Loss of heterozygosity of E-cadherin in endometrial carcinomas and endometrial hyperplasias / 대한산부인과학회지

ABSTRACT

OBJECTIVE: Microsatellite alteration such as loss of heterozygosity (LOH) has been reported to be a novel mechanism for the inactivation of tumor suppressor gene and related to carcinogenesis in many malignant tumors. E-cadherin protein coded by gene on chromosome 16q22.1 may play a principal role for tumor suppression. However LOH of E-cadherin has been rarely studied in endometrial carcinoma. The purpose of this study was to investigate the loss of heterozygosity (LOH) of E-cadherin in endometrial carcinoma and endometrial hyperplasia and to correlate their results with various clinicopathological factors. METHODS: LOH of E-cadherin on the chromosome 16q22.1 analysis was performed by using polymerase chain reaction (PCR) for three polymorphic microsatellite markers (D16S419, D16S3106, D16S498) and automatic laser fluorescent DNA sequencer in 30 cases of endometrioid endometrial adenocarcinomas and in 20 cases of endometrial hyperplasias. The relationship between LOH of E-cadherin and clinical profile was analyzed. RESULTS: Increased LOH of E-cadherin was found in endometrial carcinomas (50%) compared to endometrial hyperplasias (5%) (P=0.01, Fisher's exact test). The incidence of LOH of E-cadherin in endometrial carcinomas also showed significantly lower in stage below Ia. (P=0.034, Fisher's exact test) LOH of E-cadherin was not associated with histologic grade and lymph node metastasis. (P=0.42, P=0.5, Fisher's exact test) CONCLUSIONS: These results suggests that LOH of E-cadherin may contribute to the development of endometrial carcinoma, especially in above stage Ib.