1993 Fiscal Year Final Research Report Summary
Analysis genetic changes in human endocrine tumors
| Project/Area Number |
04671484
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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 |
内分泌・代謝学
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| Research Institution | The University of Tokushima |
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Principal Investigator |
YOSHIMOTO Katsuhiko The University of Tokushima, School of Medicine, Associate Professor, 医学部, 客員助教授 (90201863)
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| Co-Investigator(Kenkyū-buntansha) |
SANO Toshiaki The University of Tokushima, School of Medicine, Assistant Professor, 医学部, 講師 (80154128)
IWAHANA Hiroyuki The University of Tokushima, School of Medicine, Research Associate, 医学部, 寄附講座担当教員
ITAKURA Mitsuo The University of Tokushima, School of Medicine, Professor, 医学部, 客員教授 (60134227)
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| Project Period (FY) |
1992 – 1993
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| Keywords | endocrine tumors / mutation / ras gene / p53 gene / Gsalpha gene |
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| Research Abstract |
To elucidate the molecular basis for endocrine tumorigenesis, ras, p53, and Gsalpha mutations in human endocrine tumors were analyzed.
1. ras mutations
Mutations of the H-, K-, N-ras genes were examined from 171 tumors by polymerase chain reaction-single strand conformation polymorphism(PCR-SSCP). Four out of 24 thyroid follicular adenomas contained mutated N-ras codon 61, and one contained the mutated H-ras codon 61. One of the 19 pheochromocyttomas revealed mutation of the H-ras codon 13. One of the 2 pituitary carcinomas contained mutation of the H-ras codon 12.
2. p53 mutations
Exons 5 through 10 of the p53 gene were studied from 134 tumors and 6 human endocrine cancer-derived cell lines by PCR-SSCP.Mutations were detected in 4 tumors, including one parathyroid adenomas and 3 throid carcinoma cell lines. In all of 3 tumor cell lines, the normal allele including the p53 gene was lost.
3. Gsalpha mutations
Mutation at codons 201 or 227 of the Gsalpha gene were screened from 197 tumors by PCR-primer-introduced restriction analysis(PIRA). The Gsalpha mutations were present in 4 of 43 GH-secreting pituitary adenomas, 4 of 30 papillary thyroid carcinomas, and 1 of 19 adrenocortical adenomas.
Conclusion : Mutation of the ras, p53, and Gsalpha genes may not involved in the pathogenesis of a large population of human endocine tumors.
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Research Products
(10 results)
