ArticleMolecular systems biology2015
Cancer type-dependent genetic interactions between cancer driver alterations indicate plasticity of epistasis across cell types.
Article in Molecular systems biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 65 citations in OpenAlex.
- Synthetic lethality in cancer drug discovery: challenges and opportunities.Nature reviews. Drug discovery · 2026Review
- Drug molecular representations for drug response predictions: a comprehensive investigation via machine learning methods.Scientific reports · 2025Article
- Considerations in the search for epistasis.Genome biology · 2024Review
- Synergistic epistasis among cancer drivers can rescue early tumors from the accumulation of deleterious passengers.PLoS computational biology · 2024Article
- Non-Association of Driver Alterations in PTEN with Differential Gene Expression and Gene Methylation in IDH1 Wildtype Glioblastomas.Brain sciences · 2023Article
- Mutational signatures are markers of drug sensitivity of cancer cells.Nature communications · 2022Article
- Immunohistochemical Assays for Bladder Cancer Molecular Subtyping: Optimizing Parsimony and Performance of Lund Taxonomy Classifiers.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2022Article
- Higher order genetic interactions switch cancer genes from two-hit to one-hit drivers.Nature communications · 2021Article
- The somatic molecular evolution of cancer: Mutation, selection, and epistasis.Progress in biophysics and molecular biology · 2021Article
- Identification of putative actionable alterations in clinically relevant genes in breast cancer.British journal of cancer · 2021Article
- Evolutionary dependencies show paths to cancer development.Nature genetics · 2020Article
- Discovering functional evolutionary dependencies in human cancers.Nature genetics · 2020Article
- Clonal evolution driven by superdriver mutations.BMC evolutionary biology · 2020Article
- Genetic Interaction-Based Biomarkers Identification for Drug Resistance and Sensitivity in Cancer Cells.Molecular therapy. Nucleic acids · 2019Article
- Changes in gene expression predictably shift and switch genetic interactions.Nature communications · 2019Article
- Leveraging genetic interactions for adverse drug-drug interaction prediction.PLoS computational biology · 2019Article
- Clinical validation of coexisting driver mutations in colorectal cancers.Human pathology · 2019Article
- Passenger mutations accurately classify human tumors.PLoS computational biology · 2019Article
- Predicting drug response of tumors from integrated genomic profiles by deep neural networks.BMC medical genomics · 2019Article
- Identifying Mutually Exclusive Gene Sets with Prognostic Value and Novel Potential Driver Genes in Patients with Glioblastoma.BioMed research international · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancers, like many diseases, are normally caused by combinations of genetic alterations rather than by changes affecting single genes. It is well established that the genetic alterations that drive cancer often interact epistatically, having greater or weaker consequences in combination than expected from their individual effects. In a stringent statistical analysis of data from > 3,000 tumors, we find that the co-occurrence and mutual exclusivity relationships between cancer driver alterations change quite extensively in different types of cancer. This cannot be accounted for by variation in tumor heterogeneity or unrecognized cancer subtypes. Rather, it suggests that how genomic alterations interact cooperatively or partially redundantly to driver cancer changes in different types of cancers. This re-wiring of epistasis across cell types is likely to be a basic feature of genetic architecture, with important implications for understanding the evolution of multicellularity and human genetic diseases. In addition, if this plasticity of epistasis across cell types is also true for synthetic lethal interactions, a synthetic lethal strategy to kill cancer cells may frequently work in one type of cancer but prove ineffective in another.
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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.