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Review
. 2004 Mar;4(3):177-83.
doi: 10.1038/nrc1299.

A census of human cancer genes

P Andrew Futreal  1 , Lachlan Coin, Mhairi Marshall, Thomas Down, Timothy Hubbard, Richard Wooster, Nazneen Rahman, Michael R Stratton
Affiliations
Review

A census of human cancer genes

P Andrew Futreal et al. Nat Rev Cancer. 2004 Mar.

Abstract

A central aim of cancer research has been to identify the mutated genes that are causally implicated in oncogenesis (‘cancer genes’). After two decades of searching, how many have been identified and how do they compare to the complete gene set that has been revealed by the human genome sequence? We have conducted a ‘census’ of cancer genes that indicates that mutations in more than 1% of genes contribute to human cancer. The census illustrates striking features in the types of sequence alteration, cancer classes in which oncogenic mutations have been identified and protein domains that are encoded by cancer genes.

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Figures

Figure 1
Figure 1. Mutation types in human cancer
Cancer genes showing somatic mutations, germline mutations or both somatic and germline mutations in human cancers.
Figure 2
Figure 2. Proportion of translocated genes in human cancer
Somatically mutated cancer genes with translocations, with mutations other than translocations or with both.
Figure 3
Figure 3. Dominant and recessive mutations in human cancer
a | Cancer genes with germline mutations acting in a dominant or recessive manner. b | Cancer genes with somatic mutations acting in a dominant or recessive manner.
Figure 4
Figure 4. Proportion of genes associated with different tumour types
a | Cancer genes with germline mutations by tumour class (for definitions see text and supplementary tables, the category ‘numerous’ refers to cancer genes with combinations of two or more classes). b | Cancer genes with somatic mutations by tumour class.
See this image and copyright information in PMC

References

    1. Reddy EP, Reynolds RK, Santos E, Barbacid M. A point mutation is responsible for the acquisition of transforming properties by the T24 human bladder carcinoma oncogene. Nature. 1982;300:149–152. - PubMed
    1. Tabin CJ, et al. Mechanism of activation of a human oncogene. Nature. 1982;300:143–149. [References 1 and 2 are seminal papers that defined the existence of oncogene sequences in cancer-cell genomes and that first identified a mutation involved in human cancer.] - PubMed
    1. Parsons R, et al. Hypermutability and mismatch repair deficiency in RER+ tumor cells. Cell. 1993;75:1227–1236. - PubMed
    1. Fishel R, et al. The human mutator gene homolog MSH2 and its association with hereditary nonpolyposis colon cancer. Cell. 1993;75:1027–1038. - PubMed
    1. Leach FS, et al. Mutations of a mutS homolog in hereditary nonpolyposis colorectal cancer. Cell. 1993;75:1215–1225. - PubMed