Cancer initiation and progression are driven by a series of genetic and epigenetic alterations that cause either activation (gain-of-function) of oncogenes, or inactivation (loss-of-function) of tumor suppressor genes, - both accompanied by broad alterations in genome utilization and gene expression programs. The nature of these alterations and the mechanisms that lead to such genomic changes is the focus of this GRC series. The field has seen a dramatic shift in the past decade from a pure genetic to a mixed genetic/epigenetic explanation of cancer. Another dramatic shift has consisted in the emergence of increasingly powerful technologies for genome-wide analysis of genetic, epigenetic, or other mechanistic alterations. These changes will have far-reaching implications for our capacity to understand the causes of disease, to decipher the pathways and molecules involved, as well as to devise new strategies for prevention and treatment. Sessions in the meeting will be devoted to the recent developments in cancer genomics and epigenomics, to the emerging roles of non-coding RNA species, as well as to recent advances in modeling cancer development and therapy.