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Activating point mutations of the gsp oncogene in human thyroid adenomas
Author(s) -
O'Sullivan Catriona,
Barton Claire M.,
Staddon Susan L.,
Brown Christopher L.,
Lemoine Nicholas R.
Publication year - 1991
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/mc.2940040503
Subject(s) - biology , point mutation , oncogene , thyroid , adenoma , cancer research , mutation , thyroid carcinoma , gene , endocrinology , genetics , cell cycle
The gene for the alpha polypeptide chain (α s ) of the heterotrimeric G protein G s can be activated to the putative oncogene gsp by specific point mutations at codons 201 and 227. Such mutations have been reported in 40% of human growth hormone‐secreting pituitary adenomas and in a single autonomously functioning thyroid adenoma. We examined an archival series of 45 differentiated human thyroid tumors by polymerase chain reaction amplification and oligonucleotide hybridization to identify point mutations at each of the affected codons. Successful amplification was achieved in 38 cases, and activating mutations were identified in 5 of 13 (38%) autonomously functioning adenomas, but in none of 16 nonfunctioning adenomas, six papillary carcinomas, or three follicular carcinomas. Our results confirm that the gsp oncogene is involved in the pathogenesis of autonomously functioning tumors but do not support a role in other thyroid tumors.