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Repair of tobacco carcinogen-induced DNA adducts and lung cancer risk: a molecular epidemiologic study.

Publication ,  Journal Article
Wei, Q; Cheng, L; Amos, CI; Wang, LE; Guo, Z; Hong, WK; Spitz, MR
Published in: J Natl Cancer Inst
November 1, 2000

BACKGROUND: Only a fraction of cigarette smokers develop lung cancer, suggesting that people differ in their susceptibility to this disease. We investigated whether differences in DNA repair capacity (DRC) for repairing tobacco carcinogen-induced DNA damage are associated with differential susceptibility to lung cancer. METHODS: From August 1, 1995, through April 30, 1999, we conducted a hospital-based, case-control study of 316 newly diagnosed lung cancer patients and 316 cancer-free control subjects matched on age, sex, and smoking status. DRC was measured in cultured lymphocytes with the use of the host-cell reactivation assay with a reporter gene damaged by a known activated tobacco carcinogen, benzo[a]pyrene diol epoxide. Statistical tests were two-sided. RESULTS: Overall, lower DRC was observed in case patients than in control subjects (P:<.001) and was associated with a greater than twofold increased risk of lung cancer. Compared with the highest DRC quartile in the control subjects and after adjustment for age, sex, pack-years of smoking, family history of cancer, and other covariates, reduced DRC was associated with increased risk of lung cancer in a dose-dependent fashion (odds ratio [OR] = 1.8 with 95% confidence interval [CI] = 1.1-3.1, OR = 2.0 with 95% CI = 1.2-3.4, and OR = 4. 3 with 95% CI = 2.6-7.2 for the second, third, and fourth quartiles, respectively; P:(trend)<.001). Case patients who were younger at diagnosis (<60 years old), female, or lighter smokers or who reported a family history of cancer exhibited the lowest DRC and the highest lung cancer risk among their subgroups, suggesting that these subgroups may be especially susceptible to lung cancer. CONCLUSION: The results provide evidence that low DRC is associated with increased risk of lung cancer. The findings from this hospital-based, case-control study should be validated in prospective studies.

Duke Scholars

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Published In

J Natl Cancer Inst

DOI

ISSN

0027-8874

Publication Date

November 1, 2000

Volume

92

Issue

21

Start / End Page

1764 / 1772

Location

United States

Related Subject Headings

  • Transfection
  • Texas
  • Smoking
  • Sex Factors
  • Plasmids
  • Plants, Toxic
  • Oncology & Carcinogenesis
  • Nicotiana
  • Middle Aged
  • Male
 

Citation

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Wei, Q., Cheng, L., Amos, C. I., Wang, L. E., Guo, Z., Hong, W. K., & Spitz, M. R. (2000). Repair of tobacco carcinogen-induced DNA adducts and lung cancer risk: a molecular epidemiologic study. J Natl Cancer Inst, 92(21), 1764–1772. https://doi.org/10.1093/jnci/92.21.1764
Wei, Q., L. Cheng, C. I. Amos, L. E. Wang, Z. Guo, W. K. Hong, and M. R. Spitz. “Repair of tobacco carcinogen-induced DNA adducts and lung cancer risk: a molecular epidemiologic study.J Natl Cancer Inst 92, no. 21 (November 1, 2000): 1764–72. https://doi.org/10.1093/jnci/92.21.1764.
Wei Q, Cheng L, Amos CI, Wang LE, Guo Z, Hong WK, et al. Repair of tobacco carcinogen-induced DNA adducts and lung cancer risk: a molecular epidemiologic study. J Natl Cancer Inst. 2000 Nov 1;92(21):1764–72.
Wei, Q., et al. “Repair of tobacco carcinogen-induced DNA adducts and lung cancer risk: a molecular epidemiologic study.J Natl Cancer Inst, vol. 92, no. 21, Nov. 2000, pp. 1764–72. Pubmed, doi:10.1093/jnci/92.21.1764.
Wei Q, Cheng L, Amos CI, Wang LE, Guo Z, Hong WK, Spitz MR. Repair of tobacco carcinogen-induced DNA adducts and lung cancer risk: a molecular epidemiologic study. J Natl Cancer Inst. 2000 Nov 1;92(21):1764–1772.

Published In

J Natl Cancer Inst

DOI

ISSN

0027-8874

Publication Date

November 1, 2000

Volume

92

Issue

21

Start / End Page

1764 / 1772

Location

United States

Related Subject Headings

  • Transfection
  • Texas
  • Smoking
  • Sex Factors
  • Plasmids
  • Plants, Toxic
  • Oncology & Carcinogenesis
  • Nicotiana
  • Middle Aged
  • Male