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The COSMIC Cancer Gene Census: describing genetic dysfunction across all human cancers

Nature Reviews Cancervolume 18pages696705 (2018) | Download Citation


The Catalogue of Somatic Mutations in Cancer (COSMIC) Cancer Gene Census (CGC) is an expert-curated description of the genes driving human cancer that is used as a standard in cancer genetics across basic research, medical reporting and pharmaceutical development. After a major expansion and complete re-evaluation, the 2018 CGC describes in detail the effect of 719 cancer-driving genes. The recent expansion includes functional and mechanistic descriptions of how each gene contributes to disease generation in terms of the key cancer hallmarks and the impact of mutations on gene and protein function. These functional characteristics depict the extraordinary complexity of cancer biology and suggest multiple cancer-related functions for many genes, which are often highly tissue-dependent or tumour stage-dependent. The 2018 CGC encompasses a second tier, describing an expanding list of genes (currently 145) from more recent cancer studies that show supportive but less detailed indications of a role in cancer.

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COSMIC Cancer Gene Census: Database:


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The authors would like to thank J. Tate, who created the web pages presenting the functional descriptions of cancer genes. They also thank C. Rye, N. Bindal and C. Ramshaw as well as the COSMIC and Open Targets teams for testing and improving these pages. This work was supported by the Wellcome Trust (grant 206194) and by Open Targets (grant OTAR007).

Reviewer information

Nature Reviews Cancer thanks F. Ciccarelli, J. Korbel and the other anonymous reviewer(s) for their contribution to the peer review of this work.

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  1. Wellcome Sanger Institute, Wellcome Genome Campus, Hinxton, Cambridge, UK

    • Zbyslaw Sondka
    • , Sally Bamford
    • , Charlotte G. Cole
    • , Sari A. Ward
    •  & Simon A. Forbes
  2. Open Targets, Wellcome Genome Campus, Hinxton, Cambridge, UK

    • Zbyslaw Sondka
    •  & Ian Dunham
  3. European Molecular Biology Laboratory, European Bioinformatics Institute (EMBL-EBI), Wellcome Genome Campus, Hinxton, Cambridge, UK

    • Ian Dunham


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Z.S. researched data for the article, substantially contributed to the discussion of content and wrote, reviewed and edited the article. S.B., C.G.C. and S.A.W. researched data and reviewed and edited the article. I.D. substantially contributed to the discussion of content and reviewed and edited the article. S.A.F. substantially contributed to the discussion of content and wrote, reviewed and edited the article.

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The authors declare no competing interests.

Corresponding author

Correspondence to Zbyslaw Sondka.


Synthetic lethality

A mechanism using a combination of genetic and induced effects (for example, by a therapeutic agent) working together to induce cell death, where any single one of these effects is non-lethal.

Gain of function

A type of mutation resulting in an altered gene product with intensified activity or with a new biological function (neomorphic mutation).

Loss of function

A type of mutation resulting in an altered gene product with lower or no biological function.

Nucleotide excision repair

(NER). A DNA repair mechanism that removes DNA damage induced by ultraviolet light — mostly thymine dimers — and uses the complementary undamaged strand as a template to repair the damage.

Wilms tumour

Another name for nephroblastoma, a malignant embryonal neoplasm of the kidney.

Epithelial-to-mesenchymal transition

(EMT). A process in which epithelial cells lose cell polarity and cell–cell adhesion with accompanying increases in migratory and invasive capacities; EMT occurs during embryogenesis, fibrosis and wound healing but may also be an early event in cancer metastasis.


A form of programmed cell death triggered in anchorage-dependent cells by detachment of the cell from the extracellular matrix.

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