| Project/Area Number |
03454169
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
FUKUMOTO Manabu Kyoto University Faculty of Medicine, Associate Professor, 医学部, 助教授 (60156809)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1992: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1991: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Keywords | Carcinogenesis / Gene Amplification / Human cancer / Southern hybridization / In-situ hybridization / In-gel DNA hybridization / Northern hybridization / RT-PCR / ゲル内再会合法 / ノーザンハイブリダイゼーション / サザ-ンハイブリダイゼ-ション / Inーsituハイブリダイゼ-ション |
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| Research Abstract |
1. Overexpression of the c-myc gene in serous adenocarcinoma especially at stage III was significant, suggesting that the c-myc gene plays an important role for tumorigenesis of ovarian cancer at later stages.
2. The structure and location of amplicons in two independent cell lines which have coamplification of the c-myc and the Ki-ras genes were analyzed. Each one of amplicons shared one chromosome in both the cell lines. We conclude that amplification of copy number occurred in a form of episome and these two independent amplified genes got associated at chromosomal level by a common mechanism.
3. Amplification of either c-myc, erbB or bcl-1 gene was found in more than 50% or human esophageal carcinoma cell lines. The incidence of coamplification of the c-myc gene and other genes was significant. Although bcl-1 gene amplification was found in 39% of cell lines, its expression is undetectable in one cell line. The bcl-1 gene is mapped to the chromosomal locus 11q13 where several oncogenes form cluster. Therefore, the investigation whether there is a target gene which is overexpressed in the amplicon is ongoing.
4. An autocrine mechanism through basic fibroblast growth factor we applied neutralizing antibody against bFGF to inhibit growth of glioma cells by blocking the autocrine mechanism. This strategy would be a potential therapy to control gliomas.
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