p53 is an important gene, involved in apoptosis (programmed cell
death), DNA repair, and cell cycle progression. We explore the
selective advantages and disadvantages of mutations in the p53 gene
on tumor cells, and the heterogeneity of tumor cell populations.
Based on an evolutionary computational approach, our model considers
changes in mutation rate caused by lack of DNA repair processes, and
the lack of apoptosis caused by mutations in p53. We find that the
degree of robustness of p53 to mutations has a significant effect on
the tumor heterogeneity and “fitness”, with clinical consequences
for people who inherit p53 mutations.
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