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 anti-estrogen 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.