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Molecular pathology of endometrial hyperplasia and carcinoma.

Abstract：

:Four different genetic abnormalities may occur in endometrioid adenocarcinomas of the endometrium (mircosatellite instability and mutations in the PTEN, k-RAS and beta-catenin genes), whereas nonendometrioid carcinomas of the endometrium often have p53 mutations and loss of heterozygosity on several chromosomes. Occasionally, a nonendometrioid carcinoma may develop as a result of dedifferentiation of a preexisting endometrioid carcinoma; in such a case, the tumor exhibits overlapping clinical, morphologic, immunohistochemical, and molecular features of the 2 types. The insaturation of microsatellite instability in endometrial carcinogenesis seems to occur late in the transition from complex hyperplasia to carcinoma, and it is preceded by progressive inactivation of MLH-1 by promoter hypermethylation. Moreover, the endometrioid adenocarcinomas that exhibit microsatellite instability show a stepwise progressive accumulation of secondary mutations in oncogenes and tumor suppressor genes that contain short-tandem repeats in their coding sequences. Mutations in the PTEN and k-RAS genes are also frequent in endometrioid adenocarcinomas of the endometrium, particularly in the tumors that exhibit microsatellite instability, whereas beta-catenin mutations do not seem to be associated with such a phenomenon.

journal_name

Hum Pathol

journal_title

Human pathology

authors

Matias-Guiu X,Catasus L,Bussaglia E,Lagarda H,Garcia A,Pons C,Muñoz J,Argüelles R,Machin P,Prat J

doi

10.1053/hupa.2001.25929

subject

Has Abstract

pub_date

2001-06-01 00:00:00

pages

569-77

issue

6

eissn

0046-8177

issn

1532-8392

pii

S0046-8177(01)10948-2

journal_volume

32

pub_type

杂志文章,评审

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