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Seminars in cancer biology
Oct, 2010;20 (5): 281-93.

DNA replication fidelity and cancer.

Bradley D Preston, Tina M Albertson, Alan J Herr
Author Information
  1. Bradley D Preston: Department of Pathology, University of Washington, Seattle, WA 98195, USA. bradp@u.washington.edu
PMID: 20951805 DOI: 10.1016/j.semcancer.2010.10.009

Abstract

Cancer is fueled by mutations and driven by adaptive selection. Normal cells avoid deleterious mutations by replicating their genomes with extraordinary accuracy. Here we review the pathways governing DNA replication fidelity and discuss evidence implicating replication errors (point mutation instability or PIN) in carcinogenesis.

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Grants

  1. P30 ES07033/NIEHS NIH HHS
  2. R01 CA098243/NCI NIH HHS
  3. P20 CA103728/NCI NIH HHS
  4. P01 AG001751/NIA NIH HHS
  5. R01 ES09927/NIEHS NIH HHS
  6. R01 CA111582/NCI NIH HHS
  7. P01 AG01751/NIA NIH HHS
  8. P01 CA077852/NCI NIH HHS
  9. P30 ES007033/NIEHS NIH HHS
  10. P01 CA77852/NCI NIH HHS

MeSH Term

Animals
Chromosome Aberrations
DNA Damage
DNA Mismatch Repair
DNA Repair
DNA Replication
DNA-Directed DNA Polymerase
Gene Rearrangement
Humans
Microsatellite Instability
Mutation
Neoplasms
Point Mutation

Chemicals

DNA-Directed DNA Polymerase
Journal Article Research Support, N.I.H., Extramural Review
Article has an altmetric score of 8

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Created with Highcharts 10.0.0replicationmutationsDNAfidelityCancerfueleddrivenadaptiveselectionNormalcellsavoiddeleteriousreplicatinggenomesextraordinaryaccuracyreviewpathwaysgoverningdiscussevidenceimplicatingerrorspointmutationinstabilityPINcarcinogenesiscancer

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