2026/06/22 更新

写真a

ハマダ　ヘイイチロウ
濵田　平一郎
Heiichiro Hamada
所属
医歯学域附属病院 附属病院 診療施設 輸血・細胞治療部 特任助教
職名
特任助教
学位
学士（医学）（1994年3月 大分医科大学）

研究キーワード

  • 細胞治療

  • 貯血

  • 膠原病1

  • リンパ腫

  • 白血病

  • 血液内科

研究分野

輸血・細胞治療領域, 血液・膠原病内科領域

経歴

  • 2014年4月 - 現在    鹿児島大学   輸血・細胞治療部   特任助教

所属学協会

  • 2015年10月 - 現在    日本血液学会

  • 1995年5月 - 現在    日本内科学会

取得資格

  • 医師

 

論文

  • Furukawa Y, Hamada H, Kamikawaji K, Unoki T, Inoue H, Tashiro Y, Okamoto M, Baba M, Hashiguchi T .  Successful treatment of an AIDS patient with prolonged Mycobacterium avium bacteremia, high HIV RNA, HBV infection, Kaposi's sarcoma and cytomegalovirus retinitis. .  Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy26 ( 2 ) 279 - 281   2020年2月

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  • Nakamura D, Ueno T, Nakabeppu SI, Shyodai A, Arima N, Kamada Y, Hamada HI, Suzuki S, Yoshimitsu M, Ishitsuka K .  Validation of prognostic indices in adult T-cell leukemia/lymphoma and their prognostic value at the start of second-line treatment. .  Leukemia & lymphoma67 ( 7 ) 1520 - 1526   2026年6月

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    記述言語：英語  

    DOI： 10.1080/10428194.2026.2645946

    PubMed

  • Arai A, Yoshimitsu M, Otsuka M, Ito Y, Miyazono T, Nakano N, Obama K, Nakashima H, Hanada S, Owatari S, Nakamura D, Tokunaga M, Kamada Y, Utsunomiya A, Haraguchi K, Hayashida M, Fujino S, Odawara J, Tabuchi T, Suzuki S, Hamada H, Kawamoto Y, Uchida Y, Hachiman M, Ishitsuka K .  Identification of putative noncanonical driver mutations in patients with essential thrombocythemia. .  European journal of haematology110 ( 6 ) 639 - 647   2023年6月

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    記述言語：英語   出版者・発行元：Wiley  

    <jats:title>Abstract</jats:title><jats:p>Essential thrombocythemia (ET) cases without canonical <jats:italic>JAK2</jats:italic>, <jats:italic>CALR</jats:italic>, or <jats:italic>MPL</jats:italic> mutations, that is, triple‐negative (TN) ET, have been found in 10%–20% of ET cases. Owing to the limited number of TN ET cases, its clinical significance remains unclear. This study evaluated TN ET's clinical characteristics and identified novel driver mutations. Among 119 patients with ET, 20 (16.8%) had no canonical <jats:italic>JAK2/CALR/MPL</jats:italic> mutations. Patients with TN ET tended to be younger and had lower white blood cell counts and lactate dehydrogenase values. We identified putative driver mutations in 7 (35%): <jats:italic>MPL</jats:italic> S204P, <jats:italic>MPL</jats:italic> L265F, <jats:italic>JAK2</jats:italic> R683G, and <jats:italic>JAK2</jats:italic> T875N were previously reported as candidate driver mutations in ET. Moreover, we identified a <jats:italic>THPO</jats:italic> splicing site mutation, <jats:italic>MPL</jats:italic>*636Wext*12, and <jats:italic>MPL</jats:italic> E237K. Four of the seven identified driver mutations were germline. Functional studies on <jats:italic>MPL</jats:italic>*636Wext*12 and <jats:italic>MPL</jats:italic> E237K revealed that they are gain‐of‐function mutants that increase MPL signaling and confer thrombopoietin hypersensitivity with very low efficiency. Patients with TN ET tended to be younger, although this was thought to be due to the inclusion of germline mutations, hereditary thrombocytosis. Accumulating the genetic and clinical characteristics of noncanonical mutations may help future clinical interventions in TN ET and hereditary thrombocytosis.</jats:p>

    DOI： 10.1111/ejh.13945

    PubMed

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