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Benzo(a)pyrene diol epoxide-induced chromosomal aberrations and risk of lung cancer.
Cancer Res. 1996 Sep 01; 56(17):3975-9.CR

Abstract

Benzo(a)pyrene is considered a classic DNA-damaging carcinogen and is one of a multitude of polycyclic aromatic hydrocarbons commonly found in tobacco smoke and in the ambient environment. In this report, we describe the characteristics of chromosomal aberrations induced in vitro by activated benzo(a)pyrene diol epoxide (BPDE) in lymphocyte cultures of 172 normal individuals ages 19-95 years and present the analysis of a pilot case-control study of 33 lung cancer patients and 96 selected controls without history of cancer and frequency matched on age (50-85 years) to the cases. The BPDE-induced chromosomal aberrations were predominantly single chromatid breaks, with few isochromatid breaks or exchange figures. In the 172 normal subjects, the frequencies of both spontaneous and BPDE-induced chromatid breaks were not correlated with age, sex, ethnicity, or tobacco use. However, the frequency of BPDE-induced chromatid breaks was significantly correlated with the frequency of spontaneous chromatid breaks (r = 0.19, P < 0.05). In addition, Hispanics had significantly higher mean BPDE-induced chromatid breaks than did non-Hispanic whites (P < 0.01). From the case-control analyses, the frequency of BPDE-induced chromosomal aberrations was significantly higher in cases (mean, 0.67 breaks/cell) than in controls (mean, 0.41 breaks/cell; P < 0.0001). An adjusted odds ratio of 6.53 (95% confidence interval, 3.74-11.4) for lung cancer was associated with increased frequency of these chromosomal aberrations. The higher rate of BPDE-induced chromosomal aberrations may be due to inefficient DNA repair. These findings warrant additional molecular epidemiological studies. The BPDE mutagen sensitivity assay will facilitate epidemiological studies of genetic susceptibility to smoking-related cancers.

Authors+Show Affiliations

Department of Epidemiology, University of Texas M. D. Anderson Cancer Center, Houston 77030, USA. qwei@request.mda.uth.tmc.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

8752166

Citation

Wei, Q, et al. "Benzo(a)pyrene Diol Epoxide-induced Chromosomal Aberrations and Risk of Lung Cancer." Cancer Research, vol. 56, no. 17, 1996, pp. 3975-9.
Wei Q, Gu J, Cheng L, et al. Benzo(a)pyrene diol epoxide-induced chromosomal aberrations and risk of lung cancer. Cancer Res. 1996;56(17):3975-9.
Wei, Q., Gu, J., Cheng, L., Bondy, M. L., Jiang, H., Hong, W. K., & Spitz, M. R. (1996). Benzo(a)pyrene diol epoxide-induced chromosomal aberrations and risk of lung cancer. Cancer Research, 56(17), 3975-9.
Wei Q, et al. Benzo(a)pyrene Diol Epoxide-induced Chromosomal Aberrations and Risk of Lung Cancer. Cancer Res. 1996 Sep 1;56(17):3975-9. PubMed PMID: 8752166.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Benzo(a)pyrene diol epoxide-induced chromosomal aberrations and risk of lung cancer. AU - Wei,Q, AU - Gu,J, AU - Cheng,L, AU - Bondy,M L, AU - Jiang,H, AU - Hong,W K, AU - Spitz,M R, PY - 1996/9/1/pubmed PY - 1996/9/1/medline PY - 1996/9/1/entrez SP - 3975 EP - 9 JF - Cancer research JO - Cancer Res VL - 56 IS - 17 N2 - Benzo(a)pyrene is considered a classic DNA-damaging carcinogen and is one of a multitude of polycyclic aromatic hydrocarbons commonly found in tobacco smoke and in the ambient environment. In this report, we describe the characteristics of chromosomal aberrations induced in vitro by activated benzo(a)pyrene diol epoxide (BPDE) in lymphocyte cultures of 172 normal individuals ages 19-95 years and present the analysis of a pilot case-control study of 33 lung cancer patients and 96 selected controls without history of cancer and frequency matched on age (50-85 years) to the cases. The BPDE-induced chromosomal aberrations were predominantly single chromatid breaks, with few isochromatid breaks or exchange figures. In the 172 normal subjects, the frequencies of both spontaneous and BPDE-induced chromatid breaks were not correlated with age, sex, ethnicity, or tobacco use. However, the frequency of BPDE-induced chromatid breaks was significantly correlated with the frequency of spontaneous chromatid breaks (r = 0.19, P < 0.05). In addition, Hispanics had significantly higher mean BPDE-induced chromatid breaks than did non-Hispanic whites (P < 0.01). From the case-control analyses, the frequency of BPDE-induced chromosomal aberrations was significantly higher in cases (mean, 0.67 breaks/cell) than in controls (mean, 0.41 breaks/cell; P < 0.0001). An adjusted odds ratio of 6.53 (95% confidence interval, 3.74-11.4) for lung cancer was associated with increased frequency of these chromosomal aberrations. The higher rate of BPDE-induced chromosomal aberrations may be due to inefficient DNA repair. These findings warrant additional molecular epidemiological studies. The BPDE mutagen sensitivity assay will facilitate epidemiological studies of genetic susceptibility to smoking-related cancers. SN - 0008-5472 UR - https://www.unboundmedicine.com/medline/citation/8752166/Benzo_a_pyrene_diol_epoxide_induced_chromosomal_aberrations_and_risk_of_lung_cancer_ L2 - http://cancerres.aacrjournals.org/cgi/pmidlookup?view=long&amp;pmid=8752166 DB - PRIME DP - Unbound Medicine ER -