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Cancer

Tumours outside the mutation box

Nature volume 506, pages 438–439 (2014)Cite this article

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Analyses of ependymoma brain tumours reveal a gene rearrangement in one subtype, but no DNA mutations in two others, suggesting that mechanisms for cancer initiation are broader than is typically thought. See Articles p.445 & p.451

Ever since the identification1,2 in 1982 of mutated human genes that drive cancer, a massive body of evidence has established the paradigm that cancer results from mutations in specific genes. The recent wave of genome sequencing of human tumours has confirmed this concept, but it has also identified some tumours with surprisingly few cancer-associated gene mutations. The results presented in this issue further urge us to revisit the role of gene mutations in cancer. In their genomic analyses of three subtypes of ependymoma brain tumour, Parker et al.3 (page 451) and Mack et al.4 (page 445) find that one subtype carries an intrachromosomal translocation that creates a new tumour-driving gene, another lacks tumour-driving mutations but has aberrant epigenetic modifications, and a third shows neither gene mutations nor epigenetic aberrations.

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Figure 1: Genomic characterization of ependymomas.

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Authors and Affiliations

  1. Rogier Versteeg is in the Department of Oncogenomics, Academic Medical Center, University of Amsterdam, 1105 AZ Amsterdam, the Netherlands.,

    Rogier Versteeg

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  1. Rogier Versteeg
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Correspondence to Rogier Versteeg.

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Versteeg, R. Tumours outside the mutation box. Nature 506, 438–439 (2014). https://doi.org/10.1038/nature13061

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