Elucidation of molecular mechanism through which MDS develops

2017 Fiscal Year Final Research Report

• Project/Area Number: 15H04857
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Hematology
• 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)
• Co-Investigator(Kenkyū-buntansha): 長町 安希子 広島大学, 原爆放射線医科学研究所, 研究員 (20585153) ; 金井 昭教 広島大学, 原爆放射線医科学研究所, 助教 (60549567)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: MDS / RAEB / モノソミー７

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

血液学