ArticleNature genetics2020
Discovering functional evolutionary dependencies in human cancers.
Article in Nature genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Evolving patterns of co-mutations from tumor initiation to metastatic progression.Nature genetics · 2026Article
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.Nature genetics · 2026Article
- Integrative proteomic characterization of human lung adenocarcinoma with KRAS G12 mutations reveals molecular pathogenesis.Journal of advanced research · 2026Article
- Using cancer profiles to identify synthetic lethal therapeutic targets and predictive biomarkers in cancer gene dependency data.Bioinformatics (Oxford, England) · 2026Article
- Carbohydrate-dependent interaction between AMY1A/AMY2B copy number variation and APOA5 rs651821 associated with hypertriglyceridemia in Korean middle-aged adults.BMC nutrition · 2026Article
- Outcomes of patients with or without DNA repair pathway alterations: the MD Anderson IMPACT2 study.NPJ precision oncology · 2026Article
- The inverse relationship between copy number variation burden and age of onset of metabolic syndrome in Korean middle-aged adults.BMC medical genomics · 2026Article
- U2AF1 mutations rescue deleterious exon skipping induced by KRAS mutations.bioRxiv : the preprint server for biology · 2025Article
- Analysis of the mRNA modification machinery alterations in breast cancer through the SCAN-B cohort.NAR cancer · 2025Article
- Precision treatment in breast cancer: Leveraging genetic interactions.Clinical and translational medicine · 2025Article
- The three YTHDF paralogs and VIRMA are strong cross-histotype tumor driver candidates among mNAR cancer · 2024Article
- Clinical and molecular correlates of tumor aneuploidy in metastatic non-small cell lung cancer.Scientific reports · 2024Article
- Evolutionary dependency of cancer mutations in gene pairs inferred by nonsynonymous-synonymous mutation ratios.Genome medicine · 2024Article
- Systematic omics analysis identifies CCR6 as a therapeutic target to overcome cancer resistance to EGFR inhibitors.iScience · 2024Article
- Cancer Evolution: A Multifaceted Affair.Cancer discovery · 2024Article
- Recent advances in anti-inflammatory active components and action mechanisms of natural medicines.Inflammopharmacology · 2023Review
- Genomic Landscapes and Hallmarks of Mutant RAS in Human Cancers.Cancer research · 2022Article
- Clonal somatic copy number altered driver events inform drug sensitivity in high-grade serous ovarian cancer.Nature communications · 2022Article
- APOBEC mutagenesis and selection for NFE2L2 contribute to the origin of lung squamous-cell carcinoma.Lung cancer (Amsterdam, Netherlands) · 2022Article
- Higher order genetic interactions switch cancer genes from two-hit to one-hit drivers.Nature communications · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells retain genomic alterations that provide a selective advantage. The prediction and validation of advantageous alterations are major challenges in cancer genomics. Moreover, it is crucial to understand how the coexistence of specific alterations alters response to genetic and therapeutic perturbations. In the present study, we inferred functional alterations and preferentially selected combinations of events in >9,000 human tumors. Using a Bayesian inference framework, we validated computational predictions with high-throughput readouts from genetic and pharmacological screenings on 2,000 cancer cell lines. Mutually exclusive and co-occurring cancer alterations reflected, respectively, functional redundancies able to rescue the phenotype of individual target inhibition, or synergistic interactions, increasing oncogene addiction. Among the top scoring dependencies, co-alteration of the phosphoinositide 3-kinase (PI3K) subunit PIK3CA and the nuclear factor NFE2L2 was a synergistic evolutionary trajectory in squamous cell carcinomas. By integrating computational, experimental and clinical evidence, we provide a framework to study the combinatorial functional effects of cancer genomic alterations.
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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.