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20 Nov 2008

Scientists identify 'gatekeepers' of breast cancer transition to invasive disease

- 5 May 2008
By Cell Press   
Page 2 of 2

“Here, we show that a key event of tumor progression is the disappearance of the myoepithelial cell layer due to defective myoepithelial cell differentiation regulated by intrinsic and microenvironment signals. Thus, myoepithelial cells can be considered gatekeepers of the in situ to invasive carcinoma transition; understanding the pathways that regulate their differentiation may open new venues for cancer therapy and prevention,” offers Dr. Polyak.

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The researchers include Min Hu and Jun Yao of Dana-Farber Cancer Institute and Harvard Medical School in Boston, MA; Danielle K. Carroll of Harvard Medical School in Boston, MA; Stanislawa Weremowicz of Brigham and Women’s Hospital and Harvard Medical School in Boston, MA; Haiyan Chen of Dana-Farber Cancer Institute and Harvard School of Public Health in Boston, MA; Daniel Carrasco of Dana-Farber Cancer Institute in Boston, MA; Andrea Richardson of Brigham and Women’s Hospital and Harvard Medical School in Boston, MA; Shelia Violette of Biogen-Idec in Cambridge, MA; Tatiana Nikolskaya and Yuri Nikolsky of GeneGo, Inc. in St. Joseph, MI; Erica L. Bauerlein and William C. Hahn of Dana-Farber Cancer Institute and Harvard Medical School in Boston, MA; Rebecca S. Gelman of Dana-Farber Cancer Institute and Harvard School of Public Health in Boston, MA; Craig Allred of Washington University School of Medicine in St. Louis, MO; Mina J. Bissell of Lawrence Berkeley National Laboratory in Berkeley, CA; Stuart Schnitt of Harvard Medical School and Beth-Israel Deaconess Medical Center in Boston, MA; and Kornelia Polyak of Dana-Farber Cancer Institute and Harvard Medical School in Boston, MA.

This work was supported in part by NIH, DOD, and ACS grants, a Susan G. Komen Foundation fellowship, Biogen-Idec., and Novartis Pharmaceuticals, Inc.

Hu et al.: “Regulation of In Situ to Invasive Breast Carcinoma Transition.” Publishing in Cancer Cell 13, 394–406, May 2008. DOI 10.1016/j.ccr.2008.03.007 www.cancercell.org

 
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