Imbalance between proliferation and apoptosis in the development of colorectal carcinoma

To evaluate the relationship between cell proliferation and apoptosis in sp oradic colorectal carcinogenesis, immunohistochemistry for proliferation-as sociated antigen Ki-67 and in situ end labelling for identifying apoptotic bodies were performed on paraffin sections from 59 adenomas and 22 carcinom as. These results were correlated with the expression of the proliferation and apoptosis modulators Bcl-2 and p53. Carcinomas showed increased prolife ration and apoptosis compared with adenomas (P<0.0001, P<0.001, respectivel y). There were positive linear correlations between proliferation and apopt osis in adenomas and carcinomas (P<0.02, P<0.05, respectively). The prolife rative rate increased significantly from mild to moderate, and from moderat e to severe dysplasia (P<0.002, P<0.001, respectively). Apoptotic rate also increased in this sequence, but the increases did not reach statistical si gnificance (both P>0.05). Expression of Bcl-2 was associated with lower apo ptotic rate in adenomas (P<0.025) but not in carcinomas (P>0.25), whereas p 53 expression was correlated with higher proliferative rate in both adenoma s and carcinomas (P<0.01, P<0.05, respectively). An inverse relationship be tween Bcl-2 and p53 expression was seen in both adenomas and carcinomas (P< 0.05, P<0.005, respectively). These data suggest that the normal balance be tween proliferation and apoptosis is disturbed in colorectal carcinogenesis , both being increased, but proliferation occurs in excess. Bcl-2 and p53 m ay each play a role in modulating cell apoptosis or proliferation during th e development of colorectal carcinoma.