ReviewCell2019
Identifying Epistasis in Cancer Genomes: A Delicate Affair.
Review in Cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed.
- Empowering Inference of Epistasis on the Basis of Mutual Exclusivity, Co-Occurrence, Functional Antagonism and Synergy in ERK-Pathway Oncogenes.International journal of cancer · 2026Article
- Review
- Review
- Identifying multigenic modules under selection in the tumor genome.Bioinformatics (Oxford, England) · 2026Article
- Evolving patterns of co-mutations from tumor initiation to metastatic progression.Nature genetics · 2026Article
- Charting cell-type-specific positive genetic interaction at single-cell resolution for lung adenocarcinoma.NPJ precision oncology · 2026Article
- Integrated in vivo combinatorial functional genomics and spatial transcriptomics of tumours to decode genotype-to-phenotype relationships.Nature biomedical engineering · 2026Article
- A pathway-informed mutual exclusivity framework to detect genetic interactions in pediatric cancer.BMC medical genomics · 2025Article
- Mutations in tumor signaling, metastases, and synthetic lethality establish distinct patterns.PLoS computational biology · 2025Article
- Combinatorial In Vivo Genome Editing Identifies Widespread Epistasis and an Accessible Fitness Landscape During Lung Tumorigenesis.Molecular biology and evolution · 2025Article
- Prevalence and Associations of Co-occurrence ofGlobal medical genetics · 2024Article
- Co-occurring Mutations in Different Genes Can Fuel Oncogenic Signaling and Serve as Metastatic Tumor Markers.bioRxiv : the preprint server for biology · 2024Article
- A latent variable model for evaluating mutual exclusivity and co-occurrence between driver mutations in cancer.bioRxiv : the preprint server for biology · 2024Article
- Network analysis of driver genes in human cancers.Frontiers in bioinformatics · 2024Article
- Conceptual breakthroughs of the long noncoding RNA functional system and its endogenous regulatory role in the cancerous regime.Exploration of targeted anti-tumor therapy · 2024Review
- Pairwise and higher-order epistatic effects among somatic cancer mutations across oncogenesis.Mathematical biosciences · 2023Article
- Novel Alzheimer's disease genes and epistasis identified using machine learning GWAS platform.Scientific reports · 2023Article
- Oncogenic context shapes the fitness landscape of tumor suppression.Nature communications · 2023Article
- Fully accessible fitness landscape of oncogene-negative lung adenocarcinoma.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Leveraging the genetic correlation between traits improves the detection of epistasis in genome-wide association studies.G3 (Bethesda, Md.) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Recent studies of the tumor genome seek to identify cancer pathways as groups of genes in which mutations are epistatic with one another or, specifically, "mutually exclusive." Here, we show that most mutations are mutually exclusive not due to pathway structure but to interactions with disease subtype and tumor mutation load. In particular, many cancer driver genes are mutated preferentially in tumors with few mutations overall, causing mutations in these cancer genes to appear mutually exclusive with numerous others. Researchers should view current epistasis maps with caution until we better understand the multiple cause-and-effect relationships among factors such as tumor subtype, positive selection for mutations, and gross tumor characteristics including mutational signatures and load.
Indexed as
Identifiers
What OpenQuestion holds
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.