Pervasive duplication of tumor suppressor genes preceded parallel evolution of large bodied Atlantogenatans

While body size and lifespan directly impact an individual's cancer risk within species, we see no such correlation when comparing cancer risk between species - a surprise that is known as Peto's Paradox. While there are many ways that Evolution can resolve this paradox, gene duplication stands out as a particularly parsimonious solution to the problem. Inspired by previous test cases where a tumor suppressor gene duplication was found in a large, long-lived species - such as in elephants - we sought to test whether or not tumor suppressor duplicates are especially enriched among duplicated genes in large *Atlantogenatans*. We find that tumor suppressor duplicates are present in all *Atlantogenatan* genomes, and occured throughout the tree. Tumor suppressor duplicates in Elephants show functional transcription, suggesting that these duplicates have preserved a functional role, and may have permitted the sudden increases in body size we observe throughout *Atlantogenata*.

A Zombie LIF Gene in Elephants Is Upregulated by TP53 to Induce Apoptosis in Response to DNA Damage

Larger organisms with increased cell counts have a theoretically increased risk of cancer; the observation that larger species do not seem to have an increased cancer risk in contradiction to the patterns observed between members within species is known as Peto's Paradox. ere, we show that elephants and their extinct relatives (proboscideans) may have resolved Peto’s paradox in part through refunctionalizing a leukemia inhibitory factor pseudogene (LIF6) with pro-apoptotic functions. LIF6 is transcriptionally upregulated by TP53 in response to DNA damage and translocates to the mitochondria where it induces apoptosis.