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PMID: 15682379 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Nucleotide excision repair as a marker for susceptibility to tobacco-related cancers: a review of molecular epidemiological studies.

Molecular carcinogenesis ·Vol. 42 ·No. 2 ·2005-02-00 ·Pages 65-92

Neumann AS, Sturgis EM, Wei Q

Abstract

DNA repair is a complicated biological process consisting of several distinct pathways that play a central role in maintaining genomic stability. Research on DNA repair and cancer risk is a vital, emerging field that recently has seen rapid advances facilitated by the completion of the Human Genome Project. In this review, we described phenotypic and genotypic markers of nucleotide excision repair (NER) that have been used in molecular epidemiology studies. We summarized the population-based studies to date that have examined the association between DNA repair capacity phenotype and genetic polymorphisms of the NER genes and risk of tobacco-related cancers, including cancers of the lung, head and neck, prostate, bladder, breast, and esophagus. We also included studies of melanoma and nonmelanoma skin cancers because individuals with defective NER, such as patients with xeroderma pigmentosum (XP) are highly susceptible to ultraviolet light (UV)-induced melanoma and nonmelanoma skin cancers. The published data provide emerging evidence that DNA repair capacity may contribute to genetic susceptibility to cancers in the general population. However, many of the studies are limited in terms of the size of the study populations. Furthermore, all published findings are still considered preliminary, the assays used in the studies have yet to be validated, and the results need to be confirmed. Large and well-designed population-based studies are warranted to assess gene-gene and gene-environment interactions and to ultimately determine, which biomarkers of DNA repair capacity are useful for screening high-risk populations for primary prevention and early detection of tobacco-related cancers.

MeSH Terms
Biomarkers, Tumor Chloramphenicol O-Acetyltransferase/metabolism Computational Biology/methods DNA Repair Databases as Topic Disease Susceptibility Genes, Reporter Genotype Humans Luciferases/metabolism Melanoma/epidemiology,etiology Models, Biological Neoplasms/epidemiology,etiology,genetics Odds Ratio Phenotype Polymorphism, Genetic Risk Skin Neoplasms/epidemiology,etiology,genetics Smoking Tobacco/adverse effects Ultraviolet Rays
Chemicals
Biomarkers, Tumor Luciferases Chloramphenicol O-Acetyltransferase
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Neumann Ana S
Department of Epidemiology, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA.
Sturgis Erich M
Wei Qingyi
Article Info
Journal
Molecular carcinogenesis
Abbr.
Mol Carcinog
ISSN
0899-1987
Published
2005-02-00
Pages
65-92
Language
English
Region
United States
NLM ID
8811105
Subset
IM
Grants
NIEHS NIH HHS · ES07784 · United States
NIEHS NIH HHS · ES11047 · United States
NIEHS NIH HHS · ES11740 · United States
NCI NIH HHS · R01 CA100264 · United States
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