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EGFR may couple moderate alcohol consumption to increased breast cancer risk

Authors Mill CP, Chester JA, Riese D

Published 5 October 2009 Volume 2009:1 Pages 31—38


Review by Single anonymous peer review

Peer reviewer comments 2

Christopher P Mill1, Julia A Chester2, David J Riese II1

1Purdue University School of Pharmacy, Purdue University Center for Cancer Research, 2Purdue University Department of Psychological Sciences, West Lafayette, IN, USA

Abstract: Alcohol consumption is an established risk factor for breast cancer. Nonetheless, the mechanism by which alcohol contributes to breast tumor initiation or progression has yet to be definitively established. Studies using cultured human tumor cell lines have identified signaling molecules that may contribute to the effects of alcohol, including reactive oxygen species and other ethanol metabolites, matrix metalloproteases, the ErbB2/Her2/Neu receptor tyrosine kinase, cytoplasmic protein kinases, adenylate cyclase, E-cadherins, estrogen receptor, and a variety of transcription factors. Emerging data suggest that the epidermal growth factor receptor (EGFR) tyrosine kinase may contribute to breast cancer genesis and progression. Here we integrate these findings and propose three mechanisms by which alcohol contributes to breast cancer. A common feature of these mechanisms is increased EGFR signaling. Finally, we discuss how these mechanisms suggest strategies for addressing the risks associated with alcohol consumption.

Keywords: alcohol, breast cancer risk factor, EGF receptor, matrix metalloprotease

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