The Prognostic Value and Reciprocity of p53 and bcl-2 Expression in Colorectal Carcinoma

Park, Sang Heon; Min, Young Don; Kim, Jeong Yong; Kim, Kweon Cheon; Kim, Seong Hwan; Lim, Seong Cheol

Abstract

p53 is a tumor suppressor gene product identified in a wide range of tumor including colorectal carcinoma. Genetic alterations in the p53 tumor suppressor gene are common in human colorectal carcinoma. bcl-2 is a protooncogene that inhibits apoptosis. The products of mutant p53 gene and bcl-2 have been associated with prognosis in several malignancies including colorectal carcinomas. This study was undertaken to evaluate values of p53 and bcl-2 oncoproteins as prognostic factors relative to clinicopathological factors and correlation of their expression. Analyses were made on achieval pathologic tissues of 80 patients with colorectal carcinomas including 34 patients able to follow-up over 5 years. The oncoproteins were localized using commercially available monoclonal antibodies:DO-7 for p53, clone124 for bcl-2. Expression of bcl-2 was cytoplasmic, whereas nuclear p53 expression was localized in carcinoma cells. The patients were 17 to 83 years of age. The expression of p53 and bcl-2 was determined respectively in 30 (37.5%) and 21 (26.3%)cases. The expression of p53 nuclear expression was not correlated with tumor location, size, histologic grade, Duke's classification, regional lymph node metastasis and tumor recurrence. The cytoplasmic expression of bcl-2 was not correlated with tumor location, size, histologic grade, Duke's classification, regional lymph node metastasis and recurrence. Univariate analysis showed that patients with p53 nuclear expression were not associated with poorer overall survival than patients with p53 negative, and also showed in patients with bcl-2 expression. The expression of p53 did not affect to that of bcl-2. We concluded that the p53 nuclear and bcl-2 cytoplasmic expression were not independent prognostic factors in colorectal carcinomas. Evidence of reciprocity of bcl-2 and p53 expression was not found.