Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Although it has long been recognized that the exonucleolytic proofreading activity intrinsic to the replicative DNA polymerases Pol δ and Pol ε is essential for faithful replication of DNA, evidence that defective DNA polymerase proofreading contributes to human malignancy has been limited. However, recent studies have shown that germline mutations in the proofreading domains of Pol δ and Pol ε predispose to cancer, and that somatic Pol ε proofreading domain mutations occur in multiple sporadic tumours, where they underlie a phenotype of 'ultramutation' and favourable prognosis. In this Review, we summarize the current understanding of the mechanisms and consequences of polymerase proofreading domain mutations in human malignancies, and highlight the potential utility of these variants as novel cancer biomarkers and therapeutic targets.

Original publication

DOI

10.1038/nrc.2015.12

Type

Journal article

Journal

Nat Rev Cancer

Publication Date

02/2016

Volume

16

Pages

71 - 81

Keywords

DNA Polymerase II, DNA Polymerase III, DNA Replication, DNA-Directed DNA Polymerase, Endometrial Neoplasms, Female, Genetic Predisposition to Disease, Humans, Mutation, Neoplasms, Poly-ADP-Ribose Binding Proteins, Prognosis, Saccharomyces cerevisiae