Reciprocal expression of Bcl-2 and p53 in breast ductal carcinoma.
Apoptosis or programmed cell death represents a mechanism by which tumor cells with DNA damage can be deleted. Bcl-2 and p53 gene products have 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 similar effect. The purpose of this study was to investigate the relationship between bcl-2 and p53 expression and to clarify their roles in apoptosis in different histological graded breast carcinomas. We analysed 101 invasive ductal carcinomas of the breast for the expression of bcl-2, p53, c-erbB-2, estrogen and progesterone receptors using immunohistochemistry. Reciprocal expression of bcl-2 and p53 was present in 71.3% of cases. The bcl-2+/p53-expression pattern was prevalent in histological grade I and II tumors (77.4% and 59.3% respectively) and rarely present in histological grade III (6.3%). Conversely, bcl-2-/p53+ expression 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, and negatively correlated with cerbB-2 expression. Bcl-2 expression was involved in tumor progression in well-differentiated tumors and mutant p53 could substitute for bcl-2 function in poorly differentiated tumors. The bcl-2/p53 expression pattern of tumors may be of value in predicting therapeutic response and prognosis. Bcl-2 expression was correlated with other well-established prognostic factors and bcl-2 could be an estrogen-related protein.
Lee
W Y
WY
Department of Pathology, National Cheng Kung University Medical Center, Tainan, Taiwan.
Jin
Y T
YT
Tzeng
C C
CC
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017209:Apoptosis / Q000235:genetics*; D001940:Breast / Q000378:metabolism; D001943:Breast Neoplasms / Q000378:metabolism* / Q000473:pathology; D018270:Carcinoma, Ductal, Breast / Q000378:metabolism* / Q000473:pathology; D005260:Female; D019254:Genes, bcl-2 / Q000502:physiology*; D016158:Genes, p53 / Q000502:physiology*; D006801:Humans; D008875:Middle Aged; D009363:Neoplasm Proteins / Q000378:metabolism*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*
D009363:Neoplasm Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53