Abstract
Classically tumor evolution is considered to be driven by serial acquisition of mutations that increase the fitness of the tumor and evolve its phenotypes until a malignant lesion develops. I will discuss data and analysis from kidney (and other) cancers that challenges the canonical view. Specifically, genomic data from many sequencing projects is challenging this paradigm, identifying cancers that do not appear to have driving mutations (at least as they are classically understood), identifying clear examples of branched evolution, and examples of sub-clones that appear to have synergistic fitness.