damaged breast cells
http://news.softpedia.com/news/Plast...bs-82216.shtml
http://www.sciencedaily.com/releases...0401231554.htm
THE ABSTRACT:
Bisphenol A Induces a Profile of Tumor Aggressiveness in High-Risk Cells from Breast Cancer Patients
Shanaz H. Dairkee1, Junhee Seok2, Stacey Champion1, Aejaz Sayeed1, Michael Mindrinos2, Wenzhong Xiao2, Ronald W. Davis2 and William H. Goodson1
1 California Pacific Medical Center Research Institute, San Francisco, California and 2 Stanford Genome Technology Center, Stanford University School of Medicine, Palo Alto, California
Requests for reprints: Shanaz H. Dairkee and William H. Goodson, California Pacific Medical Center Research Institute, 475 Brannan Street, San Francisco, CA 94107. Phone: 415-600-1653; Fax: 415-600-1725; E-mail:
dairkes@cpmcri.org (S.H. Dairkee) and Phone: 415-923-3925; Fax: 415-776-1977; E-mail:
goodsow@cpmcri.org (W.H. Goodson).
Key Words: RPFNA • Xenoestrogen • Gene expression • Histologic grade • Prognosis
Breast cancer outcome is highly variable. Whether inadvertent exposure to environmental xenobiotics evokes a biological response promoting cancer aggressiveness and a higher probability of tumor recurrence remains unknown. To determine specific molecular alterations which arise in high-risk breast tissue in the presence of the ubiquitous xenoestrogen, bisphenol A (BPA), we used nonmalignant random periareolar fine-needle aspirates in a novel functional assay. Early events induced by BPA in epithelial-stromal cocultures derived from the contralateral tissue of patients with breast cancer included gene expression patterns which facilitate apoptosis evasion, endurance of microenvironmental stress, and cell cycle deregulation without a detectable increase in cell numbers. This BPA response profile was significantly associated with breast tumors characterized by high histologic grade (P < 0.001) and large tumor size (P = 0.002), resulting in decreased recurrence-free patient survival (P < 0.001). Our assays show a biological "fingerprint" of probable prior exposure to endocrine-disrupting agents, and suggest a scenario in which their presence in the microenvironmental milieu of high-risk breast tissue could play a deterministic role in establishing and maintaining tumor aggressiveness and poor patient outcome. [Cancer Res 2008;68(7):2076–80]
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