Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins.

ABSTRACT: Genotypic differences greatly influence susceptibility and resistance to disease. Understanding genotype-phenotype relationships requires that phenotypes be viewed as manifestations of network properties, rather than simply as the result of individual genomic variations. Genome sequencing efforts have identified numerous germline mutations, and large numbers of somatic genomic alterations, associated with a predisposition to cancer. However, it remains difficult to distinguish background, or 'passenger', cancer mutations from causal, or 'driver', mutations in these data sets. Human viruses intrinsically depend on their host cell during the course of infection and can elicit pathological phenotypes similar to those arising from mutations. Here we test the hypothesis that genomic variations

SUBMITTER: Rozenblatt-Rosen O 

PROVIDER: S-EPMC3408847 | biostudies-literature | 2012 Jul

REPOSITORIES: biostudies-literature