ArticleNature biotechnology2016
Identifying recurrent mutations in cancer reveals widespread lineage diversity and mutational specificity.
Article in Nature biotechnology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04872036 (Investigation of Prognostic Biomarkers in Patients With Urothelial Carcinoma Treated With Platinum Regimens), which is not on this map. Cited by 535 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Investigation of Prognostic Biomarkers in Patients With Urothelial Carcinoma Treated With Platinum Regimens
Who cites it
535 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Standards for the classification of pathogenicity of somatic variants in cancer (oncogenicity): Joint recommendations of Clinical Genome Resource (ClinGen), Cancer Genomics Consortium (CGC), and Variant Interpretation for Cancer Consortium (VICC).Genetics in medicine : official journal of the American College of Medical Genetics · 2022Guideline
- Randomized phase II study of preoperative afatinib in untreated head and neck cancers: predictive and pharmacodynamic biomarkers of activity.Scientific reports · 2023Trial
- AKT mutant allele-specific activation dictates pharmacologic sensitivities.Nature communications · 2022Trial
- FGFR4-associated APOBEC3 mutagenesis characterizes HER2-enriched subtype of human breast cancer.British journal of cancer · 2026Article
- Precision oncology in advanced melanoma: molecular landscapes and personalized therapy recommendations from the Molecular Tumor Board Freiburg.NPJ precision oncology · 2026Article
- Functional characterization of the 9q34.13 locus identifies RAPGEF1 as a candidate gene modulating risk for melanoma and nevi via RAS activation.American journal of human genetics · 2026Article
- HER2 targeted therapy resistance in breast cancer: from molecular landscape to clinical aspects.Science China. Life sciences · 2026Review
- Distinct mutational landscapes for germline and somatic cancer variants in forty tumor suppressor genes.American journal of human genetics · 2026Article
- Validation structures for sequence variants of uncertain significance in hereditary cancer.European journal of human genetics : EJHG · 2026Review
- Clinical usability of an explainable AI decision support tool and evaluation of multimodal models in NSCLC.Nature medicine · 2026Observational
- Mutational Landscape ofCurrent issues in molecular biology · 2026Article
- Lipid Metabolism, Lipogenesis, and Resistance to Third Generation EGFR-TKIs.Journal of clinical laboratory analysis · 2026Review
- Melanoma-patient-derived xenograft multi-omics resource melPDomiX maps gain- and loss-of-function alterations.Cell reports · 2026Article
- Long-term competition experiments reveal limited adaptive evolution in human cell lines.Scientific reports · 2026Article
- Convergent Evolution in Tumor Genomes Targets Functional Domains.bioRxiv : the preprint server for biology · 2026Article
- Enhancer and metabolic rewiring by KMT2C-COMPASS or KMT2D-COMPASS family loss in cancer creates druggable vulnerabilities.Nature reviews. Cancer · 2026Review
- Age distinguishes selection from causation in cancer genomes.Nature genetics · 2026Article
- Oncogenicity Variant Interpreter (OncoVI) Supports Harmonized Somatic Variant Interpretation in Precision Oncology.The Journal of molecular diagnostics : JMD · 2026Article
- Whole genome sequencing in oesophageal adenocarcinoma unmasks potential precision therapies.BMC cancer · 2026Article
- Cancer type-specific variation in patterns of driver alterations across 50,000 tumors.Cancer cell · 2026Article
475 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
Mutational hotspots indicate selective pressure across a population of tumor samples, but their prevalence within and across cancer types is incompletely characterized. An approach to detect significantly mutated residues, rather than methods that identify recurrently mutated genes, may uncover new biologically and therapeutically relevant driver mutations. Here, we developed a statistical algorithm to identify recurrently mutated residues in tumor samples. We applied the algorithm to 11,119 human tumors, spanning 41 cancer types, and identified 470 somatic substitution hotspots in 275 genes. We find that half of all human tumors possess one or more mutational hotspots with widespread lineage-, position- and mutant allele-specific differences, many of which are likely functional. In total, 243 hotspots were novel and appeared to affect a broad spectrum of molecular function, including hotspots at paralogous residues of Ras-related small GTPases RAC1 and RRAS2. Redefining hotspots at mutant amino acid resolution will help elucidate the allele-specific differences in their function and could have important therapeutic implications.
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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.