EXPRESSION OF THE ANTIAPOPTOTIC PROTEIN BCL-2 IS NOT DEPENDENT ON THETUMOR-SUPPRESSOR P53 PROTEIN IN INDIAN BREAST-CARCINOMA

Tissue homeostasis and the maintenance of cell populations depend on a delicate balance between the rates of cell proliferation and cell dea th. Programmed cell death or apoptosis is believed to play a major rol e in physiological processes which, when defective, could contribute t o the pathogenesis and progression of tumors. A role for altered progr ammed cell death in cancer stems from the description of alterations o f tumor-associated genes involved in the regulation of apoptosis such as p53 and bcl-2. The p53 gene promotes apoptosis in cells with geneti c damage, while bcl-2 is an antiapoptotic gene. It is therefore possib le that the balance between p53 and bcl-2 may have significant implica tions for the pathobiology of breast cancer. This study was therefore undertaken to evaluate the expression of these two proteins with oppos ite functions and their relation to the total growth fraction of the t umor as measured by PCNA immunoreactivity. A significant correlation w as observed between expression of p53 and PCNA. In contrast, bcl-2 exp ression did not correlate with the expression of p53. There was also n o correlation observed between expression of bcl-2 and PCNA. A signifi cant correlation was observed between expression of p53 and the grade of the tumor and stage of the disease. Our results thus support the hy pothesis that accumulation of p53 is associated with a high tumor prol iferation rate, an association that might be expected in view of the r ole of wild-type p53 as a negative regulator of cell proliferation. An other important observation was the lack of relationship between bcl-2 expression and PCNA immunoreactivity, supporting the hypothesis that bcl-2 is not a major regulator of proliferation.