p53 and beta-catenin expression in gallbladder tissues and correlation with tumor progression in gallbladder cancer

The inactivation of the tumor suppressor gene and activation of the proto-oncogene are key steps in the development of human cancer. p53 and beta-catenin are examples of such genes, respectively. In the present study, our aim was to determine the role of these genes in the carcinogenesis of the gallbladder by immunohistochemistry.

Sections from paraffin-embedded blocks of surgically resected specimens of gallbladder cancer (GBC) (80 cases), chronic cholecystitis (60 cases), and control gallbladders (10 cases) were stained with the monoclonal antibody p53, and polyclonal antibody beta-catenin. Results were scored semiquantitatively and statistical analysis performed. p53 expression was scored as percentage of the nuclei stained. Beta-catenin expression was scored as type of expression-membranous, cytoplasmic, and nuclear staining. Beta-catenin expression was correlated with tumor invasiveness, differentiation, and stage.

Over-expression of p53 was seen in 56.25% of GBC cases and was not seen in chronic cholecystitis or in control gallbladders. p53 expression in gallbladder cancer was significantly higher than in inflammatory or control gallbladders (P < 0.0001). p53 expression increased with increasing tumor grade (P = 0.039). Beta-catenin nuclear expression was seen in 75% cases of gallbladder cancer and in no case of chronic cholecystitis and control gallbladder. Beta-catenin nuclear expression increased with tumor depth invasiveness, and grade (P = 0.028 and P = 0.0152, respectively).

p53 and beta-catenin nuclear expression is significantly higher in GBC. p53 expression correlates with increasing tumor grade while beta-catenin nuclear expression correlates with tumor grade and depth of invasion, thus suggesting a role for these genes in tumor progression of GBC.