No evidence for oncogenic mutations in the adrenocorticotropin receptor gene in human adrenocortical neoplasms.

Abstract

The mechanism(s) of tumorigenesis for the majority of adrenocortical neoplasms remain unknown. G-Protein-coupled receptors were recently proposed as candidate protooncogenes. That activating mutations of this class of receptors might be important for tumor induction or progression of endocrine neoplasms was strengthened by the recent identification of such mutations in hyperfunctioning thyroid adenomas. To examine whether the ACTH receptor (ACTH-R) gene could be an oncogene in human adrenocortical tumors, we amplified by the polymerase chain reaction and directly sequenced the entire exon of the ACTH-R gene in 25 adrenocortical tumors (17 adenomas and 8 carcinomas) and 2 adrenocortical cancer cell lines. We found no missense point mutations or even silent polymorphisms in any of the tumors and cell lines studied. We conclude that activating mutations of the ACTH-R gene do not represent a frequent mechanism of human adrenocortical tumorigenesis.

• Authors: A C Latronico, M Reincke, B B Mendonça, K Arai, P Mora, B Allolio, B L Wajchenberg, G P Chrousos, C Tsigos
• Journal: The Journal of clinical endocrinology and metabolism (J Clin Endocrinol Metab) Vol. 80 Issue 3 Pg. 875-7 (Mar 1995) ISSN: 0021-972X [Print] United States
• PMID: 7883845 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Receptors, Corticotropin

Topics

• Adolescent
• Adrenal Cortex Neoplasms (etiology, genetics)
• Adult
• Aged
• Base Sequence
• Child
• Female
• Humans
• Male
• Middle Aged
• Molecular Sequence Data
• Mutation
• Receptors, Corticotropin (genetics)