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Biomarkers in the endometrium
Author(s) -
Berchuck Andrew
Publication year - 1995
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240590923
Subject(s) - endometrial cancer , carcinogenesis , cancer research , microsatellite instability , endometrium , biology , point mutation , oncogene , tumor suppressor gene , mutation , malignant transformation , gene , cancer , medicine , cell cycle , allele , genetics , microsatellite
A number of oncogenes and tumor suppressor genes that may serve as surrogate biomarkers of transformation are altered during the process of endometrial carcinogenesis. Overexpression of HER‐2/ neu occurs in 10% of endometrial adenocarcinomas and correlates with intraperitoneal spread of disease and poor survival. The c ‐ myc oncogene is amplified in 10% of cases. Point mutations in codon 12 of the K‐ ras oncogene have been reported to occur in 10–20% of endometrial cancers. K‐ ras mutations also have been noted in some endometrial hyperplasias, which may represent an early event in the development of some endometrial cancers. Mutation of the p53 tumor suppressor gene, with resultant overexpression of mutant p53 protein, occurs in 20% of endometrial adenocarcinomas. Overexpression of p53 is associated with advanced stage and poor survival. Because p53 mutations have not been observed in endometrial hyperplasias, this is thought to be a relatively late event in endometrial carcinogenesis. Microsatellite instability has also been noted in approximately 15% of sporadic endometrial cancers, but mutations in DNA repair genes have not yet been reported. Chemoprevention trials in endometrial cancer may be feasible due to the existence of a premalignant lesion and surrogate biomarkers.