ArticleNature communications2021
Cancer gene mutation frequencies for the U.S. population.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 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.
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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.
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Who cites it
132 citing papers in PubMed, 194 citations in OpenAlex.
- Chromatin modifiers KMT2D, cBAF, and p300 cooperatively facilitate de novo binding of transcription factors on enhancers.Nature communications · 2026Article
- Rewiring Cellular Context as A Central Mechanism Governing Cancer Stem Cell Survival: Insights from ESC Comparisons.Stem cell reviews and reports · 2026Review
- Bioengineered systems to exploit tumor microenvironment metabolism.Trends in cancer · 2026Review
- Targeting thymine DNA glycosylase induces synthetic lethality in p53-deficient cancers.Nature chemical biology · 2026Article
- Unbiased assessment of APR-246 responsive p53 mutants in ovarian cancer.Cell death discovery · 2026Article
- A catalogue of missense and nonsense mutation abundances for the U.S. cancer patient population.medRxiv : the preprint server for health sciences · 2026Article
- Rescuing TP53 from nonsense: novel triazoles for translational readthrough via optimized drug design.Scientific reports · 2026Article
- Emerging evidence on micro- and nanoplastics carcinogenicity: mechanisms, models, and signaling networks.Molecular cancer · 2026Review
- Discovery of BBO-11818, a Potent and Selective Noncovalent Inhibitor of (ON) and (OFF) KRAS with Activity against Multiple Oncogenic Mutants.Cancer discovery · 2026Article
- The GF-NEO discovery platform unveils a [KQE][DG] sequence motif within fusion neoantigens in pediatric cancer.iScience · 2026Article
- Pan-cancer analysis of cholesterol metabolism reveals the uptake as a modulator of tumor immune features and of the KRAS pathway.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Review
- The impact of AI on modern oncology from early detection to personalized cancer treatment.NPJ precision oncology · 2026Review
- Dominant-negative TP53 mutations potentiated by the HSF1-regulated proteostasis network.Molecular cell · 2026Article
- KRAS Inhibition in Pancreatic Ductal Adenocarcinoma.Journal of clinical medicine · 2026Review
- Molecular grammars of predicted intrinsically disordered regions that span the human proteome.Cell · 2026Article
- Prognostic impact of p53 and HER2 immunohistochemistry profiles in colorectal carcinoma.Pathology oncology research : POR · 2026Article
- Tumor microenvironment-activated ferritin nanovector enables enhanced tumor delivery of KRASFrontiers in cell and developmental biology · 2026Article
- Integrated Proteogenomic Characterization Identifies Breast Cancer Immune Subgroups and Subtype-Specific Therapeutic Strategies.Research (Washington, D.C.) · 2026Article
- Geometrically Encoded Positioning of Introns, Intergenic Segments, and Exons in the Human Genome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
72 more citing papers are in PubMed but not listed here.
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 at 2 institutions in 1 country.
Funding
Abstract
Mutations play a fundamental role in the development of cancer, and many create targetable vulnerabilities. There are both public health and basic science benefits from the determination of the proportion of all cancer cases within a population that include a mutant form of a gene. Here, we provide the first such estimates by combining genomic and epidemiological data. We estimate KRAS is mutated in only 11% of all cancers, which is less than PIK3CA (13%) and marginally higher than BRAF (8%). TP53 is the most commonly mutated gene (35%), and KMT2C, KMT2D, and ARID1A are among the ten most commonly mutated driver genes, highlighting the role of epigenetic dysregulation in cancer. Analysis of major cancer subclassifications highlighted varying dependencies upon individual cancer drivers. Overall, we find that cancer genetics is less dominated by high-frequency, high-profile cancer driver genes than studies limited to a subset of cancer types have suggested.
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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.