| Project/Area Number |
01570571
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
YASUNO Hirokazu Kyoto Prefectural University of Medicine, Department of Dermatology, Professor, 医学部, 教授 (20079908)
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| Co-Investigator(Kenkyū-buntansha) |
YAMANISHI Kiyofumi Kyoto Prefectural University of Medicine, Department of Dermatology, Research As, 医学部, 助手 (10182586)
池田 佳弘 京都府立大学, 医学部, 助手 (50202908)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1990: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1989: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Skin tumor / Oncogene / Ras gene / Point mutation / PCR / Tumor suppressor gene / p53 / ゲノム解析 / PCR |
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| Research Abstract |
The oncogenes and tumor suppressor genes have been suggested to be involved in tumorigenesis of human cell. In this project, on the basis of mechanisms of epidermal keratinocytes growth and its deregulation, we tried to detect the mutations of these genes in human skin tumors, especially derived from keratinocytes. The growth of keratinocytesis regulated by various growth control system including cAMP system. We first showed that the expression of Ha-ras oncogene introduced into cultured keratinocytes caused deregulation of the growth of the cells. Then we investigated the significance of the mutations of the Ha-ras gene in several kinds of human epidermal tumors. DNA from paraffin-embedded tissues of benign and malignant human epidermal tumors (27 samples from 25 patients ; seborrheic keratosis, keratoacanthoma, Bowen's disease, basal cell epithelioma, squamous cell carcinoma) were prepared and examined for point mutations of codons 12, 13, and 61 of Ha-ras gene by polymerase chain reaction and oligonucleotide hybridization. Only one sample of basal cell epithelioma and one sample of keratoacanthoma were found to carry an A to T transversion at the second position of codon 61. Th low incidence of Ha-ras mutations suggests that the mutational activation of the gene may not be primarily involved in human epidermal tumorigenesis. In addition, the research examining the tumor suppressor gene p53 mutations in 4 hot spots of mutation in various skin tumors is in progress.
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