Tumour growth and cell kinetics in variants of a human endometrial adenocarcinoma expressing either wild-type or mutant p53.

We have compared the baseline cell proliferation and tumour growth in two variants of a human endometrial adenocarcinoma grown in nude mice. One of these tumour variants expressed wild-type p53 whereas the other had mutations of the p53 gene at codon 175 in both alleles and at codon 248 in one allele. There was no difference in growth rate between the tumour variants. Cell proliferation parameters, such as labelling index and S-phase fraction, were significantly increased in the tumour with mutated p53 and consequently there was a significantly lower proportion of cells in the G1-phase, proposing an at least partial loss of suppressor function in this tumour. Semi-quantitative analysis of the p53 and bcl-2 proteins showed a significant overexpression of p53 and a decreased expression of the bcl-2 protein in the p53 mutated tumour variant compared with the variant with wild-type p53. We conclude that wild-type p53 protein acts as an active suppressor in the regulation of the baseline growth and cell kinetics of this tumour and could be linked through a p53--bcl-2 system in human endometrial adenocarcinomas.