Positive selection in the evolution of cancer

We hypothesize that forms of antagonistic coevolution have forged strong links between positive select' n at the molecular level and increased cancer risk. By this hypothesis, evolutionary conflict between males and females, mothers and foetuses, hosts and parasites, and other parties with divergent fitness interests has led to rapid evolution of genetic systems involved in control over fertilization and cellular resources. The genes involved in such systems promote cancer risk as a secondary effect of their roles in antagonistic coevolution, which generates evolutionary, disequflibrium and malaclaptation. Evidence from two sources: (1) studies on specific genes, including SPAXV cancer/ testis antigen genes, several Y-linked genes, thepem homebox gene, centromeric histone genes, die breast cancer gene BRCA1, the angiogenesis gene AXG, cadherin genes, cytochrome P450 genes, and viral oncogenes; and (2) large-scale database studies of selection on different functional categories of genes, supports our hypothesis. These results have important implications for understanding the evolutionary underpinnings of cancer and the dynamics of antagonistically-coevolving molecular systems.