Loss of PTEN Expression in Breast Cancers.
- Author:
Sun Hee CHANG
1
;
Shi Nae LEE
;
Min Sun CHO
;
Heasoo KOO
;
Woon Sup HAN
;
Seock Ah IM
;
Byung In MOON
;
Hyun Suk SUH
;
Hye Young CHOI
;
Sun Hee SUNG
Author Information
1. Department of Pathology, InJe University Ilsan Paik Hospital, Korea.
- Publication Type:Original Article
- Keywords:
PTEN;
Invasive ductal carcinoma;
Breast;
Promoter hypermethylation
- MeSH:
Breast Neoplasms;
Breast*;
Carcinoma, Ductal;
Diagnosis;
Female;
Genes, Tumor Suppressor;
Humans;
Incidence;
Loss of Heterozygosity;
Lymph Nodes;
Methylation;
Neoplasm Metastasis;
Polymerase Chain Reaction
- From:Korean Journal of Pathology
2005;39(4):236-241
- CountryRepublic of Korea
- Language:English
-
Abstract:
Background : PTEN, located on chromosome 10q23.31, is a novel tumor suppressor gene. In the sporadic breast cancers, the incidence of the loss of heterozygosity of PTEN is approximately 10% to 40%, but the incidence of intragenic mutation of PTEN is less than 1%. To as- sess the role of the PTEN in the invasive ductal breast cancer, we studied the frequency of the loss of PTEN expression, its correlation with the commonly used prognostic factors of the breast cancer and with PTEN promoter hypermethylation status. Methods : Immunohistochemical staining with an anti-PTEN protein antibody was performed on the paraffin-embedded breast tissues from 129 women with a diagnosis of invasive ductal carcinoma. Methylation specific PCR was performed to detect hypermethylation in the PTEN gene on the 28 cases with the loss of PTEN expression. Results : Sixty-two (48%) of 129 breast tumors had the loss of PTEN expression. The loss of PTEN expression was correlated with lymph node metastasis and stage, and there was a near-significant correlation with the tumor size. PTEN promoter hypermethylation was found in five (18%) out of 28 patients. Conclusion : These results suggest that the loss of PTEN expression might play a role in the progression of the breast cancer and that the aberrant promoter methylation is one of the silencing mechanisms of PTEN.
