1990 Fiscal Year Final Research Report Summary
Analysis of Oncogene and Tumor Suppressor Gene Mutations in Human Kin Tumors
| 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)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Skin tumor / Oncogene / Ras gene / Point mutation / PCR / Tumor suppressor gene / p53 |
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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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Research Products
(6 results)
