Background and Objectives : bcl-2 and p53 gene products have both been linked to apoptosis. bcl-2 plays a role as an inhibitor of apoptosis that may facilitate tumor progression. Mutant p53 has a similar effect. Overexpression of the cyclin D1 gene ca...
Background and Objectives : bcl-2 and p53 gene products have both been linked to apoptosis. bcl-2 plays a role as an inhibitor of apoptosis that may facilitate tumor progression. Mutant p53 has a similar effect. Overexpression of the cyclin D1 gene can accelerate the progress of cells through the G1 phase and relate to tumor proliferation. Therefore, cyclin D1 may have an apoptosis inhibiting effect. The purpose of this study was to determine the significance of expression of bcl-2, p53 and cyclin D1 in invasive breast carcinoma. Materials and Methods : Expression of bcl-2, p53 and cyclin D1 gene was detected by immunohistochemistry using paraffin sections in 128 cases of invasive ductal carcinoma of breast. The results were correlated with survival rate and clinicopathologic variables, including patient’s age, histologic grade, lymph node status, tumor size, estrogen receptor (ER) and progesterone receptor (PR). Results : Our results showed that bcl-2 expression was positively correlated with ER and PR, and involved in low histologic grade. The expression of p53 protein showed a significant relationship to high histologic grade. An inverse relationship was shown between bcl-2 and p53 expression. Cyclin D1 expression was significantly more often found in tumor with bcl-2 and in tumors with low histologic grade expressing ER and PR. No association was seen between cyclin D1 and p53 expression. In survival analysis, no definite association between bcl-2, p53, and cyclin D1 and survival rate was found. Conclusion : bcl-2 and cyclin D1 expression was involved in tumor progression in well-differentiated tumors and could be an estrogen and progesterone related protein. Mutant p53 could substitute for bcl-2 function in poorly differentiated tumors. In multivariate analysis, the expression of bcl-2, p53, and cyclin D1 were not themselves independent predictors for clinical outcome.