Assistant Professor, Department of BiochemistryTumor Cell Biology ProgramPhD, Biomedical Sciences, 2002, University of Chile, Santiago, ChilePostdoctoral fellow, 2002-04, University of Chile, Santiago, ChilePostdoctoral fellow, 2004-08, Northwestern University, Evanston, ILProfessional Associate in Research, 2008-11, Mayo Clinic, Rochester, MN
Contact information2500 N State St, Room G760Jackson, MS 39216Phone: (601) 815-3511E-mail: email@example.com
Progression of cancer is linked to the expression of myriad proteins; among them, angiogenic factors that induce blood vessel formation and tumor growth play an important role. In breast cancer, the pro-angiogenic factor Cyr61 is expressed in about 30% of highly aggressive triple negative breast carcinomas and is also expressed in a subpopulation of Estrogen Receptor positive (ER+) breast carcinomas. In ER+ breast tumors it induces estrogen independence and antiestrogen resistance. We have shown that the interaction of Cyr61 and integrin receptors generates differential response to chemotherapeutic drugs. These studies have put in the map Cyr61 as a potential target for breast cancer. Based on these results, an ongoing clinical trial blocking Cyr61/αvβ3 integrin interaction in cancer patients has been opened.
Currently I am focused in studying the role of Notch signaling in ER+ breast carcinomas. Dr. Miele's work has demonstrated that in ER+ breast cancer cells Notch signaling is inhibited by Estrogen and reactivated by 4-OH-Tamoxifen. It increases the cell dependence on Notch signaling for survival. In vivo studies using xenografts models, showed that Tamoxifen and a pharmacological Notch inhibitor (γ-secretase inhibitor, GSI) caused tumor regression. Based on these data a pilot clinical trial using a combination regimen including endocrine therapy (Letrozole or Tamoxifen) and GSI is currently underway. The goal of these studies is to define new targeted therapies for ER+ breast cancer patients that have developed resistance to endocrine therapy.
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