| Project/Area Number |
10670935
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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 | Chiba University |
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Principal Investigator |
SATO Takeyuki Chiba University, School of Medicine, Associate Professor, 医学部, 教授 (30187207)
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| Co-Investigator(Kenkyū-buntansha) |
OHKI Misao National Cancer Institute, Department of Radiology, Chief of the department, 国立がんセンター研究所, 部長 (00158792)
TANZAWA Hideki Chiba University, School of Medicine, Professor, 医学部, 教授 (50236775)
FUSE Akira National Institute of Infections Disease, Department of Oral Surgery, Professor, 国立感染症研究所, 室長 (60110300)
野口 靖 千葉大学, 医学部・附属病院, 医員
白澤 浩 千葉大学, 医学部, 教授 (00216194)
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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 |
¥3,700,000 (Direct Cost: ¥3,700,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | Megakaryoblastic leukemia / Cell line / Chromosome 17 / Gene cloning / 癌遺伝子 / 癌抑制遺伝子 |
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| Research Abstract |
All for megakaryoblastic leukemia cell lines, which were establish in our laboratory, showed the abnormalities of chromosome 17. CMK and CMY showed the chromosomal translocation of 17p13 and deletion of chromosome17, CMS showed the chromosomal translocation of 17P13 and CTS showed the deletion of chromosome 17. There findings suggested that some gene, which is related to oncogenacity (especially to magakaryoblastic leukemia), located in chromosome 17, especially in 17P13. The blasts of the patient before establishment of CMY did not reveal the abnormalities of chromosome 17, then the blasts which showed the same chromosomal abnormalities of CMY increased in blood of patient according to the resistance to chemotherapy. This finding suggested that CMY was established fun the minor clone which was undetectable by conventional Karyotype analysis. Then this minor clone increased according to the resistance to chemotherapy. Taken together, some gene which was related to the resistance to chemotherapy and establishment of cell lines.
Because P53 suppressor gene locates on chromosome P17, expressions of P53 gene in CMY and original blasts were analyzed by SSCP method. CMY showed the abnormality of exon 5 of P53 gene, whereas the blasts of the patient did not show the abnormalities. There findings indicated that the abnormality of P53 gene might occurred during the process of establishment of CMY, and did not relate to the chromosomal abnormality of 17P of the blasts the patient.
We now study the locus of the translocation which is common in CMK,CMY and CMS or not by FISH analysis using several genes which locate chromosome 17P13. Furthemore, we try the gene cloning using differential display method and representational difference analysis.
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