Analysis genetic changes in human endocrine tumors

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To elucidate the molecular basis for endocrine tumorigenesis, ras, p53, and Gsalpha mutations in human endocrine tumors were analyzed.1. ras mutationsMutations 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 mutationsExons 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 mutationsMutation 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.