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Abstract
Egypt shows a parallel increase in premenopausal breast cancer and environmental pollution. The purpose of this study is to explore a possible relationship between oxidative DNA damage, urinary estrogen metabolites and breast cancer in Egyptian premenopausal women. We conducted a pilot study of Egyptian breast cancer involving 29 cases and 32 controls and analysed lymphocyte DNA levels of 7,8-dihydro-8-oxo-2′-deoxyguanine (8-oxo-dG), a measure of oxidative DNA damage using high performance liquid chromatography with electro-chemical detection (HPLC-ECD) method. We analysed levels of urinary estrogen metabolites, 2-hydroxyestrone (2-OHE) and 16α-hydroxyestrone (16α-OHE) by an enzyme immuno assay. We also collected residential, occupational, and reproductive histories of all study subjects. We detected, in all subjects, exceptionally high levels of 8-oxo-dG and thus oxidative DNA damage, the levels (mean 8-oxo-dG/105 dG ± SD) were significantly (P < 0.01) higher in breast cancer cases (139.4 ± 78.4) than in controls (60.9 ± 51.5). Urinary 2-OHE and 16α-OHE or their ratio was not significantly different between cases and controls. However, 8-oxo-dG levels were positively correlated (P < 0.05) with 2-OHE and 16α-OHE from cases while controls showed a negative correlation (P < 0.05). Urban residence (Odds Ratio [OR] 3.1; Confidence interval [CI], 1.1 – 9.3), infertility (OR [9.8]; CI [1.1 – 89.7]), age (OR [2.6]; CI [1.4 – 4.6]) and 8-oxo-dG (OR 5.8; CI 1.9 – 17.5) levels were found to be significant predictors of breast cancer. Our finding of exceptionally high levels of 8-oxo-dG, a common result of oxidative DNA damage, warrant future studies on a larger population of premenopausal women in Egypt with consideration of other susceptibility markers and dietary characteristics.
Acknowledgements
We appreciate the excellent editorial comments of Jude Richard in the Department of Scientific Publications, M.D. Anderson Cancer Center and the secretarial support of Joyce Brown in the Department of Epidemiology at M.D. Anderson Cancer Center. This work was supported in part by a pilot grant from the Center for Research on Environmental Disease, NIEHS (ES 07784), a grant from the Middle East Cancer Consortium (MECC No. 99003), and a fellowship from the Cancer Research Foundation of America and a grant from the National Cancer Institute (K07-90241).
