Cancer Institute

  • Ingrid Espinoza

    espinoza_ingrid.jpgAssistant Professor, Department of Biochemistry
    Tumor Cell Biology Program
    PhD, Biomedical Sciences, 2002, University of Chile, Santiago, Chile
    Postdoctoral fellow, 2002-04, University of Chile, Santiago, Chile
    Postdoctoral fellow, 2004-08, Northwestern University, Evanston, IL
    Professional Associate in Research, 2008-11, Mayo Clinic, Rochester, MN

    Contact information
    2500 N State St, Room G760
    Jackson, MS 39216
    Phone: (601) 815-3511
    E-mail: iespinoza@umc.edu

    Research interests

    • Development of combinatorial targeted therapies for breast cancer
    • Drug delivery systems
    • Notch and other developmental pathways as therapeutic targets in cancer

    Research synopsis

    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.

    Recent accomplishments and honors

    • 2007 AACR-WICR Brigid G. Leventhal Scholar Award in Cancer Research, Los Angeles, CA.
    • 2008 Young Investigator Award. Mayo Clinic Angiogenesis Symposium. Rochester, MN,
    • 2008 Susan G. Komen for the Cure-AACR Minority Scholar Award. San Antonio, TX

    Selected publications

    • Espinoza, I. and Miele, L. Notch inhibitors for cancer treatment. In press. Pharmacology & Therapeutics, 2013.
    • Espinoza, I. and Miele, L. Development of Notch Pathway Inhibitors for Cancer Therapy. Breast Cancer Metastasis and Drug Resistance. Progress and Prospects. Springer. Editor: Aamir Ahmad. 17: 291-327, 2013.
    • Espinoza I et al. CCN1 a Candidate Target for Zoledronic Acid Treatment in Breast Cancer. Mol Cancer Ther. 10:732-41, 2011.
    • Cabrera G et al. Mesocestoides corti: morphological features and glycogen mobilization during in vitro differentiation from larva to adult worm. Parasitology 137:373-84, 2010
    • Deshet N et al. Plasminogen-induced aggregation of PANC-1 cells requires conversion to plasmin and is inhibited by endogenous plasminogen activator inhibitor-1. J Cell Physiol. 216:632-9, 2008.
    • Espinoza I et al. Developmental expression pattern of histone H4 gene associated to DNA synthesis in the endoparasitic platyhelminth Mesocestoides corti. GENE 386:35-41, 2007.
    • Espinoza I et al. Early post-larval development of the endoparasitic platyhelminth Mesocestoides corti: Trypsin provokes reversible tegumental damage leading to serum-induced cell proliferation and growth. J Cell Physiol. 205:211-7, 2005.