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PTEN methylation is associated with advanced stage and microsatellite instability in endometrial carcinoma
Author(s) -
Salvesen Helga B.,
MacDonald Nicola,
Ryan Andy,
Jacobs Ian J.,
Lynch Eric D.,
Akslen Lars A.,
Das Soma
Publication year - 2000
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/1097-0215(20010101)91:1<22::aid-ijc1002>3.0.co;2-s
Subject(s) - pten , microsatellite instability , loss of heterozygosity , cancer research , endometrial cancer , tumor suppressor gene , carcinoma , methylation , biology , dna methylation , population , oncology , cancer , gene , microsatellite , medicine , genetics , carcinogenesis , gene expression , allele , pi3k/akt/mtor pathway , apoptosis , environmental health
Loss of heterozygosity and mutations in the PTEN ( MMAC1 ) tumor suppressor gene are frequent in endometrial carcinoma. Promoter hypermethylation has recently been identified as an alternative mechanism of tumor suppressor gene inactivation in cancer, but its importance in the PTEN gene in endometrial carcinoma is unknown. The purpose of our study was to assess the frequency of promoter methylation of the PTEN gene and to determine its correlation with clinicopathologic variables in a prospective and population‐based series of endometrial carcinomas with complete follow‐up. Presence of PTEN promoter methylation was seen in 26 of 138 patients (19%). Methylation was significantly associated with metastatic disease ( p = 0.01) and a microsatellite unstable phenotype ( p = 0.006). In conclusion, we find that PTEN promoter methylation is relatively frequent in endometrial carcinoma. Its association with metastatic disease and microsatellite instability implicates its importance in the development of this tumor type. Int. J. Cancer 91:22–26, 2001. © 2001 Wiley‐Liss, Inc.