研究者詳細 - 冨樫　庸介

論文 - 冨樫　庸介

分割表示 155 件中 61 - 80 件目／全件表示 >>

Selective inhibition of low-affinity memory CD8⁺ T cells by corticosteroids. 査読国際誌

Tokunaga A, Sugiyama D, Maeda Y, Warner AB, Panageas KS, Ito S, Togashi Y, Sakai C, Wolchok JD, Nishikawa H

The Journal of experimental medicine 216 ( 12 ) 2701 - 2713 2019年9月

Analysis of the Tumor Reactivity of Tumor-Infiltrating Lymphocytes in a Metastatic Melanoma Lesion that Lost Major Histocompatibility Complex Class I Expression after Anti-PD-1 Therapy. 査読国際誌

Takashi Inozume, Tomonori Yaguchi, Ryo Ariyasu, Yosuke Togashi, Takehiro Ohnuma, Akiko Honobe, Hiroyoshi Nishikawa, Yutaka Kawakami, Tatsuyoshi Kawamura

The Journal of investigative dermatology 139 ( 7 ) 1490 - 1496 2019年7月

記述言語：英語掲載種別：研究論文（学術雑誌）

Major histocompatibility complex class I loss due to the abnormality of β2-microglobulin gene is one of the mechanisms underlying delayed relapses in melanoma patients long after the initial positive responses to anti-PD-1 therapy. However, the tumor-specific reactivity of tumor-infiltrating lymphocytes in tumor lesions that lost major histocompatibility complex class I expression has not been well evaluated. We report the case of a 55-year-old woman with two metastatic melanoma lesions. After a 12-month period of successful tumor suppression by anti-PD-1 antibody therapy, one lesion started to grow again. We resected both lesions and examined the tumor cells and tumor-infiltrating lymphocytes. The shrinking lesion consisted of necrotic tissue and macrophages, and the enlarged lesion consisted of both necrotic tissue and viable tumor cells. The tumor cells completely lost major histocompatibility complex class I expression, but it was restored upon retroviral transduction of the normal β2-microglobulin gene. When we checked the tumor-specific reactivity of tumor-infiltrating lymphocytes derived from the relapsing lesion, we found that these tumor-infiltrating lymphocytes failed to recognize the native tumor cells derived from the lesion, but strongly recognized the major histocompatibility complex class-I-recovered cells by β2-microglobulin transduction. Our report emphasizes the limitations of T-cell-based immunotherapy and highlights the importance of developing alternative strategies for such cases.

DOI： 10.1016/j.jid.2019.01.007

PubMed

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Immune suppression by PD-L2 against spontaneous and treatment-related antitumor immunity. 査読

Tanegashima T, Togashi Y, Azuma K, Kawahara A, Ideguchi K, Sugiyama D, Kinoshita F, Akiba J, Kashiwagi E, Takeuchi A, Irie T, Tatsugami K, Hoshino T, Eto M, Nishikawa H

Clinical cancer research : an official journal of the American Association for Cancer Research 25 ( 15 ) 4808 - 4819 2019年5月

PD-1⁺ regulatory T cells amplified by PD-1 blockade promote hyperprogression of cancer. 査読国際誌

Kamada T, Togashi Y, Tay C, Ha D, Sasaki A, Nakamura Y, Sato E, Fukuoka S, Tada Y, Tanaka A, Morikawa H, Kawazoe A, Kinoshita T, Shitara K, Sakaguchi S, Nishikawa H

Proceedings of the National Academy of Sciences of the United States of America 116 ( 20 ) 9999 - 10008 2019年4月

Mutational activation of the epidermal growth factor receptor down-regulates major histocompatibility complex class I expression via the extracellular signal-regulated kinase in non-small cell lung cancer. 査読国際誌

Satomi Watanabe, Hidetoshi Hayashi, Koji Haratani, Shigeki Shimizu, Junko Tanizaki, Kazuko Sakai, Hisato Kawakami, Kimio Yonesaka, Junji Tsurutani, Yosuke Togashi, Kazuto Nishio, Akihiko Ito, Kazuhiko Nakagawa

Cancer science 110 ( 1 ) 52 - 60 2019年1月

記述言語：英語掲載種別：研究論文（学術雑誌）

The efficacy of programmed cell death-1 (PD-1) blockade in patients with non-small cell lung cancer (NSCLC) positive for epidermal growth factor receptor (EGFR) gene mutations has been found to be limited, but the underlying mechanisms for this poor response have remained obscure. Given that the recognition by T cells of tumor antigens presented by major histocompatibility complex class I (MHC-I) molecules is essential for an antitumor immune response, we examined the effects of EGFR tyrosine kinase inhibitors (TKIs) on MHC-I expression in NSCLC cell lines. Appropriate EGFR-TKIs increased MHC-I expression at the mRNA and cell surface protein levels in NSCLC cells positive for EGFR mutations including those with the T790M secondary mutation. Trametinib, an inhibitor of the extracellular signal-regulated kinase (ERK) kinase MEK, also increased MHC-I expression, whereas the phosphatidylinositol 3-kinase (PI3K) inhibitor buparlisib did not, suggesting that the MEK-ERK pathway mediates the down-regulation of MHC-I expression in response to EGFR activation. Immunohistochemical analysis of EGFR-mutated NSCLC specimens obtained before and after EGFR-TKI treatment also revealed down-regulation of phosphorylated forms of EGFR and ERK in association with up-regulation of MHC-I, an increased number of infiltrating CD8+ T cells, and increased PD-1 ligand 1 expression after such treatment. Our results thus suggest that mutational activation of EGFR inhibits MHC-I expression through the MEK-ERK pathway in NSCLC and thereby contributes to the poor response of such tumors to immunotherapy. Further studies are warranted to evaluate the relation between EGFR-MEK-ERK signaling in and the immune response to EGFR-mutated NSCLC. .

DOI： 10.1111/cas.13860

PubMed

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Regulatory T cells in cancer immunosuppression - implications for anticancer therapy. 査読

Togashi Y, Shitara K, Nishikawa H

Nature reviews. Clinical oncology 16 ( 6 ) 356 - 371 2019年1月

非小細胞肺癌において上皮成長因子受容体が変異活性化すると細胞外シグナル調節キナーゼを介して主要組織適合遺伝子複合体クラスIの発現が下方制御される(Mutational activation of the epidermal growth factor receptor down-regulates major histocompatibility complex class I expression via the extracellular signal-regulated kinase in non-small cell lung cancer)

Watanabe Satomi, Hayashi Hidetoshi, Haratani Koji, Shimizu Shigeki, Tanizaki Junko, Sakai Kazuko, Kawakami Hisato, Yonesaka Kimio, Tsurutani Junji, Togashi Yosuke, Nishio Kazuto, Ito Akihiko, Nakagawa Kazuhiko

Cancer Science 110 ( 1 ) 52 - 60 2019年1月

Targeting VEGFR2 with Ramucirumab strongly impacts effector/ activated regulatory T cells and CD8⁺ T cells in the tumor microenvironment. 査読国際誌

Tada Y, Togashi Y, Kotani D, Kuwata T, Sato E, Kawazoe A, Doi T, Wada H, Nishikawa H, Shitara K

Journal for immunotherapy of cancer 6 ( 1 ) 106 - 106 2018年10月

Clinicopathological features of 22C3 PD-L1 expression with mismatch repair, Epstein–Barr virus status, and cancer genome alterations in metastatic gastric cancer 査読

Akihito Kawazoe, Kohei Shitara, Yasutoshi Kuboki, Hideaki Bando, Takashi Kojima, Takayuki Yoshino, Atsushi Ohtsu, Atsushi Ochiai, Yosuke Togashi, Hiroyoshi Nishikawa, Toshihiko Doi, Takeshi Kuwata

Gastric Cancer 1 - 8 2018年6月

Immunological impact of ramucirumab on tumor microenvironment in advanced gastric cancer. 査読

Togashi Yosuke, Tada Yasuko, Kotani Daisuke, Kawazoe Akihito, Doi Toshihiko, Nishikawa Hiroyoshi

https://jitc.biomedcentral.com 36 ( 5 ) 2018年2月

Suppression from beyond the grave 査読

Yosuke Togashi, Hiroyoshi Nishikawa

NATURE IMMUNOLOGY 18 ( 12 ) 1285 - 1286 2017年12月

Tumor immune microenvironment and nivolumab efficacy in EGFR mutation-positive non-small-cell lung cancer based on T790M status after disease progression during EGFR-TKI treatment 査読

K. Haratani, H. Hayashi, T. Tanaka, H. Kaneda, Y. Togashi, K. Sakai, K. Hayashi, S. Tomida, Y. Chiba, K. Yonesaka, Y. Nonagase, T. Takahama, J. Tanizaki, K. Tanaka, T. Yoshida, K. Tanimura, M. Takeda, H. Yoshioka, T. Ishida, T. Mitsudomi, K. Nishio, K. Nakagawa

ANNALS OF ONCOLOGY 28 ( 7 ) 1532 - 1539 2017年7月

Clinical significance of Akt2 in advanced pancreatic cancer treated with erlotinib 査読

Eri Banno, Yosuke Togashi, Marco A. De Velasco, Takuro Mizukami, Yu Nakamura, Masato Terashima, Kazuko Sakai, Yoshihiko Fujita, Ken Kamata, Masayuki Kitano, Masatoshi Kudo, Kazuto Nishio

INTERNATIONAL JOURNAL OF ONCOLOGY 50 ( 6 ) 2049 - 2058 2017年6月

Efficacy of irreversible EGFR-TKIs for the uncommon secondary resistant EGFR mutations L747S, D761Y, and T854A 査読

Masato Chiba, Yosuke Togashi, Eri Bannno, Yoshihisa Kobayashi, Yu Nakamura, Hidetoshi Hayashi, Masato Terashima, Marco A. De Velasco, Kazuko Sakai, Yoshihiko Fujita, Tetsuya Mitsudomi, Kazuto Nishio

BMC CANCER 17 ( 1 ) 281 2017年4月

Characterization of EGFR T790M, L792F, and C797S Mutations as Mechanisms of Acquired Resistance to Afatinib in Lung Cancer 査読

Yoshihisa Kobayashi, Koichi Azuma, Hiroki Nagai, Young Hak Kim, Yosuke Togashi, Yuichi Sesumi, Masato Chiba, Masaki Shimoji, Katsuaki Sato, Kenji Tomizawa, Toshiki Takemoto, Kazuto Nishio, Tetsuya Mitsudomi

MOLECULAR CANCER THERAPEUTICS 16 ( 2 ) 357 - 364 2017年2月

Significance of FGF9 gene in resistance to anti-EGFR therapies targeting colorectal cancer: A subset of colorectal cancer patients with FGF9 upregulation may be resistant to anti-EGFR therapies 査読国際誌

Takuro Mizukami, Yosuke Togashi, Saeko Naruki, Eri Banno, Masato Terashima, Marco A. de Velasco, Kazuko Sakai, Azusa Yoneshige, Hidetoshi Hayashi, Yoshihiko Fujita, Shuta Tomida, Takako Eguchi Nakajima, Takashi Fujino, Narikazu Boku, Akihiko Ito, Kazuhiko Nakagawa, Kazuto Nishio

Molecular Carcinogenesis 56 ( 1 ) 106 - 117 2017年1月

MOLECULAR CARCINOGENESIS 56 ( 1 ) 106 - 117 2017年1月

Regulatory T Cells: Molecular and Cellular Basis for Immunoregulation 査読

Yosuke Togashi, Hiroyoshi Nishikawa

EMERGING CONCEPTS TARGETING IMMUNE CHECKPOINTS IN CANCER AND AUTOIMMUNITY 410 3 - 27 2017年

MEK inhibitors against MET-amplified non-small cell lung cancer 査読

Masato Chiba, Yosuke Togashi, Shuta Tomida, Hiroshi Mizuuchi, Yu Nakamura, Eri Banno, Hidetoshi Hayashi, Masato Terashima, Marco A. De Velasc, Kazuko Sakai, Yoshihiko Fujita, Tetsuya Mitsudomi, Kazuto Nishio

INTERNATIONAL JOURNAL OF ONCOLOGY 49 ( 6 ) 2236 - 2244 2016年12月

FGFR gene alterations in lung squamous cell carcinoma are potential targets for the multikinase inhibitor nintedanib 査読

Masaaki Hibi, Hiroyasu Kaneda, Junko Tanizaki, Kazuko Sakai, Yosuke Togashi, Masato Terashima, Marco Antonio De Velasco, Yoshihiko Fujita, Eri Banno, Yu Nakamura, Masayuki Takeda, Akihiko Ito, Tetsuya Mitsudomi, Kazuhiko Nakagawa, Isamu Okamoto, Kazuto Nishio

CANCER SCIENCE 107 ( 11 ) 1667 - 1676 2016年11月

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