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The burden of faulty proofreading in colon cancer

A Corrigendum to this article was published on 26 September 2013

This article has been updated

Our understanding of inherited risk factors for colorectal cancer (CRC) is incomplete. A new study reports the identification of germline CRC risk variants that adversely affect the proofreading function of DNA polymerases encoded by POLE and POLD1.

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Figure 1: Inherited DNA replication defects lead to CRC risk.

Change history

  • 05 September 2013

    In the version of the article initially published, reference 6 (J. Biol. Chem. 281, 4486–4494, 2006) should have been Genome 49, 403–410, 2006. Part of the associated sentence, "Alteration of this amino acid has been shown to lead to mutator phenotypes in yeast6," was revised to "Alteration of the equivalent residue in a related polymerase, POLD1, leads to mutator phenotypes in yeast6." In paragraph 4, alteration of a POLD1 residue in yeast, given as arginine, should have been asparagine. A sentence with an error in paragraph 7, "Similarly, tumors reported by Palles et al.4 that carried the POLE p.Leu424Val exonuclease-deficient germline variant also carried APC alterations," has been changed to state that the POLE p.Leu424Val variant alters an amino acid in the active site of the exonuclease domain. The revised sentence reads "Similarly, tumors reported by Palles et al.4 that carried the POLE p.Leu424Val germline variant, which maps to the active site of the exonuclease domain, also carried APC alterations." The legend for Figure 1 has been amended to include "Adapted with permission from ref. 5."

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Correspondence to Somasekar Seshagiri.

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The author is an employee of Genentech Inc. and holds Roche stocks.

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Seshagiri, S. The burden of faulty proofreading in colon cancer. Nat Genet 45, 121–122 (2013). https://doi.org/10.1038/ng.2540

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