rap1 signal modulators control the maintenance of hematopoietic progenitors in bone marrow and adult long-term hematopoiesis. Rap1 signal modulators control the maintenance of hematopoietic progenitors in bone marrow and adult long-term hematopoiesis. Cancer science, 110, 4, 1317-1330 Cancer science, 110, 4, 1317-1330 Cancer science, 110, 4, 1317-1330 2019/04 公開
Xu Y, Ikeda S, Sumida K, Yamamoto R, Tanaka H, Minato N Xu Y, Ikeda S, Sumida K, Yamamoto R, Tanaka H, Minato N Xu Y, Ikeda S, Sumida K, Yamamoto R, Tanaka H, Minato N Sipa1 deficiency unleashes a host-immune mechanism eradicating chronic myelogenous leukemia-initiating cells. Sipa1 deficiency unleashes a host-immune mechanism eradicating chronic myelogenous leukemia-initiating cells. Sipa1 deficiency unleashes a host-immune mechanism eradicating chronic myelogenous leukemia-initiating cells. Nature communications, 9, 1, 914 Nature communications, 9, 1, 914 Nature communications, 9, 1, 914 2018/03 公開
Makihara H, Inaba H, Enomoto A, Tanaka H, Tomono Y, Ushida K, Goto M, Kurita K, Nishida Y, Kasahara K, Goto H, Inagaki M Makihara H, Inaba H, Enomoto A, Tanaka H, Tomono Y, Ushida K, Goto M, Kurita K, Nishida Y, Kasahara K, Goto H, Inagaki M Makihara H, Inaba H, Enomoto A, Tanaka H, Tomono Y, Ushida K, Goto M, Kurita K, Nishida Y, Kasahara K, Goto H, Inagaki M Desmin phosphorylation by Cdk1 is required for efficient separation of desmin intermediate filaments in mitosis and detected in murine embryonic/newborn muscle and human rhabdomyosarcoma tissues. Desmin phosphorylation by Cdk1 is required for efficient separation of desmin intermediate filaments in mitosis and detected in murine embryonic/newborn muscle and human rhabdomyosarcoma tissues. Desmin phosphorylation by Cdk1 is required for efficient separation of desmin intermediate filaments in mitosis and detected in murine embryonic/newborn muscle and human rhabdomyosarcoma tissues. Biochemical and biophysical research communications, 478, 3, 1323-1329 Biochemical and biophysical research communications, 478, 3, 1323-1329 Biochemical and biophysical research communications, 478, 3, 1323-1329 2016/09 公開
Goto H, Tanaka H, Kasahara K, Inagaki M Goto H, Tanaka H, Kasahara K, Inagaki M Goto H, Tanaka H, Kasahara K, Inagaki M Phospho-Specific Antibody Probes of Intermediate Filament Proteins. Phospho-Specific Antibody Probes of Intermediate Filament Proteins. Phospho-Specific Antibody Probes of Intermediate Filament Proteins. Methods in enzymology, 568, 85-111 Methods in enzymology, 568, 85-111 Methods in enzymology, 568, 85-111 2016 公開
Tanaka H, Goto H, Inoko A, Makihara H, Enomoto A, Horimoto K, Matsuyama M, Kurita K, Izawa I, Inagaki M Tanaka H, Goto H, Inoko A, Makihara H, Enomoto A, Horimoto K, Matsuyama M, Kurita K, Izawa I, Inagaki M Tanaka H, Goto H, Inoko A, Makihara H, Enomoto A, Horimoto K, Matsuyama M, Kurita K, Izawa I, Inagaki M Cytokinetic Failure-induced Tetraploidy Develops into Aneuploidy, Triggering Skin Aging in Phosphovimentin-deficient Mice. Cytokinetic Failure-induced Tetraploidy Develops into Aneuploidy, Triggering Skin Aging in Phosphovimentin-deficient Mice. Cytokinetic Failure-induced Tetraploidy Develops into Aneuploidy, Triggering Skin Aging in Phosphovimentin-deficient Mice. The Journal of biological chemistry, 290, 21, 12984-12998 The Journal of biological chemistry, 290, 21, 12984-12998 The Journal of biological chemistry, 290, 21, 12984-12998 2015/05 公開
Matsuyama M, Tanaka H, Inoko A, Goto H, Yonemura S, Kobori K, Hayashi Y, Kondo E, Itohara S, Izawa I, Inagaki M Matsuyama M, Tanaka H, Inoko A, Goto H, Yonemura S, Kobori K, Hayashi Y, Kondo E, Itohara S, Izawa I, Inagaki M Matsuyama M, Tanaka H, Inoko A, Goto H, Yonemura S, Kobori K, Hayashi Y, Kondo E, Itohara S, Izawa I, Inagaki M Defect of mitotic vimentin phosphorylation causes microophthalmia and cataract via aneuploidy and senescence in lens epithelial cells. Defect of mitotic vimentin phosphorylation causes microophthalmia and cataract via aneuploidy and senescence in lens epithelial cells. Defect of mitotic vimentin phosphorylation causes microophthalmia and cataract via aneuploidy and senescence in lens epithelial cells. The Journal of biological chemistry, 288, 50, 35626-35635 The Journal of biological chemistry, 288, 50, 35626-35635 The Journal of biological chemistry, 288, 50, 35626-35635 2013/12 公開
Tanaka H, Tamura A, Sekai M, Hamazaki Y, Minato N Tanaka H, Tamura A, Sekai M, Hamazaki Y, Minato N Tanaka H, Tamura A, Sekai M, Hamazaki Y, Minato N Increased c-Myc activity and DNA damage in hematopoietic progenitors precede myeloproliferative disease in Spa-1-deficiency. Increased c-Myc activity and DNA damage in hematopoietic progenitors precede myeloproliferative disease in Spa-1-deficiency. Increased c-Myc activity and DNA damage in hematopoietic progenitors precede myeloproliferative disease in Spa-1-deficiency. Cancer science, 102, 4, 784-791 Cancer science, 102, 4, 784-791 Cancer science, 102, 4, 784-791 2011/04 公開
Wang SF, Aoki M, Nakashima Y, Shinozuka Y, Tanaka H, Taniwaki M, Hattori M, Minato N Wang SF, Aoki M, Nakashima Y, Shinozuka Y, Tanaka H, Taniwaki M, Hattori M, Minato N Wang SF, Aoki M, Nakashima Y, Shinozuka Y, Tanaka H, Taniwaki M, Hattori M, Minato N Development of Notch-dependent T-cell leukemia by deregulated Rap1 signaling. Development of Notch-dependent T-cell leukemia by deregulated Rap1 signaling. Development of Notch-dependent T-cell leukemia by deregulated Rap1 signaling. Blood, 111, 5, 2878-2886 Blood, 111, 5, 2878-2886 Blood, 111, 5, 2878-2886 2008/03 公開
タイトル言語:
外部資金:競争的資金・科学研究費補助金
種別 代表/分担 テーマ(日本語) テーマ(英語) 期間
若手研究 代表 白血病(幹)細胞を制御するがん微小環境の分子基盤の解明 (平成30年度分) 2018/04/01〜2019/03/31