J Breast Cancer.
2005 Dec;8(4):157-164. 10.4048/jbc.2005.8.4.157.
Loss of Heterozygosity of E-Cadherin Gene and Protein Expression in Invasive Ductal Carcinomas
- Affiliations
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- 1Department of Surgery, Hallym University College of Medicine, Seoul, Korea.
- 2Department of Pathology, Hallym University College of Medicine, Seoul, Korea.
- 3Department of Pathology and Biomedical Research Center, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, korea. heej0124@medimail.co.kr
- KMID: 1963234
- DOI: http://doi.org/10.4048/jbc.2005.8.4.157
Abstract
- PURPOSE
The E-cadherin gene, located on chromosome 16q22, may play principal roles in cell adhesion with the loss of E-cadherin expression leading to a propensity for a great number of malignant properties. The loss of heterozygosity (LOH) on 16q22 has rarely been studied in invasive ductal carcinomas. Our objectives were to evaluate the LOH of E-cadherin and the protein expression in invasive ductal carcinomas and their correlation with various clinicopathological factors. METHODS: The LOH analysis was performed using polymerase chain reactions with three polymorphic microsatellite markers (D16S419, D16S3106 and D16S498) in 50 surgically resected tumors and their non-tumorous counterparts. The E-cadherin protein expression was studied using immunohistochemistry. RESULTS: The LOH and loss of protein expression were detected in 54% and 46% of the tumors, respectively. There was no LOH or protein loss detected in the non-tumor lesions. The LOH results were well correlated with the tumor size and lymph node metastasis. The protein loss results were well correlated with tumor histological grade. No correlation was found between LOH and protein loss. CONCLUSION: These results suggest that the LOH of E-cadherin may be associated with tumor metastasis and tumor progression and E-cadherin protein loss may be related with the dedifferentiation in some portions of invasive ductal carcinomas. We propose the LOH of E-cadherin and protein loss may contribute to tumor progression by independent mechanism.
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