ArticleNature2012
Interpreting cancer genomes using systematic host network perturbations by tumour virus proteins.
Article in Nature, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05381038 (Optimizing and Personalising Azacitidine Combination Therapy for Treating Solid Tumours Using the Quadratic Phenotypic Optimization Platform), which is not on this map. Cited by 262 papers, 2 of them syntheses that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Optimizing and Personalising Azacitidine Combination Therapy for Treating Solid Tumours Using the Quadratic Phenotypic Optimization Platform (QPOP) and an Artificial Intelligence-based Platform (CURATE.AI)
Who cites it
262 citing papers in PubMed, 2 syntheses or guidelines pooled it, 396 citations in OpenAlex.
- Integration of TP53, DREAM, MMB-FOXM1 and RB-E2F target gene analyses identifies cell cycle gene regulatory networks.Nucleic acids research · 2016Pooled it
- Systems Genetics Analysis of Genome-Wide Association Study Reveals Novel Associations Between Key Biological Processes and Coronary Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2015Pooled it
- The diverse functions of viral microproteins.bioRxiv : the preprint server for biology · 2026Article
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- NeuroViOme: a viral orfeome collection for studies of neurodegenerative disease.Journal of neurovirology · 2026Review
- Effector-host interactome map links type III secretion systems in healthy gut microbiomes to immune modulation.Nature microbiology · 2026Article
- Pharmacologic reversion of Merkel cell carcinoma via CBP/p300 inhibition.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Systematic Discovery of Pathogen Effector Functions across Human Pathogens and Pathways.bioRxiv : the preprint server for biology · 2025Article
- The adenovirus E4orf1 protein initiates a feedback loop involving insulin and growth factor receptors, AKT, and NF-κB, leading to abnormal DNA content in infected cells.PLoS pathogens · 2025Article
- The coming era of proteomics-driven precision medicine.National science review · 2025Review
- Structural host-virus interactome profiling of intact infected cells.Nature communications · 2025Article
- Yellow Fever Virus Interactomes Reveal Common and Divergent Strategies of Replication and Evolution for Mosquito-borne Flaviviruses.bioRxiv : the preprint server for biology · 2025Article
- Metabolic modeling elucidates phenformin and atpenin A5 as broad-spectrum antiviral drugs against RNA viruses.Communications biology · 2025Article
- Intrinsic p53 activation restricts gammaherpesvirus driven germinal center B cell expansion during latency establishment.Nature communications · 2025Article
- Review
- The Expression of HPV-16 E5 Oncoprotein Impacts the Transcript Profiles of FGFR2 and EMT-Related Genes in Preneoplastic Anal Epithelium Lesions.International journal of molecular sciences · 2024Article
- Merkel cell polyomavirus small tumor antigen contributes to immune evasion by interfering with type I interferon signaling.PLoS pathogens · 2024Article
202 more citing papers are in PubMed but not listed here.
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Authors and funding
52 authors at 8 institutions in 4 countries.
Funding
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 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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.