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.