Nucleotide-excision repair and prostate cancer risk

Kristin L. Lockett, Isaac V. Snowhite, Jennifer J. Hu

Research output: Contribution to journalShort survey

27 Scopus citations

Abstract

Prostate cancer (CaP) is the most commonly diagnosed nonskin cancer and the second leading cause of cancer death in American men. Its etiology is not fully understood. Ethnicity/race and family history are associated with it, and incidence increases with age. As with other solid tumors, accumulation of mutations and decline in DNA repair during aging may lead to CaP. However, we believe that conducting a large population screening for every cancer susceptibility gene (e.g. DNA repair) is only meaningful, if we can predict to what extent genetic variants contribute to DNA-repair functional phenotype and CaP risk. This review focuses on the association between CaP and nucleotide excision repair (NER), because some of the DNA adducts generated by CaP-related carcinogens are removed by the NER pathway, and our previous data showed a significant association between lower NER capacity (NERC) and CaP risk. Many laboratories, including ours, have employed a variety of approaches to evaluate the functional significance of DNA-repair single-nucleotide polymorphisms (SNPs) in human cancer risk assessment. Genetic profiling and computational modeling that can predict NERC may have great potential for CaP-risk assessment, because the current NERC assay is quite labor intensive, costly, and therefore not suitable for population-based screening.

Original languageEnglish (US)
Pages (from-to)125-135
Number of pages11
JournalCancer letters
Volume220
Issue number2
DOIs
StatePublished - Apr 8 2005
Externally publishedYes

Keywords

  • Genetic polymorphisms
  • Nucleotide excision repair
  • Prostate cancer risk

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology
  • Oncology

Fingerprint Dive into the research topics of 'Nucleotide-excision repair and prostate cancer risk'. Together they form a unique fingerprint.

  • Cite this