COSMIC: the Catalogue Of Somatic Mutations In Cancer
Open accessAbstract
COSMIC, the Catalogue Of Somatic Mutations In Cancer (https://cancer.sanger.ac.uk) is the most detailed and comprehensive resource for exploring the effect of somatic mutations in human cancer. The latest release, COSMIC v86 (August 2018), includes almost 6 million coding mutations across 1.4 million tumour samples, curated from over 26 000 publications. In addition to coding mutations, COSMIC covers all the genetic mechanisms by which somatic mutations promote cancer, including non-coding mutations, gene fusions, copy-number variants and drug-resistance mutations. COSMIC is primarily hand-curated, ensuring quality, accuracy and descriptive data capture. Building on our manual curation processes, we are introducing new initiatives that allow us to prioritize key genes and diseases, and to react more quickly and comprehensively to new findings in the literature. Alongside improvements to the public website and data-download systems, new functionality in COSMIC-3D allows exploration of mutations within three-dimensional protein structures, their protein structural and functional impacts, and implications for druggability. In parallel with COSMIC's deep and broad variant coverage, the Cancer Gene Census (CGC) describes a curated catalogue of genes driving every form of human cancer. Currently describing 719 genes, the CGC has recently introduced functional descriptions of how each gene drives disease, summarized into the 10 cancer Hallmarks.
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All of the Alzheimer's disease-enriched genes represent critical tumor suppressor genes widely implicated in various cancers and clonal hematopoiesis.
“All of these AD-enriched genes represent critical TSGs widely implicated in various cancers33 and CH34.”
From Somatic cancer variants enriched in Alzheimer’s disease microglia-like cells drive inflammatory and proliferative states (2026) · cites this paper as [33]
The Cancer gene census section (page unavailable) describes genes implicated in cancer and explains that some are classified as tumour suppressor genes. It does not identify the AD-enriched genes or establish that all of them are tumour suppressors implicated in various cancers. The separate clonal-hematopoiesis assertion is attached to citation 34, not this source. (LLM, conf=0.78)
Experimental — accuracy not yet measuredTP53 was primarily mutated at known hotspots R175, R248, R273, and R282, or had nonsense or frameshift mutations.
“TP53 was primarily mutated at known hotspots R175, R248, R273, and R282 (refs. 59–61), or had nonsense or frameshift mutations”
From The origins and genetic interactions of KRAS mutations are allele- and tissue-specific (2021) · cites this paper as [61]
MAP2K4 primarily had missense mutations at known mutational hotspots.
“MAP2K4 primarily had missense mutations at known mutational hotspots61”
From The origins and genetic interactions of KRAS mutations are allele- and tissue-specific (2021) · cites this paper as [61]
All TP53 mutations were either predicted to be deleterious or previously identified recurrent mutations.
“All were either predicted to be deleterious76,77 or previously identified recurrent mutations61”
From The origins and genetic interactions of KRAS mutations are allele- and tissue-specific (2021) · cites this paper as [61]
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- Authors
- Tate, J. G., Bamford, S., Jubb, H. C., Sondka, Z., Beare, D. M., Bindal, N., Boutselakis, H., Cole, C. G., Creatore, C., Dawson, E., Fish, P., Harsha, B., Hathaway, C., Jupe, S. C., Kok, C. Y., Noble, K., Ponting, L., Ramshaw, C. C., Rye, C. E., Speedy, H. E., Stefancsik, R., Thompson, S. L., Wang, S., Ward, S., Campbell, P. J., & Forbes, S. A.
- Affiliations
- Wellcome Sanger Institute (GB)
- Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge CB10 1SA, UK
- Corresponding author
- Tate, John G
- ORCID
- Venue
- Nucleic Acids Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-10-29
- Volume
- 47
- Issue
- D1
- Pages
- D941-D947
- ISSN
- 0305-1048 (ISSN-L)
- 1362-4962
- PMC
- PMC6323903
- OpenAlex
- W2898789672
- Cited by
- 4,867
- References
- 22
- Citations by year
- 2026: 358 · 2025: 565 · 2024: 740 · 2023: 806 · 2022: 789 · 2021: 829 · 2020: 545 · 2019: 205 · 2018: 14 · 2017: 5 · 2016: 2 · 2013: 1 · 2012: 1
- FWCI
- 124.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Nucleic Acids Research (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust (206194)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genomics and Rare Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Keywords
- COSMIC, somatic mutations, cancer genomics, coding mutations, non-coding mutations, gene fusion, copy number variation, drug resistance mutations, manual curation, protein structure, druggability, Cancer Gene Census, cancer hallmarks
- MeSH terms
- Genes, Humans, Mutation, Neoplasms, Protein Conformation, Databases, Nucleic Acid
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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