N-methylpurine DNA glycosylase and OGG1 DNA repair activities: Opposite associations with lung cancer risk

Yael Leitner-Dagan, Ziv Sevilya, Mila Pinchev, Ran Kramer, Dalia Elinger, Laila C. Roisman, Hedy S. Rennert, Edna Schechtman, Laurence Freedman, Gad Rennert, Zvi Livneh, Tamar Paz-Elizur

Research output: Contribution to journalArticlepeer-review

52 Scopus citations

Abstract

Only a minority of smokers develop lung cancer, possibly due to genetic predisposition, including DNA repair deficiencies. To examine whether inter-individual variations in DNA repair activity of N-methylpurine DNA glycosylase (MPG) are associated with lung cancer, we conducted a blinded, population-based, case-control study with 100 lung cancer case patients and 100 matched control subjects and analyzed the data with conditional logistic regression. All statistical tests were two-sided. MPG enzyme activity in peripheral blood mononuclear cells from case patients was higher than in control subjects, results opposite that of 8-oxoguanine DNA glycosylase (OGG1) DNA repair enzyme activity. For lung cancer associated with one standard deviation increase in MPG activity, the adjusted odds ratio was 1.8 (95% confidence interval [CI] 1.2 to 2.6; P . 006). A combined MPG and OGG1 activities score was more strongly associated with lung cancer risk than either activity alone, with an odds ratio of 2.3 (95% CI 1.4 to 3.6; P <. 001). These results form a basis for a future panel of risk biomarkers for lung cancer risk assessment and prevention.

Original languageEnglish
Pages (from-to)1765-1769
Number of pages5
JournalJournal of the National Cancer Institute
Volume104
Issue number22
DOIs
StatePublished - 21 Nov 2012
Externally publishedYes

Bibliographical note

Funding Information:
This work was supported the Early Detection Research Network of the National Cancer Institute, National Institutes of Health (U01 CA111219 to ZL, TP-E, and GR) and the Flight Attendant Medical Research Institute, Florida (part of a Center of Excellence Award, 032001 to ZL and TP-E).

Funding

This work was supported the Early Detection Research Network of the National Cancer Institute, National Institutes of Health (U01 CA111219 to ZL, TP-E, and GR) and the Flight Attendant Medical Research Institute, Florida (part of a Center of Excellence Award, 032001 to ZL and TP-E).

FundersFunder number
National Institutes of Health
National Cancer InstituteU01CA111219
Flight Attendant Medical Research Institute032001

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