The molecular mechanism of prognostic exacerbation by the addition of KIT mutations in CBF leukemia
Project/Area Number |
22790911
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Hematology
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Research Institution | Osaka University |
Principal Investigator |
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Project Period (FY) |
2010 – 2012
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Project Status |
Completed (Fiscal Year 2012)
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Budget Amount *help |
¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
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Keywords | CBF 白血病 / KIT 遺伝子変異 / 薬剤耐性遺伝子 / DNA 修復遺伝子 / CBF白血病 / 予後 / KIT遺伝子 / DNA修復 / KITV814 / CBFβ-MYH11 / レトロウィルス / 白血病 / シグナル伝達 / 肥満細胞腫瘍 / c-Kit遺伝子 |
Research Abstract |
Core binding factor (CBF) acute myeloid leukemia (AML) has a relatively favorable prognosis. However, activating KIT mutations are reported to be associated with higher risk of relapse and shorter survival. This project aims to clarify the molecular mechanism of such unfavorable effects by KIT mutations. The applicant explained that KIT mutations give poor prognosis to CBF leukemia through the induction of drug resistance genes and the reduction of DNA repair-related genes.
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Report
(4 results)
Research Products
(20 results)
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[Journal Article] BCR-ABL but not JAK2 V617F inhibits erythropoiesis through the Rassignal by inducing p21CIP1/WAF1.2010
Author(s)
Tokunaga M, Ezoe S, Tanaka H, Satoh Y, Fukushima K, Matsui K, Shibata M, Tanimura A, Oritani K, Matsumura I, Kanakura Y.
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Journal Title
Journal of Biological Chemistry
Volume: 285
Pages: 31774-31782
Related Report
Peer Reviewed
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