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

ROZENBLATT-ROSEN, Orit ; DEO, Rahul C ; PEVZNER, Samuel J ; ABDERAZZAQ, Fieda ; BYRDSON, Danielle ; CARVUNIS, Anne-Ruxandra ; CHEN, Alyce A ; JINGWEI CHENG ; CORRELL, Mick ; DUARTE, Melissa ; CHANGYU FAN ; FELTKAMP, Mariet C ; PADI, Megha ; FICARROL, Scott B ; FRANCHI, Rachel ; GARG, Brijesh K ; GULBAHCE, Natali ; TONG HAO ; HOLTHAUS, Amy M ; JAMES, Robert ; KORKHIN, Anna ; LITOVCHICK, Larisa ; MAR, Jessica C ; ADELMANT, Guillaume ; PAK, Theodore R ; RABELLO, Sabrina ; RUBIO, Renee ; YUN SHEN ; SINGH, Saurav ; SPANGLE, Jennifer M ; TASAN, Murat ; WANAMAKER, Shelly ; WEBBER, James T ; ROECKLEIN-CANFIELD, Jennifer ; CALDERWOOD, Michael A ; JOHANNSEN, Eric ; BARABASI, Albert-László ; BEROUKHIM, Rameen ; KIEFF, Elliott ; CUSICK, Michael E ; HILL, David E ; MÜNGER, Karl ; MARTO, Jarrod A ; QUACKENBUSH, John ; ROTH, Frederick P ; ROLLAND, Thomas ; DECAPRIO, James A ; VIDAL, Marc ; GRACE, Miranda ; DRICOT, Amélie ; ASKENAZI, Manor ; TAVARES, Maria

Nature (London), 2012-07, Vol.487 (7408), p.491-495 [Periódico revisado por pares]

London: Nature Publishing Group

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Título:
Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins
Autor: ROZENBLATT-ROSEN, Orit ; DEO, Rahul C ; PEVZNER, Samuel J ; ABDERAZZAQ, Fieda ; BYRDSON, Danielle ; CARVUNIS, Anne-Ruxandra ; CHEN, Alyce A ; JINGWEI CHENG ; CORRELL, Mick ; DUARTE, Melissa ; CHANGYU FAN ; FELTKAMP, Mariet C ; PADI, Megha ; FICARROL, Scott B ; FRANCHI, Rachel ; GARG, Brijesh K ; GULBAHCE, Natali ; TONG HAO ; HOLTHAUS, Amy M ; JAMES, Robert ; KORKHIN, Anna ; LITOVCHICK, Larisa ; MAR, Jessica C ; ADELMANT, Guillaume ; PAK, Theodore R ; RABELLO, Sabrina ; RUBIO, Renee ; YUN SHEN ; SINGH, Saurav ; SPANGLE, Jennifer M ; TASAN, Murat ; WANAMAKER, Shelly ; WEBBER, James T ; ROECKLEIN-CANFIELD, Jennifer ; CALDERWOOD, Michael A ; JOHANNSEN, Eric ; BARABASI, Albert-László ; BEROUKHIM, Rameen ; KIEFF, Elliott ; CUSICK, Michael E ; HILL, David E ; MÜNGER, Karl ; MARTO, Jarrod A ; QUACKENBUSH, John ; ROTH, Frederick P ; ROLLAND, Thomas ; DECAPRIO, James A ; VIDAL, Marc ; GRACE, Miranda ; DRICOT, Amélie ; ASKENAZI, Manor ; TAVARES, Maria
Assuntos: Adenoviridae - genetics ; Adenoviridae - metabolism ; Adenoviridae - pathogenicity ; Apoptosis ; Binding sites ; Biological and medical sciences ; Cancer ; Computational biology ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm - genetics ; Genetic aspects ; Genome, Human - genetics ; Genomes ; Health aspects ; Herpes viruses ; Herpesvirus 4, Human - genetics ; Herpesvirus 4, Human - metabolism ; Herpesvirus 4, Human - pathogenicity ; Host-Pathogen Interactions - genetics ; Host-tumor relations. Immunology. Biological markers ; Human papillomavirus ; Humans ; Mass spectrometry ; Medical sciences ; Mutation ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - pathology ; Oncogenic Viruses - genetics ; Oncogenic Viruses - metabolism ; Oncogenic Viruses - pathogenicity ; Open Reading Frames - genetics ; Papillomaviridae - genetics ; Papillomaviridae - metabolism ; Papillomaviridae - pathogenicity ; Perturbation (Mathematics) ; Physiological aspects ; Polyomavirus - genetics ; Polyomavirus - metabolism ; Polyomavirus - pathogenicity ; Proteins ; Receptors, Notch - metabolism ; Signal Transduction ; Systems biology ; Tumors ; Two-Hybrid System Techniques ; Viral proteins ; Viral Proteins - genetics ; Viral Proteins - metabolism
É parte de: Nature (London), 2012-07, Vol.487 (7408), p.491-495
Notas: ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
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Descrição: 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 and tumour viruses may cause cancer through related mechanisms, by systematically examining host interactome and transcriptome network perturbations caused by DNA tumour virus proteins. The resulting integrated viral perturbation data reflects rewiring of the host cell networks, and highlights pathways, such as Notch signalling and apoptosis, that go awry in cancer. We show that systematic analyses of host targets of viral proteins can identify cancer genes with a success rate on a par with their identification through functional genomics and large-scale cataloguing of tumour mutations. Together, these complementary approaches increase the specificity of cancer gene identification. Combining systems-level studies of pathogen-encoded gene products with genomic approaches will facilitate the prioritization of cancer-causing driver genes to advance the understanding of the genetic basis of human cancer.
Editor: London: Nature Publishing Group
Idioma: Inglês

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

London: Nature Publishing Group

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