| Budget Amount *help |
¥17,680,000 (Direct Cost: ¥13,600,000、Indirect Cost: ¥4,080,000)
Fiscal Year 2017: ¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2015: ¥6,630,000 (Direct Cost: ¥5,100,000、Indirect Cost: ¥1,530,000)
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| 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.
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