CEBP CTRC-AACR San Antonio Breast Cancer Symposium Cancer Health Disparities Conference 2009
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Cancer Epidemiology Biomarkers & Prevention Vol. 12, 75, January 2003
© 2003 American Association for Cancer Research


Letters to the Editor

Correspondence re: Gammon et al., Environmental Toxins and Breast Cancer on Long Island. I. Polycyclic Aromatic Hydrocarbon DNA Adducts. 11, 677–685, 2002

Frederica Perera and Andrew Rundle

Columbia University Mailman School of Public Health

Gammon et al. recently reported results from the comprehensive Long Island Breast Cancer Case-Control Study1 showing no consistent elevation in risk with increasing PAH-DNA adduct levels in white blood cells (CEBP, Vol. 11, 677–685, 2002). Their results are similar to our previous findings from a hospital-based, case-control study in New York City that did not find a consistent association between PAH/aromatic adducts in white blood cells and breast cancer (A. G. Rundle, A Molecular Epidemiologic Case Control Study of Breast Cancer, Doctoral Dissertation, 2000, Department of Epidemiology, Mailman School of Public Health, Columbia University, NY). In contrast to adducts in blood, however, in our study, elevated PAH-DNA adducts measured in breast tumor tissue from cases and normal tissue from controls were significantly associated with breast cancer (odds ratio 2.56, 96% confidence interval 1.05–6.24; Carcinogenesis, Vol. 21, pp. 1281–1289, 2000).

Our study included 100 cases and 105 controls enrolled before surgery and treatment from the same source population at Columbia Presbyterian Medical Center (now New York Presbyterian Hospital) in New York City. Thus, the controls were representative of the population from which the cases arose. Women who were diagnosed with benign breast cancer (excluding atypia) considered to be at relatively low risk of subsequent breast cancer comprised the control group. We did not see a correlation between adducts in blood and breast tissue, although adducts in tumor and nontumor breast tissue from the same cases were significantly correlated (P < 0.001).

Unlike results on adducts and lung cancer (Tang et al., Cancer Res. 2001, 61:6708–6712), it appears that the blood is not a good proxy for the target tissue in this instance, possibly because the breast represents a hormonal milieu. The results underscore the importance of obtaining both surrogate, target tissue, and suggest that PAHs are a risk factor for breast cancer. If confirmed, the results would open new avenues for prevention.

Footnotes

1 The abbreviation used is: PAH, polycyclic aromatic hydrocarbon. Back

Received 8/30/02; revised 8/30/02; accepted 9/12/02.

References

  1. Gammon M. D., Santella R. M., Neugut A. I., Eng S. M., Teitelbaum S. L., Paykin A., Levin B., Terry M. B., Young T. L., Wang L. W., et al Environmental toxins and breast cancer on Long Island. I. Polycyclic aromatic hydrocarbon DNA adducts. Cancer Epidemiol. Biomarkers Prev., 11: 677-685, 2002.[Abstract/Free Full Text]




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online