| Project/Area Number |
13671087
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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, Associate Professor, 医学部, 助教授 (10203267)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | LEUKEMOGENESIS / p230 bcr / abl / transgenic mouse / mutation / CML / thrombocytosis / p63 / モデルマウス / bcr-abl / calpastatin / トランスジェニックマウス / bcr-a61 |
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| Research Abstract |
Leukemogenesis was investigated with molecular biological methods. Especially, abnormalities of novel apotosis inhibitor gene, having homology with calpastatin, in chronic myelogenous leukemia (CML) was detected. Novel apotosis inhibitor gene was expressed abnormal sized mRNA in one patient of CML. I found that some CML patients had abnormality of novel apotosis inhibitor gene. The function of the novel gene is under analyzing.
Micro type bcr-abl (p230 bcr/abl) transcript was revealed to make CML patients atypical clinical courses other than typical CML. A novel transgenic mouse expressing p230 bcr/abl cDNA was succeeded to make. The transgenic mouse has a disease phenotype of CML with thrombocytosis. Transgenic mice expressing abnormal p51/p63 or the novel gene are now under making. Biological function of abnormalities of these p51/p63 and the novel gene are investigating with mutagenesis method.
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