biostudies-literatureRozenblatt-Rosen ONHLBI NIH HHSNHGRI NIH HHSNCI NIH HHSNIGMS NIH HHS491-5https://www.ebi.ac.uk/biostudies/studies/S-EPMC3408847biostudies-literatureUnknown487(7408)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 NatureInterpreting cancer genomes using systematic host network perturbations by tumour virus proteins.PMC3408847F32 GM095284T32HL007208R01CA093804K08HL098361U01 CA141583R01 CA081135R01 CA047006R01CA063113R01CA066980F32GM095284R01 HG001715R01 CA066980P01CA050661R01 CA093804R01CA131354R01 CA063113R01CA085180P01 CA050661P50HG004233T32 HL007208R01CA081135R01 CA131354K25 HG006031R01HG001715K08 HL098361U01CA141583P50 HG004233R01CA047006K08 CA122833R01 CA085180K25HG006031Roth FPHolthaus AMPadi MBarabasi ALDuarte MGarg BKHao TRabello SGulbahce NJames RWebber JTCorrell MMunger KShen YSingh SCalderwood MARozenblatt-Rosen ODricot AByrdsong DMar JCGrace MCarvunis ARHill DETasan MTavares MQuackenbush JVidal MPevzner SJDeCaprio JAAdelmant GRolland TFeltkamp MCRubio RFranchi RSpangle JMBeroukhim RKieff EFicarro SBJohannsen EWanamaker SFan CCheng JAskenazi MRoecklein-Canfield JLitovchick LKorkhin ADeo RCAbderazzaq FChen AAMarto JAPak TRCusick MEfalseInterpreting cancer genomes using systematic host network perturbations by tumour virus proteins.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 2012-01-01T00:00:00Z2012 Jul2026-05-04T23:32:30.079Z2026-04-07T21:05:02.762ZS-EPMC34088472281058610.1038/nature11288