Relation between p53/waf1 expression to clinicopathological features of the Egyptian breast cancer

Abstract

A cell cycle inhibitory gene (WAF1/CIP1) is a gene whose protein plays an important role in cell regulation by inhibiting the formation of the engine driving the cycle (Cyclins-cdks). The induction of the expression of WAF1 gene is mediated by wild type p53 not the mutant one, consequently mutations in p53 gene may affect that gene. We studied p53/WAF1 expression in relation to the clinicopathological features of Egyptian breast cancer in an attempt for the possible use of them as genetic marker for the development and/or progression of such types of disease in Egypt. For this purpose, a series of 50 breast tumors from National Cancer Institute, Cairo University were screened for detection of p53 alterations using Western blot confirmed by PCR-SSCP, as well as the expression of WAF1 gene using Western blot technique. Our results revealed that 13/50 (26%) showed mutant-type of p53, all of them had abnormal pattern in SSCP analysis. A significant correlation was observed between histopathological type of breast cancer and presence of p53 mutations (p=0.04). On the other hand, no correlation was reported in case of tumor grade, nodal status, and metastatic potential of the tumor. Sixteen out of 50 (32%) cases showed WAF1 down-expression, 11 of them (68.8%) harbor p53 mutations. No correlation was reported between the expression of WAF1 and the clinicopathological variables. Also, no correlation was observed between deficient p53/WAF1 status with different clinicopathological variables. These data demonstrated that there is a strong negative correlation between the presence of p53 mutations and WAF1 expression in breast cancer in Egypt. The data suggested that p53 may play a role in the genesis of IDC type of Egyptian breast cancer. Also, no role for p53/WAF1 expression in breast cancer development and progression confirming the heterogeneity of breast cancer.

Publication Title

Cancer Molecular Biology

This document is currently not available here.

Share

COinS