研究者業績

三村 尚也

ミムラ ナオヤ  (Naoya Mimura)

基本情報

所属
千葉大学 医学部附属病院 輸血・細胞療法部 講師
学位
医学博士(2007年3月 千葉大学大学院)

研究者番号
00422220
J-GLOBAL ID
201801011517739316
researchmap会員ID
B000341027

論文

 131
  • Sanshiro Nakao, Shokichi Tsukamoto, Yusuke Takeda, Chikako Ohwada, Chihiro Ri, Shintaro Izumi, Yuri Kamata, Shinichiro Matsui, Asuka Shibamiya, Arata Ishii, Koji Takaishi, Kohei Takahashi, Yuki Shiko, Nagisa Oshima-Hasegawa, Tomoya Muto, Naoya Mimura, Koutaro Yokote, Chiaki Nakaseko, Emiko Sakaida
    International journal of hematology 2024年8月27日  
    Criteria for airflow obstruction (AFO) at one year after allogeneic hematopoietic stem cell transplantation (allo-HSCT) in pulmonary function tests (PFTs) are more stringent than the bronchiolitis obliterans syndrome (BOS) criteria of the National Institutes of Health. This single-center, retrospective cohort study evaluated the clinical impact of the AFO criteria at any time after transplantation. In 132 patients who underwent allo-HSCT from 2006 to 2016, the 2-year cumulative incidence of AFO was 35.0%, and the median time to diagnosis of AFO was 101 days after transplantation (range 35-716 days). Overall chronic graft-versus-host disease (cGVHD) incidence was significantly higher in patients with AFO than in those without AFO (80.4% vs. 47.7%, P < 0.01); notably, 37.0% of patients with AFO developed cGVHD after AFO diagnosis. AFO patients developed BOS with a 5-year cumulative incidence of 49.1% after AFO onset. The 5-year cumulative incidence of non-relapse mortality in the AFO group was higher than that in the non-AFO group (24.7% vs. 7.1%, P < 0.01). These results suggest that closely monitoring PFTs within two years after allo-HSCT, regardless of cGVHD status, is important for early detection of AFO and prevention of progression to BOS. (192words).
  • Arata Ishii, Shokichi Tsukamoto, Naoya Mimura, Yurie Miyamoto-Nagai, Yusuke Isshiki, Shinichiro Matsui, Sanshiro Nakao, Asuka Shibamiya, Yutaro Hino, Kensuke Kayamori, Nagisa Oshima-Hasegawa, Tomoya Muto, Yusuke Takeda, Tomoki Suichi, Sonoko Misawa, Chikako Ohwada, Koutaro Yokote, Satoshi Kuwabara, Chiaki Nakaseko, Hiroyuki Takamatsu, Emiko Sakaida
    Scientific Reports 14(1) 2024年5月6日  
    Abstract POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monoclonal protein [M-protein], and skin changes) is a rare systemic disorder characterized by various symptoms caused by underlying plasma cell (PC) dyscrasia. Detection of monoclonal PCs is mandatory for the diagnosis of POEMS syndrome; however, the usefulness of EuroFlow-based next-generation flow cytometry (EuroFlow-NGF) in POEMS syndrome for detecting monoclonal PCs in bone marrow (BM) and the gating strategy suitable for flow cytometry study of POEMS syndrome remain unknown. We employed EuroFlow-NGF-based single-tube eight-color multiparameter flow cytometry (MM-flow) and established a new gating strategy (POEMS-flow) to detect the monoclonal PCs in POEMS syndrome, gating CD38 broadly from dim to bright and CD45 narrowly from negative to dim compared to MM-flow. MM-flow detected monoclonal PCs in 9/25 (36.0%) cases, including 2/2 immunofixation electrophoresis (IFE)-negative cases (100%). However, POEMS-flow detected monoclonal PCs in 18/25 cases (72.0%), including 2/2 IFE-negative cases (100%). POEMS-flow detected monoclonal PCs with immunophenotypes of CD19 in 17/18 (94.4%). In six cases where post-treatment samples were available, the size of the clones was significantly reduced after the treatment (P = 0.031). POEMS-flow can enhance the identification rate of monoclonal PCs in POEMS syndrome and become a valuable tool for the diagnosis of POEMS syndrome.
  • Shinichiro Matsui, Chihiro Ri, Lyndsey C. Bolanos, Kwangmin Choi, Asuka Shibamiya, Arata Ishii, Koji Takaishi, Nagisa Oshima-Hasegawa, Shokichi Tsukamoto, Yusuke Takeda, Naoya Mimura, Akihide Yoshimi, Koutaro Yokote, Daniel T. Starczynowski, Emiko Sakaida, Tomoya Muto
    Leukemia 38(5) 1032-1045 2024年4月12日  
    Abstract TNF receptor associated factor 6 (TRAF6) is an E3 ubiquitin ligase that has been implicated in myeloid malignancies. Although altered TRAF6 expression is observed in human acute myeloid leukemia (AML), its role in the AML pathogenesis remains elusive. In this study, we showed that the loss of TRAF6 in AML cells significantly impairs leukemic function in vitro and in vivo, indicating its functional importance in AML subsets. Loss of TRAF6 induces metabolic alterations, such as changes in glycolysis, TCA cycle, and nucleic acid metabolism as well as impaired mitochondrial membrane potential and respiratory capacity. In leukemic cells, TRAF6 expression shows a positive correlation with the expression of O-linked N-acetylglucosamine (O-GlcNAc) transferase (OGT), which catalyzes the addition of O-GlcNAc to target proteins involved in metabolic regulation. The restoration of growth capacity and metabolic activity in leukemic cells with TRAF6 loss, achieved through either forced expression of OGT or pharmacological inhibition of O-GlcNAcase (OGA) that removes O-GlcNAc, indicates the significant role of O-GlcNAc modification in the TRAF6-related cellular and metabolic dynamics. Our findings highlight the oncogenic function of TRAF6 in leukemia and illuminate the novel TRAF6/OGT/O-GlcNAc axis as a potential regulator of metabolic reprogramming in leukemogenesis.
  • 中世古 知昭, 渡部 玲子, 大和田 千桂子, 堺田 恵美子, 三村 尚也, 塚本 祥吉
    国際医療福祉大学学会誌 28(抄録号) 194-194 2023年9月  
  • Tomoyasu Jo, Satoshi Yoshihara, Yoshiki Okuyama, Keiko Fujii, Tomoko Henzan, Kaoru Kahata, Rie Yamazaki, Wataru Takeda, Yoshihiro Umezawa, Kentaro Fukushima, Takashi Ashida, Minami Yamada-Fujiwara, Ryo Hanajiri, Noboru Yonetani, Yuma Tada, Yuji Shimura, Hidekazu Nishikii, Norio Shiba, Naoya Mimura, Jun Ando, Takayuki Sato, Yasuhiro Nakashima, Junko Ikemoto, Keita Iwaki, Shin-Ichiro Fujiwara, Masaki Ri, Tokiko Nagamura-Inoue, Ryuji Tanosaki, Yasuyuki Arai
    British journal of haematology 202(2) 256-266 2023年7月  
    For successful chimeric antigen receptor T (CAR-T) cell therapy, CAR-T cells must be manufactured without failure caused by suboptimal expansion. In order to determine risk factors for CAR-T cell manufacturing failure, we performed a nationwide cohort study in Japan and analysed patients with diffuse large B-cell lymphoma (DLBCL) who underwent tisagenlecleucel production. We compared clinical factors between 30 cases that failed (7.4%) with those that succeeded (n = 378). Among the failures, the proportion of patients previously treated with bendamustine (43.3% vs. 14.8%; p < 0.001) was significantly higher, and their platelet counts (12.0 vs. 17.0 × 104 /μL; p = 0.01) and CD4/CD8 T-cell ratio (0.30 vs. 0.56; p < 0.01) in peripheral blood at apheresis were significantly lower than in the successful group. Multivariate analysis revealed that repeated bendamustine use with short washout periods prior to apheresis (odds ratio [OR], 5.52; p = 0.013 for ≥6 cycles with washout period of 3-24 months; OR, 57.09; p = 0.005 for ≥3 cycles with washout period of <3 months), low platelet counts (OR, 0.495 per 105 /μL; p = 0.022) or low CD4/CD8 ratios (<one third) (OR, 3.249; p = 0.011) in peripheral blood at apheresis increased the risk of manufacturing failure. Manufacturing failure remains an obstacle to CAR-T cell therapy for DLBCL patients. Avoiding risk factors, such as repeated bendamustine administration without sufficient washout, and risk-adapted strategies may help to optimize CAR-T cell therapy for DLBCL patients.

MISC

 136
  • 三川紫緒, 大和田千桂子, 三村尚也, 三村尚也, 稲葉洋介, 長谷川浩子, 石井改, 高石浩司, 大島渚, 大島渚, 武藤朋也, 塚本祥吉, 竹田勇輔, 中世古知昭, 堺田惠美子, 堺田惠美子, 堺田惠美子
    日本輸血細胞治療学会誌 69(2) 2023年  
  • 西原彩佳, 西原彩佳, 塚本祥吉, 塚本祥吉, 栢森健介, 栢森健介, 日野裕太郎, 日野裕太郎, 三村尚也, 三村尚也, 三村尚也, 久保寺愛, 久保寺愛, 中島彰宏, 中島彰宏, 加藤怜, 加藤怜, 李千尋, 李千尋, 和泉真太郎, 和泉真太郎, 鎌田百合, 鎌田百合, 松井愼一郎, 松井愼一郎, 中尾三四郎, 中尾三四郎, 柴宮明日香, 柴宮明日香, 石井改, 石井改, 大島渚, 大島渚, 武藤朋也, 武藤朋也, 三川紫緒, 三川紫緒, 三川紫緒, 竹田勇輔, 竹田勇輔, 大和田千桂子, 大和田千桂子, 大和田千桂子, 中世古知昭, 堺田惠美子, 堺田惠美子, 堺田惠美子
    日本造血・免疫細胞療法学会総会プログラム・抄録集 44th 2022年  
  • 中尾三四郎, 中尾三四郎, 竹田勇輔, 竹田勇輔, 塚本祥吉, 塚本祥吉, 李千尋, 李千尋, 和泉真太郎, 和泉真太郎, 鎌田百合, 鎌田百合, 松井愼一郎, 松井愼一郎, 柴宮明日香, 柴宮明日香, 石井改, 石井改, 栢森健介, 栢森健介, 日野裕太郎, 日野裕太郎, 大島渚, 大島渚, 武藤朋也, 武藤朋也, 三川紫緒, 三川紫緒, 三川紫緒, 三村尚也, 三村尚也, 三村尚也, 大和田千桂子, 大和田千桂子, 大和田千桂子, 中世古知昭, 堺田惠美子, 堺田惠美子, 堺田惠美子
    日本造血・免疫細胞療法学会総会プログラム・抄録集 44th 2022年  
  • 堺田惠美子, 堺田惠美子, 堺田惠美子, 木村賢司, 木村賢司, 塚本祥吉, 塚本祥吉, 中尾三四郎, 中尾三四郎, 竹田勇輔, 竹田勇輔, 大和田千桂子, 大和田千桂子, 大和田千桂子, 清水亮, 田中宏明, 永尾侑平, 鐘野勝洋, 小野田昌弘, 横田朗, 新井宏典, 宇津欣和, 増田真一, 青墳信之, 仕子優樹, 小澤義人, 三川紫緒, 三川紫緒, 三川紫緒, 三川紫緒, 石井改, 石井改, 高石浩司, 高石浩司, 栢森健介, 栢森健介, 日野裕太郎, 日野裕太郎, 大島渚, 大島渚, 大島渚, 武藤朋也, 武藤朋也, 三村尚也, 三村尚也, 三村尚也, 中世古知昭, 中世古知昭, 中世古知昭
    日本造血・免疫細胞療法学会総会プログラム・抄録集 45th 2022年  
  • 中尾三四郎, 塚本祥吉, 竹田勇輔, 久保寺愛, 加藤怜, 中島彰宏, 田波貴彬, 西原彩佳, 李千尋, 和泉真太郎, 鎌田百合, 松井愼一郎, 柴宮明日香, 石井改, 高石浩司, 大島渚, 武藤朋也, 三村尚也, 大和田千桂子, 中世古知昭, 堺田惠美子, 中尾三四郎, 塚本祥吉, 竹田勇輔, 久保寺愛, 加藤怜, 中島彰宏, 田波貴彬, 西原彩佳, 李千尋, 和泉真太郎, 鎌田百合, 松井愼一郎, 柴宮明日香, 石井改, 高石浩司, 大島渚, 武藤朋也, 三村尚也, 大和田千桂子, 中世古知昭, 堺田惠美子, 大島渚, 三村尚也, 大和田千桂子, 中世古知昭, 堺田惠美子
    日本造血・免疫細胞療法学会総会プログラム・抄録集 45th 2022年  

書籍等出版物

 3

講演・口頭発表等

 81

共同研究・競争的資金等の研究課題

 12