Hypermethylation of E-cadherin in endometrial carcinoma.
10.3802/jgo.2008.19.4.241
- Author:
Jee Hyun PARK
1
;
Byung Ick LEE
;
Eun Seop SONG
;
Sung Ook WHANG
;
Woo Young LEE
;
Seong Jin CHO
Author Information
1. Department of Obstetrics and Gynecology, College of Medicine, Inha University, Incheon, Korea. p0928@inha.ac.kr
- Publication Type:Original Article
- Keywords:
E-cadherin;
Hypermethylation;
IHC;
Endometrial carcinoma
- MeSH:
Cadherins;
CpG Islands;
DNA;
Endometrial Hyperplasia;
Endometrial Neoplasms;
Female;
Genes, Tumor Suppressor;
Humans;
Lymph Nodes;
Methylation;
Neoplasm Metastasis;
Polymerase Chain Reaction;
Promoter Regions, Genetic
- From:Journal of Gynecologic Oncology
2008;19(4):241-245
- CountryRepublic of Korea
- Language:English
-
Abstract:
OBJECTIVE: Hypermethylation of CpG island is a common mechanism for the inactivation of tumor suppressor genes. Hypermethylation of the E-cadherin promoter region has been rarely studied in endometrial carcinoma of Korean women. The purpose of this study is to investigate methylation status of E-cadherin promoter region in endometrial carcinomas and endometrial hyperplasias, and analyze the correlation with clinicopathologic variables in endometrial carcinomas. METHODS: We examined the methylation status of the E-cadherin promoter region using methylation specific polymerase chain reaction and immunohistochemical expression (IHC) of E-cadherin in 30 endometrioid endometrial carcinomas and 20 endometrial hyperplasias, and correlated these results with various clinicopathological factors of endometrial carcinomas. RESULTS: Decreased expression of E-cadherin was detected in 13 of 30 (43.3%) endometrial carcinomas and in 1 of 20 (5%) endometrial hyperplasias (p=0.009). Promoter hypermethylation was detected in 12 of 30 (40%) endometrial carcinomas and 2 of 20 (10%) endometrial hyperplasias (p=0.015). Methylation status did not have a significant influence on the tumor grade and lymph node metastasis. However, the hypermethylation rate was significantly higher in stage above Ic (p=0.025). Decreased expression of E-cadherin was associated with tumor grade, tumor stage, and lymph node metastasis in endometrial carcinomas (p=0.01, p=0.02, p=0.03). There was no correlation between DNA hypermethylation and decreased expression of E-cadherin in endometrial carcinomas (p>0.05). CONCLUSION: These results indicate that hypermethylation of E-cadherin promoter region is a frequent event in endometrial carcinoma, which may play an important role in the progression of carcinogenesis. Also, the promoter methylation of E-cadherin in endometrial carcinoma was found to be significantly associated with higher stage above Ic.
