Analysis of the onset mechanism of myelomonocytic leukemia by GATA2 deficiency

Research Project

Project/Area Number	26860204
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Pathological medical chemistry
Research Institution	Tohoku University
Principal Investigator	Harada Nobuhiko 東北大学, 医学(系)研究科(研究院), 助教 (20431439)
Project Period (FY)	2014-04-01 – 2016-03-31
Project Status	Completed (Fiscal Year 2015)
Budget Amount *help	¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000) Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Keywords	単球性白血病 / 白血病 / 転写因子
Outline of Final Research Achievements	Gata2 knockdown(KD) mice showed no abnormality in complete blood count but these mice showed monocytosis　with aging, like chronic myelomonocytic leukemia patients.By using a colony-forming unit(CFU) assay, the propotion of CFU-M(monocyte) from Gata2 KD bone marrow was increased. The gene expression of Csf1 receptor and IL-6 receptor was increased in granulocyte-macrophage progenitors(GMPs) from Gata2 KD bone marrow. These results suggested that GMPs from Gata2 KD has a potential to promote aberrant monocytic differentiation.

Report

(3 results)