Cancer is sometimes depicted as a reversion to single cell behavior in cells adapted to live in a multicellular assembly. If this is the case, one would expect that mutation in cancer disrupts functional mechanisms that suppress cell-level traits detrimental to multicellularity. Such mechanisms should have evolved with or after the emergence of multicellularity. This leads to two related, but distinct hypotheses: 1) Somatic mutations in cancer will occur in genes that are younger than the emergence of multicellularity (1000 million years [MY]); and 2) genes that are frequently mutated in cancer and whose mutations are functionally important for the emergence of the cancer phenotype evolved within the past 1000 million years, and thus would exhibit an age distribution that is skewed to younger genes. In order to investigate these hypotheses we estimated the evolutionary ages of all human genes and then studied the probability of mutation and their biological function in relation to their age and genomic location for both normal germline and cancer contexts.

We observed that under a model of uniform random mutation across the genome, controlled for gene size, genes less than 500 MY were more frequently mutated in both cases. Paradoxically, causal genes, defined in the COSMIC Cancer Gene Census, were depleted in this age group. When we used functional enrichment analysis to explain this unexpected result we discovered that COSMIC genes with recessive disease phenotypes were enriched for DNA repair and cell cycle control. The non-mutated genes in these pathways are orthologous to those underlying stress-induced mutation in bacteria, which results in the clustering of single nucleotide variations. COSMIC genes were less common in regions where the probability of observing mutational clusters is high, although they are approximately 2-fold more likely to harbor mutational clusters compared to other human genes. Our results suggest this ancient mutational response to stress that evolved among prokaryotes was co-opted to maintain diversity in the germline and immune system, while the original phenotype is restored in cancer. Reversion to a stress-induced mutational response is a hallmark of cancer that allows for effectively searching “protected” genome space where genes causally implicated in cancer are located and underlies the high adaptive potential and concomitant therapeutic resistance that is characteristic of cancer.

The space occupied by evolutionarily advanced ant societies can be subdivided into functional sites, such as broodchambers; peripheral nest chambers; kitchen middens; and foraging routes. Many predators and social parasites are specially adapted to make their living inside specific niches created by ants. In particular, the foraging paths of certain ant species are frequented by predatory and kleptoparasitic arthropods, including one striking example, the nitidulid beetle, Amphotis marginata. Adults of this species obtain the majority of their nutrition by acting as a kind of “highwayman” on the foraging trails of the ant Lasius fuliginosus, where they solicit regurgitation from food laden ant-workers by mimicking the ant’s food-begging signals. Employing food labeled with the radio isotope [superscript 32]P, we assessed the quantities of food the beetles siphoned-off of food-laden ants, and we investigated the site preferences, behavioral mechanisms and possible morphological adaptations underlying the food kleptoparasitism of A. marginata.