Open Accessras Mutations in Endocrine Tumors: Mutation Detection by Polymerase Chain Reaction‐Single Strand Conformation Polymorphism
Author(s) -
Yoshimoto Katsuhiko,
Iwahana Hiroyuki,
Fukuda Ayumi,
Sano Toshiaki,
Katsuragi Kiyonori,
Kinoshita Moritoshi,
Saito Shiro,
Itakura Mitsuo
Publication year - 1992
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1992.tb02722.x
Subject(s) - multiple endocrine neoplasia , carcinogenesis , biology , endocrine system , mutation , single strand conformation polymorphism , polymerase chain reaction , gene , thyroid , adenoma , microbiology and biotechnology , gene mutation , men1 , cancer research , genetics , endocrinology , hormone
To elucidate the molecular basis for endocrine tumorigenesis, ras mutations in human endocrine tumors were analyzed using polymerase chain reaction‐single strand conformation polymorphism (PCR‐SSCP) analysis. Mutations of the H‐, K‐, N‐ ras genes were examined in genomic DNAs from 169 successfully amplified primary endocrine tumors out of 189 samples. Four out of 24 thyroid follicular adenomas analyzed contained mutated N‐ ras codon 61, and one contained the mutated H‐ ras codon 61. One of the 19 pheochromocytomas revealed mutation of the H‐ ras codon 13. No mutations of the ras gene were detected in pituitary adenomas, parathyroid tumors, thyroid cancers, endocrine pancreatic tumors, and adrenocortical tumors. Based on these findings we conclude that activation of the ras gene may play a role in the tumorigenesis of a limited number of thyroid follicular adenomas and pheochromocytomas, and that mutation of the ras gene is not frequent in other human endocrine tumors.