| Project/Area Number |
11671018
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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 |
Hematology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
INOKUCHI Koiti Nippon Medical School, Dept.of Internal Medicine, Lecturer, 医学部, 助教授 (10203267)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2000: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | LEUKEMOGENESIS / c-kit / c-mpl / mutation / calpastatin |
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| Research Abstract |
Leukemogenesis was investigated with molecular biological methods. Especially, abnormalities of c-kit and novel apotosis inhibitor genes in chronic myelogenous leukemia (CML) were detected. I found that some CML patients had abnormality of novel apotosis inhibitor gene, and others had a point mutation of c-kit genes. Minor type bcr-abl transcript was revealed to make CML patients atypical clinical courses other than typical CML.Acute lymphoblastic leukemia with atypical P180 BCR/ABL protein was also atypical clinical course with chemo-resistance. Novel apotosis inhibitor gene, which had homology with the caplastatin gene, was expressed abnormal sized mRNA in one patient of CML.The function of the novel gene is under analyzing. Four out of 80 CML patients had point mutation of codon 541 of c-kit. The same point mutation of codon 541 was occurred in three CML patients at blastic crisis, whose skin has no mutation of codon 541.
One CML patient had point mutation of codon 564 of c-kit. These abnormal c-kit had relatively higher tyrosine activity. These CML had remarkable leukocytosis. Biological function of abnormalities of these c-kit and c-mpl proteins are investigating with mutagenesis method.
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