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To support the free and open dissemination of research findings and information on alcoholism and alcohol-related problems. To encourage open access to peer-reviewed articles free for all to view.

For full versions of posted research articles readers are encouraged to email requests for "electronic reprints" (text file, PDF files, FAX copies) to the corresponding or lead author, who is highlighted in the posting.

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Monday, October 5, 2009

EGFR may couple moderate alcohol consumption to increased breast cancer risk
Breast Cancer: Targets and Therapy 2009:1 31–38

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.

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