Abstract: The risk of developing cancer is correlated with body size and lifespan within species. Between species, however, there is no correlation between cancer and either body size or lifespan, indicating that large, long-lived species have evolved enhanced cancer protection mechanisms. Elephants and their relatives (Proboscideans) are a particularly interesting lineage for the exploration of mechanisms underlying the evolution of augmented cancer resistance because they evolved large bodies recently within a clade of smaller bodied species (Afrotherians). Here, we explore the contribution of gene duplication to body size and cancer risk in Afrotherians. Through comparative genomics we identified a duplicate SOD1 gene Proboscideans that we functionally characterize and show may underlie some aspects of their remarkable anti-cancer cell biology. These data suggest that duplication of tumor suppressor genes facilitated the evolution of increased body size by compensating for decreasing intrinsic cancer risk.

Biography: Received my BS University at Albany and worked with Caro-Beth Stewart on sperm protein evolution in humans and other primates. Received by PhD and did a post-doc with Günter Wagner at Yale, working on the evolution of pregnancy and how transcription factor proteins evolve new functions. Moved on to an Assistant Prof position in the Dept. of Human Genetics at the University of Chicago, where I still worked on the evolution of pregnancy but started a new research project on why some animals seem to be (almost) cancer free. Moved last year to the University at Buffalo and still work on the evolution of pregnancy and how that impacts human pregnancy complications, and expanded the research program on cancer-free species to elephants, armadillos, whales, bats, and most recently Galapagos tortoises.