CARCINOGEN-DNA ADDUCTS IN HUMAN BREAST-TISSUE

Citation
Fp. Perera et al., CARCINOGEN-DNA ADDUCTS IN HUMAN BREAST-TISSUE, Cancer epidemiology, biomarkers & prevention, 4(3), 1995, pp. 233-238
Citations number
61
Categorie Soggetti
Public, Environmental & Occupation Heath
ISSN journal
10559965
Volume
4
Issue
3
Year of publication
1995
Pages
233 - 238
Database
ISI
SICI code
1055-9965(1995)4:3<233:CAIHB>2.0.ZU;2-Y
Abstract
Breast cancer is the second leading cause of cancer death among Americ an women. Known risk factors account for only approximately one-third of the 182,000 new cases diagnosed each year in the United States. The re is both concern and debate over the contribution of environmental e xposures related to lifestyle, occupation, and ambient pollution, part icularly in high risk areas such as Long Island, NY and the rest of th e northeastern United States. Biomarkers such as carcinogen-DNA adduct s can help to explore the role of environmental risk factors for breas t cancer by documenting DNA damage from specific carcinogens directly in human tissue. In this pilot study, a fetal of 31 breast tissue samp les were analyzed by the P-32-postlabeling method for carcinogen-DNA a dducts characteristic of complex mixtures of aromatic compounds (such as polycyclic aromatic hydrocarbons) and tobacco smoke. The samples in cluded tumor and tumor-adjacent tissues from 15 women with breast canc er and normal tissue samples from 4 women undergoing breast reduction, Among the breast canter cases, the mean aromatic/hydrophobic-DNA addu ct level in all tissues assayed was 5.3 +/- 2.4 (SD) adducts/10(8) 10( 8) nucleotides compared to 2.3 +/- 1.5 among the samples from the nonc ancer patients. Breast tissue (tumor and/or nontumor) from 30% (5 of 1 5) of women with breast cancer displayed a pattern of adducts (referre d to as a diagonal zone of radioactivity) associated previously, in st udies of other tissues, with exposure to tobacco smoke. The 5 positive samples were from current smokers; tissue samples from the 8 nonsmoki ng eases did not show this characteristic pattern (P < 0.01). While th e nature of the study precludes an inference of causality, these resul ts demonstrate the presence in human breast cells of DNA damage charac teristic of environmental carcinogens (complex mixtures of polycyclic aromatic hydrocarbons and tobacco smoke) to which women are widely exp osed. Although limited, our results indicate that biomarkers such as D NA adducts may be useful in investigating specific environmental expos ures that may contribute to breast cancer causation as well as the pop ulations and individuals most affected. If so, they might be helpful i n suggesting new strategies for prevention of breast cancer.