| Project/Area Number |
10670768
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Hyogo College of Medicine |
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Principal Investigator |
YAMAMOTO Masuji Associate Professor, Department of Pediatrics, Hyogo College of Medicine, 医学部, 助教授 (40200844)
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| Co-Investigator(Kenkyū-buntansha) |
TSUJINO Yoshiaki Research Associate, Department of Pediatrics, Hyogo College of Medicine, 医学部, 助手 (60268547)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | cell cycle / MDS (myelodysplastic syndrome) / Leukemic change |
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| Research Abstract |
The expression patterns of D-type cyclins and cyclin-dependent kinases (cdks) in SKM-1 myelodyaplastic syndrome (MDS) cells co-cultured with granulocyte-macrophage colonystimulating factor (GM-CSF) and/or transforming growth factor-β1 (TGF-β1) was analyzed. Our results indicated that TGF-β1-mediated G1 arrest correlated with the downregulation of cdk4, cdk6 and cyclin D2, and that abrogation of TGF-β1-mediated G1 arrest by GM-CSF was caused by the constitutive overexpression of cyclin D2 and cdk6 but not cdk4. These results suggest the importance of cyclin D2/cdk6 levels in abrogating G1 arrest in cells exposed to TGF-β1, and raise the possibility that the GM-CSF-mediated upregulatory pathway of signal transduction through cyclin D2/cdk6 play an important roles in the induction of leukemic change of patients with myelodysplastic syndrome.
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