|
Affiliation |
Faculty of Medicine College Hospital Department of Blood Medicine |
|
Title |
Lecturer |
|
External Link |
|
|
Related SDGs |
|
SHIDE Kotaro
|
|
|
Research Areas 【 display / non-display 】
-
Life Science / Hematology and medical oncology
Education 【 display / non-display 】
-
Kyushu University Graduate School, Division of Medical Sciences
- 2008.3
Country：Japan
-
Kyushu University Faculty of Medicine Department of Medicine
- 2001.3
Country：Japan
Professional Memberships 【 display / non-display 】
-
日本血液学会
2006.3
-
American Society of Hematology
2008.8
Qualification acquired 【 display / non-display 】
-
日本内科学会認定内科医
-
日本内科学会総合内科専門医
-
日本血液学会 血液専門医
-
日本血液学会 指導医
-
日本輸血・細胞治療学会 認定医
Papers 【 display / non-display 】
-
Fibrocytes drive JAK2V617F-mutated myelofibrosis: pitavastatin reverses marrow fibrosis and anemia Reviewed International journal
Uchida T., Shide K., Kameda T., Ozono Y., Kubuki Y., Tahira Y., Kamiunten A., Marutsuka K., Akizuki K., Karasawa M., Uehira Y., Ueno H., Yamaguchi H., Shimoda K.
Blood 2026.7
Language：English Publishing type：Research paper (scientific journal) Publisher：Blood
Bone marrow (BM) fibrosis in primary and post–polycythemia vera/essential thrombocythemia myelofibrosis (MF) has traditionally been considered a reactive process driven by cytokines, such as transforming growth factor β1 (TGF-β1), primarily produced by neoplastic megakaryocytes and platelets. These cytokines promote the differentiation of wild-type mesenchymal stromal cells into collagen- and fibronectin-producing myofibroblasts, thereby inducing BM fibrosis. However, hematopoietic-derived collagen-producing cells of monocyte lineage, termed fibrocytes, have also been implicated in this process. Here, we demonstrate that fibrocytes constitute a major collagen-producing cell population in the BM of patients with JAK2V617F-mutated MF, with additional contributions from myofibroblasts. Analysis of BM samples from patients with JAK2V617F-mutated myeloproliferative neoplasms (MPNs) revealed that fibrocytes accounted for nearly two-thirds of collagen-producing cells, whereas myofibroblasts represented a smaller subset. Using BM-derived fibrocytes from Jak2V617F transgenic mice (Jak2V617F mice), we performed a high-throughput drug screen and identified statins as inhibitors of fibrocyte proliferation in vitro. In vivo, pitavastatin treatment reduced fibrocyte numbers, ameliorated BM fibrosis, and improved anemia in Jak2V617F mice. Pitavastatin also decreased TGF-β1 production by neoplastic fibrocytes, resulting in reduced myofibroblast expansion. Peripheral blood–derived fibrocytes from patients with JAK2V617F-mutated MPNs were similarly sensitive to pitavastatin in vitro. Together, these findings suggest that fibrocytes substantially contribute to BM fibrosis in JAK2V617F-mutated MF and support further investigation of pitavastatin as a potential antifibrotic strategy in this molecular subset.
Other Link： https://ashpublications.org/blood/article/doi/10.1182/blood.2025032693/569496
-
TYK2 is essential for the therapeutic effect of IFN-α in Jak2V617F-induced murine myeloproliferative neoplasms Reviewed International journal
Yuki Tahira, Kotaro Shide, Takuro Kameda, Taisuke Uchida, Ayako Kamiunten, Keiichi Akizuki, Yoko Kubuki, Masayoshi Karasawa, Ryoma Ikeda, Kengo Matsumoto, Jie Bai, Minoru Terashima, Koji Kato, Tomofumi Uto, Tomohiro Fukaya, Shuya Mitoma, Katsuaki Sato, Yudai Uehira, Hiroaki Ueno, Goro Sashida, Hideki Yamaguchi, Kazuya Shimoda
Blood Neoplasia 2025.3
Language：English Publishing type：Research paper (scientific journal) Publisher：the American Society of Hematology
-
Real-world clinical characteristics of post-essential thrombocythemia and post-polycythemia vera myelofibrosis Reviewed International journal
Shide K., Takenaka K., Kitanaka A., Numata A., Kameda T., Yamauchi T., Inagaki A., Mizuno S., Takami A., Ito S., Hagihara M., Usuki K., Maekawa T., Sunami K., Ueda Y., Tsutsui M., Ando M., Komatsu N., Ozawa K., Kurokawa M., Arai S., Mitani K., Akashi K., Shimoda K.
Annals of Hematology 103 ( 1 ) 97 - 103 2024.1
Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：Annals of Hematology
There are few prospective studies on patients with post-essential thrombocythemia myelofibrosis (PET-MF) and post-polycythemia vera myelofibrosis (PPV-MF). Therefore, we conducted a nationwide longitudinal prospective survey to clarify the clinical characteristics of these diseases. A total of 197 PET-MF and 117 PPV-MF patients diagnosed between 2012 and 2021 were analyzed. The median age at diagnosis was 70.0 years for both diseases. The time from diagnosis of ET or PV to that of MF was 9.6 and 10.4 years, respectively, with no significant difference. Patients with PPV-MF had higher hemoglobin levels and white blood cell counts than those with PET-MF, whereas those with PET-MF had higher platelet counts than those with PPV-MF. Although splenomegaly was more frequent in patients with PPV-MF at diagnosis, there was no difference in the frequency of constitutional symptoms. Ruxolitinib was the most common treatment administered to 74.6% and 83.8% of patients with PET-MF and PPV-MF, respectively. Patients with PET-MF and PPV-MF had similar prognoses, with 3-year overall survival (OS) of 0.742 in PET-MF and 0.768 in PPV-MF patients. In both diseases, leukemic transformation was the leading cause of death, followed by infection. The 3-year OS for patients with PET/PPV-MF and primary MF diagnosed during the same period was 0.754 and 0.626, respectively, with no significant difference. This survey provides real-world clinical features and prognostic data on secondary myelofibrosis in the ruxolitinib era.
-
Nationwide prospective survey of secondary myelofibrosis in Japan: superiority of DIPSS-plus to MYSEC-PM as a survival risk model Reviewed International journal
Shide K., Takenaka K., Kitanaka A., Numata A., Kameda T., Yamauchi T., Inagaki A., Mizuno S., Takami A., Ito S., Hagihara M., Usuki K., Maekawa T., Sunami K., Ueda Y., Tsutsui M., Ando M., Komatsu N., Ozawa K., Kurokawa M., Arai S., Mitani K., Akashi K., Shimoda K.
Blood Cancer Journal 13 ( 110 ) 2023.7
Authorship：Lead author Publishing type：Research paper (scientific journal) Publisher：Blood Cancer Journal
DOI： 10.1038/s41408-023-00869-9
Other Link： https://www.nature.com/articles/s41408-023-00869-9
-
SDHAF1 confers metabolic resilience to aging hematopoietic stem cells by promoting mitochondrial ATP production Reviewed International journal
Watanuki S, Kobayashi H, Sugiura Y, Yamamoto M, Karigane D, Shiroshita K, Sorimachi Y, Morikawa T, Fujita S, Shide K, Haraguchi M, Tamaki S, Mikawa T, Kondoh H, Nakano H, Sumiyama K, Nagamatsu G, Goda N, Okamoto S, Nakamura-Ishizu A, Shimoda K, Suematsu M, Suda T, Takubo K
Cell Stem Cell 2024.5
Language：English Publishing type：Research paper (scientific journal)
Books 【 display / non-display 】
-
「血小板増多の鑑別診断」とことん読み解く「血算」ーこの数字は何を伝えようとしているのか？ 編集 神田善伸
幣光太郎（ Role： Contributor , 血小板増多の鑑別診断）
南江堂 2026.4 （ ISBN:978-4-524-27288-4 ）
Total pages：193 Responsible for pages：106-113 Language：Japanese Book type：Scholarly book
-
「骨髄線維症(原発性, 二次性)の治療」 新・白血病学(下), -病態・診断・治療-
幣 光太郎（ Role： Contributor , 骨髄線維症(原発性, 二次性)の治療）
日本臨床社 2025.5
Responsible for pages：242-248 Language：Japanese Book type：Scholarly book
-
Primary myelofibrosis. TODAY'S THERAPY 2025
（ Role： Contributor）
2025.1 （ ISBN:978-4-260-05718-9 ）
Total pages：2 Responsible for pages：678-679 Language：Japanese Book type：Scholarly book
-
「原発性骨髄線維症, 真性多血症, 本態性血小板血症」最新の臨床WEB
幣 光太郎（ Role： Contributor , 原発性骨髄線維症, 真性多血症, 本態性血小板血症）
南江堂 2024.4
Language：Japanese Book type：Textbook, survey, introduction
-
22.分子標的治療薬 19) JAK2阻害薬 新臨床腫瘍学改訂第７版
幣 光太郎（ Role： Contributor , 22.分子標的治療薬 19) JAK2阻害薬）
南江堂 2024.2
Language：Japanese Book type：Scholarly book
MISC 【 display / non-display 】
-
Pathogenesis and advances in therapy of myelofibrosis: JAK inhibitors and allogenic hematopoietic cell transplantation. Invited Reviewed
Kotaro Shide, Kazuya Shimoda
Journal of the Japanese Society of Internal Medicine 115 ( 7 ) 1170 - 1175 2026.7
Authorship：Lead author, Corresponding author Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (scientific journal)
-
ルキソリチニブ(ジャカビ), モメロチニブ(オムジャラ)(特集 最近よく聞く他科の薬－先生の外来にこの薬を使っている患者さんがきますよ－) Invited
幣 光太郎
臨床雑誌 内科 136 ( 3 ) 499 - 502 2025.9
Authorship：Lead author, Corresponding author Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media) Publisher：南江堂
-
Ruxolitinib and momelotinib for myelofibrosis : their effects and positioning Invited
Hematology 90 ( 5 ) 553 - 559 2025.5
Authorship：Lead author, Corresponding author Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)
-
The impact of JAK2 allele burden in the management of patients with myeloproliferative neoplasms. Invited
Kotaro Shide
Hematology 90 ( 3 ) 277 - 283 2025.3
Authorship：Lead author, Corresponding author Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)
-
骨髄増殖性腫瘍におけるゲノム異常と臨床的有用性(特集 ゲノム解析時代の血液腫瘍学) Invited
幣 光太郎
医学のあゆみ 292 ( 1 ) 54 - 60 2025.1
Authorship：Lead author, Corresponding author Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (scientific journal) Publisher：医歯薬出版株式会社
Presentations 【 display / non-display 】
-
Neoplastic fibrocytes as key effectors of bone marrow fibrosis in myelofibrosis and their suppression by statins / Symposium 5 Development of novel therapies for myeloproliferative neoplasms Invited International conference
Kotaro Shide
The 87th Annual Meeting of the Japanese Society of Hematology (Kobe, Japan) 2025.10.12 The Japanese Society of Hematology
Event date： 2025.10.10 - 2025.10.12
Language：English Presentation type：Symposium, workshop panel (nominated)
Venue：Kobe, Japan Country：Japan
-
A mouse model of aggressive ATL associated with oncogenic mutations and an HBZ-expressing hematopoietic environment International conference
Takuro Kameda, Kotaro Shide, Yuki Tahira, Taisuke Uchida, Ayako Kamiunten, Keiichi Akizuki, Masayoshi Karasawa, Kengo Matsumoto, Ryoma Ikeda, Koshiro Nagamine, Ayuka Kuroki, Yoko Kubuki, Kazuya Shimoda
The 67th ASH Annual Meeting (Orlando, Florida) 2025.12.1 The American Society of Hematology
Event date： 2025.12.6 - 2025.12.9
Language：English Presentation type：Poster presentation
Venue：Orlando, Florida Country：United States
Other Link： https://www.sciencedirect.com/science/article/pii/S0006497125042296
-
Impact of Cooperating Myeloid Gene Mutations on Disease Progression and Survival in Japanese MPN Patients: A Multicenter Study International conference
Saki Ogawa, Kotaro Shide, Masami Takeuchi, Kosei Matsue, Takuro Kameda, Masato Yasumi, Takahiro Karasuno, Taizo Shimomura, Hitoshi Suzushima, Kiyoshi Yamashita, Noriaki Kawano, Osamu Imataki, Norimitsu Kadowaki, Akihito Yonezawa, Eiichi Otsuka, Yoshio Saburi, Yuki Tahira, Ayako Kamiunten, Keiichi Akizuki, Masayoshi Karasawa, Ryoma Ikeda, Kengo Matsumoto, Ayuka Kuroki, Koshiro Nagamine, Yoko Kubuki, Kazuya Shimoda
The 66th ASH Annual Meeting (San Diego, CA) 2024.12.7 米国血液学会
Event date： 2024.12.7 - 2024.12.10
Language：English Presentation type：Poster presentation
Venue：San Diego, CA Country：United States
-
TYK2 Is Essential for IFNα-Induced Resolution of MPN Features in a Murine Jak2V617F PMF Model International conference
Yuki Tahira, Kotaro Shide, Takuro Kameda, Ayako Kamiunten, Keiichi Akizuki, Masayoshi Karasawa, Ryoma Ikeda, Kengo Matsumoto, Yoko Kubuki, and Kazuya Shimoda
The 65th ASH Annual Meeting (San Diego, CA) 2023.12.11 米国血液学会
Event date： 2023.12.9 - 2023.12.12
Language：English Presentation type：Oral presentation (general)
Venue：San Diego, CA Country：United States
-
Significance of C-terminal amino acid sequence of CALR mutant proteins in inducing MPNs
The 85th Annual Meeting of the Japanese Society of Hematology (Tokyo) 2023.10.14 The Japanese Society of Hematology
Event date： 2023.10.13 - 2023.10.15
Language：Japanese Presentation type：Oral presentation (general)
Venue：Tokyo Country：Japan
Industrial property rights 【 display / non-display 】
-
骨髄線維症治療薬
下田 和哉、幣 光太郎、内田 泰介、大園 芳範
Applicant：宮崎大学
Application no：2024-011961 Date applied：2024.1.30
Announcement no：2025-117227 Date announced：2025.8.12
Country of applicant：Domestic
Awards 【 display / non-display 】
-
2025.3 公益財団法人 新日本先進医療研究財団 Calreticulinが関わる造血シグナル伝達機構、およびその破綻による骨髄増殖性腫瘍発症機序の解明
幣 光太郎
Award type：Award from publisher, newspaper, foundation, etc.
-
公益信託日本白血病研究基金一般研究賞
2017.11 公益信託日本白血病研究基金 骨髄増殖性腫瘍の発症・進展における、calreticulin機能不全の分子機構解明と治療法への展開
幣 光太郎
Award type：Award from publisher, newspaper, foundation, etc. Country：Japan
-
平成25年度日本血液学会奨励賞
2013.10 日本血液学会
幣 光太郎 宮崎大学 内科学講座 消化器血液学分野
Award type：Award from Japanese society, conference, symposium, etc. Country：Japan
Grant-in-Aid for Scientific Research 【 display / non-display 】
-
骨髄線維症における線維細胞標的療法開発のためのトランスレーショナル研究基盤の構築
Grant number：26K11330 2026.04 - 2029.03
日本学術振興会 科学研究費基金 基盤研究(C) 小区分54010:血液および腫瘍内科学関連
Authorship：Principal investigator
骨髄線維症（myelofibrosis: MF）の病態に深く関与する線維細胞を標的とする新規治療法を、第Ⅱ相医師主導治験へと発展させる基盤を確立する。そのため、①疾患マウスモデルを活用した前臨床proof of conceptの確立、②治療に特化したMF患者レジストリの構築、を戦略的に推進する。前臨床データと臨床リソースを同時に整備し、アカデミア発の革新的治療開発を実現可能とする体制を確立する。成果は、MFにおける新たな治療選択肢の創出に直結するのみならず、アカデミアから発信するトランスレーショナルリサーチのモデルケースとして、今後の本邦の血液腫瘍研究全体にも波及的な影響が期待される。
-
炎症と血栓形成の新仮説に基づく骨髄増殖性腫瘍の病態制御
Grant number：23K07817 2023.04 - 2026.03
日本学術振興会 科学研究費基金 基盤研究(C)
Authorship：Principal investigator
-
腫瘍性fibrocyteの本態解明と、骨髄線維症診断・治療への展開
Grant number：23H02938 2023.04 - 2026.03
独立行政法人日本学術振興会 科学研究費補助金 基盤研究(B)
下田 和哉
Authorship：Coinvestigator(s)
-
CALR変異幹細胞の増幅機構及び変異体の機能モチーフを標的とした骨髄線維症の制御
Grant number：19K08819 2019.04 - 2022.03
科学研究費補助金 基盤研究(C)
Authorship：Principal investigator
-
CALRが関わる造血シグナル伝達と、その破綻による骨髄増殖性腫瘍発症機序の解明
Grant number：16K09852 2016.04 - 2019.03
科学研究費補助金 基盤研究(C)
Authorship：Principal investigator