The relationship between genetic damage from polycyclic aromatic hydrocarbons in breast tissue and breast cancer

Citation
A. Rundle et al., The relationship between genetic damage from polycyclic aromatic hydrocarbons in breast tissue and breast cancer, CARCINOGENE, 21(7), 2000, pp. 1281-1289
Citations number
56
Categorie Soggetti
Onconogenesis & Cancer Research
Journal title
CARCINOGENESIS
ISSN journal
01433334 → ACNP
Volume
21
Issue
7
Year of publication
2000
Pages
1281 - 1289
Database
ISI
SICI code
0143-3334(200007)21:7<1281:TRBGDF>2.0.ZU;2-K
Abstract
A number of polycyclic aromatic hydrocarbons (PAH) are widespread environme ntal contaminants that cause mammary cancer experimentally. We investigated whether exposure and susceptibility to PAH, as measured by PAH-DNA adducts in breast tissue, are associated with human breast cancer. We carried out a hospital-based case-control study using immunohistochemical methods to an alyze PAH-DNA adducts in tumor and nontumor breast tissue from cases and be nign breast tissue from controls. The subjects were white, African-American and Latina women without prior cancer or treatment, including 119 women wi th breast cancer and 108 with benign breast disease without atypia, PAN-DNA adducts measured in breast tumor tissue of 100 cases and in normal tissue from 105 controls were significantly associated with breast cancer (OR = 4. 43, 96% CI 1.09-18.01) after controlling for known breast cancer risk facto rs and current active and passive smoking, and dietary PAH, There was subst antial interindividual (17-fold) variability in adducts overall, with 27% o f cases and 13% of controls having elevated adducts, The odds ratio for ele vated adducts in tumor tissue compared with control tissue was 2.56 (1.05-6 .24), after controlling for potential confounders. Adduct levels in tumor t issue did not vary by stage or tumor size. Among 86 cases with paired tumor and nontumor tissue, adducts levels in these two tissues were highly corre lated (r = 0.56, P<0.001). However, the corresponding associations between case-control status and adducts measured in nontumor tissue from 90 cases a nd in normal tissue from 105 controls were positive but not statistically s ignificant. Overall, neither active nor passive smoking, or dietary PAH wer e significantly associated with PAH-DNA adducts or breast cancer case-contr ol status. These results suggest that genetic damage reflecting Individual exposure and susceptibility to PAH may play a role in breast cancer; but mo re research is needed to determine whether the findings are relevant to cau sation or progression of breast cancer.