Journal Article

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

Andrew Rundle, Deliang Tang, Hanina Hibshoosh, Allison Estabrook, Freya Schnabel, Wangfen Cao, Surah Grumet and Frederica P. Perera

in Carcinogenesis

Volume 21, issue 7, pages 1281-1289
Published in print July 2000 | ISSN: 0143-3334
Published online July 2000 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/21.7.1281
The relationship between genetic damage from polycyclic aromatic hydrocarbons in breast tissue and breast cancer

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A number of polycyclic aromatic hydrocarbons (PAH) are widespread environmental 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 analyze PAH–DNA adducts in tumor and nontumor breast tissue from cases and benign breast tissue from controls. The subjects were white, African-American and Latina women without prior cancer or treatment, including 119 women with breast cancer and 108 with benign breast disease without atypia. PAH–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 factors and current active and passive smoking, and dietary PAH. There was substantial interindividual (17-fold) variability in adducts overall, with 27% of cases and 13% of controls having elevated adducts. The odds ratio for elevated adducts in tumor tissue compared with control tissue was 2.56 (1.05–6.24), after controlling for potential confounders. Adduct levels in tumor tissue 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 correlated (r=0.56, P<0.001). However, the corresponding associations between case-control status and adducts measured in nontumor tissue from 90 cases and in normal tissue from 105 controls were positive but not statistically significant. Overall, neither active nor passive smoking, or dietary PAH were significantly associated with PAH–DNA adducts or breast cancer case-control status. These results suggest that genetic damage reflecting individual exposure and susceptibility to PAH may play a role in breast cancer; but more research is needed to determine whether the findings are relevant to causation or progression of breast cancer.

Keywords: BBD, benign breast disease; BPDE, benzo[a]pyrene diol epoxide; CPMC, Columbia Presbyterian Medical Center; DCIS, ductal carcinoma in situ; GSD; geometric standard deviation; OD; optical density; PAH; polycyclic aromatic hydrocarbons.

Journal Article.  7721 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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