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Affiliation |
Hospital Internal MedicineⅢ |
Graduating School 【 display / non-display 】
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-2009.03
Akita University Faculty of Medicine Graduated
Graduate School 【 display / non-display 】
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-2016.03
Akita University Graduate School, Division of Medicine Doctor's Course Completed
Campus Career 【 display / non-display 】
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2023.04-Now
Akita University Hospital Internal MedicineⅢ Lecturer
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2022.04-2023.03
Akita University Hospital Pharmaceutical Management Center Lecturer
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2020.09-2022.03
Akita University Hospital Pharmaceutical Management Center Assistant Professor
Research Areas 【 display / non-display 】
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Life Science / Hematology and medical oncology
Thesis for a degree 【 display / non-display 】
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MicroRNA-16 mediates the regulation of a senescence-apoptosis switch in cutaneous T-cell and other non-Hodgkin lymphomas.
Akihiro Kitadate, Sho Ikeda, KazuakiTeshima, Mitsugu Ito, Ikumi Toyota, Naoko Hasunuma, Naoto Takahashi, Tomomitsu Miyagaki, Makoto Sugaya, Hiroyuki Tagawa
Oncogene 35 ( 28 ) 3692 - 3704 2016.03 [Refereed]
Domestic Co-author
Research Achievements 【 display / non-display 】
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Comment on skin biopsies for diagnosing intravascular lymphoma: A retrospective study of diagnostic accuracy.
Naoko Enzan, Akihiro Kitadate, Michihiro Kono
Journal of the American Academy of Dermatology 2023.01 [Refereed]
Research paper (journal) Domestic Co-author
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High baseline total lesion glycolysis predicts early progression of disease within 24 months in patients with high-tumor-burden follicular lymphoma.
Wataru Kuroki, Akihiro Kitadate, Koichi Ishiyama, Yoshihiro Kameoka, Naoto Takahashi
International Journal of Hematology 116 ( 5 ) 712 - 722 2022.11 [Refereed]
Research paper (journal) Domestic Co-author
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Multiple myeloma with t(11;14)-associated immature phenotype has lower CD38 expression and higher BCL2 dependence
Akihiro Kitadate
Cancer Science 112 ( 9 ) 3645 - 3654 2021.09 [Refereed]
Research paper (journal) Domestic Co-author
CD38 expression on myeloma cells is a critical factor affecting the early response to the anti-CD38 antibody daratumumab. However, factors affecting CD38 expression in untreated multiple myeloma are not fully elucidated. In this study, we found that CD38 expression was significantly lower in myeloma patients with the translocation t(11;14)-associated immature plasma cell phenotype, and particularly in those expressing B-cell-associated genes such as PAX5 and CD79A. CD138, a representative marker of plasmacytic differentiation, was also significantly lower in these patients, suggesting that CD38 expression may be associated with the differentiation and maturation stages of myeloma cells. Furthermore, the BCL2/BCL2L1 ratio, a response marker of the BCL2 inhibitor venetoclax, was significantly higher in patients with the immature phenotype expressing B-cell-associated genes. The BCL2/BCL2L1 ratio and CD38 expression were significantly negatively correlated. We also confirmed that patients with translocation t(11;14) expressing B-cell-associated genes were indeed less sensitive to daratumumab-mediated direct cytotoxicity but highly sensitive to venetoclax treatment in ex vivo assays. Moreover, all-trans-retinoic acid, which enhances CD38 expression and induces cell differentiation in myeloma cells, reduced B-cell marker expression and the BCL2/BCL2L1 ratio in myeloma cell lines, leading to reduced efficacy of venetoclax. Venetoclax specifically induces cell death in myeloma with t(11;14), although why patients with translocation t(11;14) show BCL2 dependence is unclear. These results suggest that BCL2 dependence, as well as CD38 expression, are deeply associated with the differentiation and maturation stages of myeloma cells. This study highlights the importance of examining t(11;14) and considering cell maturity in myeloma treatment strategies.
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Kitadate A.
Cancer Medicine 9 ( 15 ) 5509 - 5518 2020.08 [Refereed]
Research paper (journal) Domestic Co-author
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Terao T, Machida Y, Tsushima T, Miura D, Narita K, Kitadate A, Takeuchi M, Matsue K.
British Journal of Haematology 2020 [Refereed]
Research paper (journal) Domestic Co-author
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Ikeda S, Abe F, Matsuda Y, Kitadate A, Takahashi N, Tagawa H.
Cancer Science 2020 [Refereed]
Domestic Co-author
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Abe F, Kitadate A, Ikeda S, Yamashita J, Nakanishi H, Takahashi N, Asaka C, Teshima K, Miyagaki T, Sugaya M, Tagawa H.
Oncotarget 8 ( 5 ) 7572 - 7585 2017
Domestic Co-author
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FUJISHIMA Masumi, TAKAHASHI Naoto, FUJISHIMA Naohito, KITADATE Akihiro, GUO Yongmei, WATANABE Atsushi, UBUKAWA Kumi, NARA Miho, YOSHIOKA Tomoko, KAMEOKA Yoshihiro
Rinsho Ketsueki ( The Japanese Society of Hematology ) 58 ( 7 ) 743 - 748 2017
<p>A 64-year-old woman was admitted to our hospital to undergo allogeneic stem cell transplantation. She was diagnosed with polycythemia vera with a JAK2 V617F mutation 7 years ago. She was administered ruxolitinib for splenomegaly two years prior to admission but this was discontinued because of progressive pancytopenia. One months after cessation of ruxolitinib, she developed acute myeloid leukemia transformed from post-polycythemia vera myelofibrosis. Although she achieved complete remission after induction therapy, 8-finger-breadth splenomegaly remained below the left costal margin. Ruxolitinib was re-administered following two courses of consolidation therapy. She underwent unrelated peripheral blood stem cell transplantation. Ruxolitinib was administered until the day before transplantation, and the spleen was palpated in 4-finger breadth below costal arc. Neutrophil engraftment was achieved 13 days after transplantation. In allogeneic stem cell transplantation, splenomegaly is one of the risk factors for engraftment failure and/or therapy-related mortality. Hence, a smaller spleen size can theoretically improve the outcome after transplantation. The administration of ruxolitinib prior to transplantation may have contributed to engraftment with a non-invasive reduction in the size of the spleen.</p>