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The diverse, specialized genes in today's lifeforms evolved from a commoncore of ancient, elementary genes. However, these genes did not evolveindividually: gene expression is controlled by a complex network ofinteractions, and alterations in one gene may drive reciprocal changes in itsproteins' binding partners. We show that the topology of a leukemia generegulatory network is strongly coupled with evolutionary properties.Slowly-evolving ("cold"), old genes tend to interact with each other, as dorapidly-evolving ("hot"), young genes, causing genes to evolve in clusters. Weargue that gene duplication placed old, cold genes at the center of thenetwork, and young, hot genes on the periphery, and demonstrate this withsingle-node centrality measures and two new measures of efficiency. Integratingcentrality measures with evolutionary information, we define amedically-relevant "cancer network core," strongly enriched for common cancermutations ($p=2\times 10^{-14}$). This could aid in identifying drivermutations and therapeutic targets.

Evolutionary and topological properties of gene modules and driver mutations in a leukemia gene regulatory network