RECIPROCAL EXPRESSION OF BCL-2 AND P53 IN BREAST DUCTAL CARCINOMA

Apoptosis of programmed cell death represents a mechanism by which tum or cells with DNA damage can be deleted. Bcl-2 and p53 gene products h ave both been linked to apoptosis. Bcl-2 plays a role as an inhibitor of apoptosis that may extend the viability of cells containing genetic alterations and facilitate tumor progression. Mutant p53 has a simila r effect The purpose of this study was to investigate the relationship between bcl-2 and p53 expression and to clarify their roles in apopto sis in different histological graded breast carcinomas. We analysed 10 1 invasive ductal carcinomas of the breast for the expression of bcl-2 , p53, c-erbB-2, estrogen and progesterone receptors using immunohisto chemistry. Reciprocal expression of bcl-2 and p53 was present in 71.3% of cases. The bcl-2+/p53-expression pattern was prevalent in histolog ical grade I and II tumors (77.4% and 59.3% respectively) and rarely p resent in histological grade III (6.3%). Conversely, bcl-2-/p53+ expre ssion pattern was rarely present in histological grade I and II tumors (3.2% and 11.1% respectively) and prevalent in histological grade III (50.0%). Our results also showed that Bcl-2 expression was positively correlated with ER and PR, more prevalent in pre-menopausal status, a nd negatively correlated with cerbB-2 expression. Bcl-2 expression was involved in tumor progression in well-differentiated tumors and mutan t p53 could substitute for bcl-2 function in poorly differentiated tum ors. The bcl-2/p53 expression pattern of tumors may be of value in pre dicting therapeutic response and prognosis. Bcl-2 expression was corre lated with other well-established prognostic factors and bcl-2 could b e an estrogen-related protein.