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セミナー第16回応用幹細胞医科学部門セミナー【Dr. Simón Méndez-Ferrer】

  • [開催日時]2018年10月23日(火)17:30-19:00
  • [開催場所]総合研究棟 1階105セミナー室
  • [対象]
備考・問合せ先
 10月23日(火)に以下のセミナーを開催いたします。
皆様方のご来聴を心よりお待ちしております
どうぞ宜しくお願い致します。

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【第16回 応用幹細胞医科学部門セミナー】

日時:2018年10月23日 (月) 17:30〜19:00 (質疑応答時間を含みます)
場所:総合研究棟 1階105セミナー室

演者:Dr. Simón Méndez-Ferrer
所属: Welcome-Trust Medical Research Council Cambridge Stem Cell Institute and Department of Haematology, University of Cambridge, and National Health Service Blood and Transplant, Cambridge Biomedical Campus, Cambridge, UK
講演タイトル:Microenvironmental contributions to myeloproliferative disorders

講演要旨:
Myeloproliferative neoplasms (MPNs) can be considered preleukemic disorders because MPN patients have a higher risk of developing acute myeloid leukaemia (AML). However, for reasons not fully clear, the transformation rates are very different across distinct MPN subsets (primary myelofibrosis > polycythemia vera (PV) > essential thrombocythemia (ET)). Although PV and ET can originate from hematopoietic stem and progenitor cells (HSPCs) activating the same overall JAK-STAT oncogenic pathway, the transformation rate into secondary myelofibrosis and leukemia is higher for PV than for ET. Whereas in some cases secondary mutations might cause transformation, it remains unclear whether distinct bone marrow (BM) microenvironments can influence the progression of MPNs or any preleukemic disorder. I will present evidence indicating that niche heterogeneity impacts evolution of MPNs driven by the same oncogenic pathway.

AML is also a heterogeneous disease characterised by the proliferation of clonal stem-cell-like blasts in the BM. Previous studies have demonstrated that the BM microenvironment (niche) contributes to AML development and chemoresistance. However, most BM stromal cells are reduced in AML and the mechanisms by which the surviving stromal cells promote leukaemogenesis remain incompletely understood. I will show that, unlike the bulk of stromal cells, BM mesenchymal stem cells (BMSCs) identified by the expression of the intermediate filament protein nestin are not diminished in AML patients or an inducible MLL-AF9 leukaemic mouse model. I will show how nestin+ BMSCs provide leukaemic blasts with increased bioenergetics and essential ROS detoxifying tools for AML development and chemoresistance.

Together, these studies highlight the active role and therapeutic potential of the BM microenvironment in the development and chemoresistance of myeloproliferative disorders.

Key Publications:
1. Del Toro R, et al. Nestin(+) cells direct inflammatory cell migration in atherosclerosis. Nat Commun. 2016 2. Sánchez-Aguilera A, et al. Estrogen signaling selectively induces apoptosis of hematopoietic progenitors and myeloid neoplasms without harming steady-state hematopoiesis. Cell Stem Cell 15: 791-780, 2014 3. Isern J, et al. The neural crest is a source of mesenchymal stem cells with specialized haematopoietic stem cell niche function. eLife 2014 4. Arranz L, et al. Neuropathy of haematopoietic stem cell niche is essential for myeloproliferative neoplasms. Nature 512: 78-81, 2014 5. Méndez-Ferrer S, et al. Mesenchymal and haematopoietic stem cells form a unique bone marrow niche. Nature 466:829-834, 2010


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新井 文用

九州大学大学院医学研究院
応用幹細胞医科学部門
幹細胞再生修復医学分野

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