A major premise of this GRC series, now titled DNA Damage, Mutation, and Cancer, has been that much of the cancer associated with environmentally-induced and endogenous DNA damage is linked to damage-dependent mutagenesis. Cells use a network of interconnected pathways to suppress such mutagenesis and thus avoid carcinogenesis. They repair damaged DNA and bypass DNA-replication-blocking lesions by processes that balance efficiency and fidelity. Damage-triggered signaling pathways delay cycling of genetically-compromised cells and may eventually eliminate them. The 2008 conference will place a major emphasis on consequences for human health. A pair of keynote talks that describe "genetic landscapes" of cancer will set the stage for subsequent sessions concerned with specific genetic alternations in cancer cells and with the genetic epidemiology of sporadic cancer. Two additional sessions concerned with health endpoints will focus on cellular responses to chemotherapy-induced DNA damage that may induce secondary cancers, and consider consequences of processing of damaged DNA for tissue growth and development and for aging. Some of these talks will emphasize the value of new model systems - Arabidopsis and zebrafish - to the DNA repair and mutagenesis community. Two sessions will be concerned with molecular starting points of damage-processing pathways: the structural biology and theory of DNA-damage recognition and effects of sequence context and consequences of novel structures in lesion-free DNA. One session aims at biochemical understanding of the balance between error-prone vs. high-fidelity responses to blocked replication forks. One will consider multi-step processing pathways initiated by specific DNA lesions.