Role of apoptosis, proliferating cell nuclear antigen and p53 protein in the immune response of rat colon cells to cancer and vaccination with anti-p53 polyclonal antibodies.

BACKGROUND

Previously it was shown that rabbit anti-p53 antibodies can exert tumor-suppressive effects on chemically induced rat colon cancer (Cancer J, 10:116-120, 1997). This work examines the role of some components of the immune system in the response of the rat colon cells to treatment with a carcinogen and anti-p53 antibodies.

METHODS

The following groups of rats were studied: a) control non treated rats; b) tumor-free non vaccinated rats treated with a carcinogen; c) tumor-bearing non vaccinated rats; d) tumor-free vaccinated rats exposed to a carcinogen; e) tumor-bearing vaccinated rats. The manifestation of apoptosis, proliferating cell nuclear antigen (PCNA), mitotic index, T lymphocytes and p53 protein was compared between the different groups of rats.

RESULTS

The apoptotic index and the number of p53-positive cells and T lymphocytes were significantly higher in colon adenocarcinomas obtained from vaccinated rats than in unvaccinated rats. PCNA was lower in tumors from the vaccinated rats, whereas the proliferating cell index was not different between the both groups of rats. An inverse relationship was seen between apoptosis and most other parameters studied. The inverse correlation found between apoptosis and p53 protein in this study demonstrated that apoptosis acts as a p53-independent parameter in chemically induced rat colon cancer.

CONCLUSIONS

Our findings demonstrated that vaccination significantly activated apoptosis in both types of colon tissue, and induced synthesis of p53 protein in tumor tissue. Vaccination with anti-p53 polyclonal antibodies seemed to activate the immune system and to stimulate some of its cellular components responsible for tumor suppression.