Distributions of p53 codon 72 polymorphism in bladder cancer – proline form is prominent in invasive tumor

Abstract

Abnormal function of p53 is commonly associated with various cancer formations. High-grade and late-stage bladder cancers have been reported to have mutated or become inactive p53 when using immunohistochemical stains. Recently, p53 codon 72 polymorphism was extensively studied to determine the risk factors responsible for cancer formation. There was a general population of codon 72 sequence polymorphism of the wild type p53. A single base change from G to C caused the alteration of amino acid residue 72 from arginine to proline. The arginine form is considered to be a significant risk factor in the development of cancer. However, various reports had indicated discrepancies with regard to this polymorphism; some showed no significant difference between the control and cancer groups, while other series were associated with high risks in the proline form homozygotes. To resolve the undefined distribution of this polymorphism in bladder cancers, 58 patients with bladder cancer were enrolled onto this study. When checked using the Chi-squared test (P=0.952) there were no differences between the control subjects and bladder cancer patients in the distribution of polymorphism. However, proline form homozygotes were more frequently found in the invasive group than the non-invasive group by Fisher's exact test (25% and 2.9%, respectively, P < 0.001). More than 70% of the non-invasive bladder cancers were the arginine form homozygotes. This result is consistent with those reported for hepatocellular carcinoma that showed a history of chronic liver disease and proline form homozygotes in a report by Yu et al. Our data suggest that proline form homozygotes are associated with invasive bladder cancer.