Identification of genes involved in the development of MDS as a tool of elucidation of hematopoiesis.

2014 Fiscal Year Final Research Report

• Project Area: Molecular mechanisms of cell fate determination in the cells that undergo stepwise differentiation to multiple pathways
• Project/Area Number: 22118005
• Research Category: Grant-in-Aid for Scientific Research on Innovative Areas (Research in a proposed research area)
• Allocation Type: Single-year Grants
• Review Section: Biological Sciences
• Research Institution: Hiroshima University
• Principal Investigator: INABA Toshiya 広島大学, 原爆放射線医科学研究所, 教授 (60281292)
• Project Period (FY): 2010-04-01 – 2015-03-31
• Keywords: MDS / モノソミー7 / 片アレル欠失不全 / 分裂期制御 / エンドソーム蛋白質 / Samd9 / Samd9L / Miki

Outline of Final Research Achievements

To elucidate mechanisms through which a hematopoietic stem cell differentiates to mature blood cells, myelodysplastic syndromes (MDS) may be a good material. We identified three responsible genes for the deletion of the long arm of chromosome 7, which is most frequently observed as a non-random chromosome abnormality in patients with MDS. Both the homo- and hetero-deficient mice of Samd9/Samd9L genes, which encode endosome proteins developed MDS at their advanced age, mimics human diseases. Lack of Miki, which encodes a centrosome protein prolongs prometaphase, resulting in abnormal morphology of nuclei, which strikingly resembles those routinely observed in bone marrow preparations of MDS patients. Those three genes located in chromosome 7 were considered to be responsible for the development of MDS.

Free Research Field

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