Anika Agarwal, MD, MPhil
Tufts Medical Center
Targeting the Synergy Between the Protease-Activated Receptor-1 and Inflammatory Chemokine Receptors in the Ovarian Tumor Microenvironment
Bio
Anika Agarwal, MD MPhil is an Instructor in the Department of Medicine and the Molecular Oncology Research Institute at Tufts University Medical Center. Her research interests are understanding tumor stromal interactions in ovarian tumor microenvironment that promote angiogenesis, ascites and peritoneal spread, and also to identifying target receptors to develop therapeutic strategies for complementing current treatment regimens in ovarian cancer. She received her clinical training at the Institute of Medical Science, BHU, Varanasi, India, and received her MPhil in Reproductive Biology from the University of Hong Kong, Hong Kong. In addition to her 2008 Liz Tilberis Award from OCRF, she is the winner of the Endocine Society’s 2002 Women in Endocrine Travel Award, and the 2004 Eastern Cooperative Oncology Group Aventis Young Investigator travel Award.
Project Summary
Poor survival in ovarian cancer is attributed to late detection leading to widespread dissemination and lack of adequate treatment modalities. This study focuses on understanding interactions in ovarian tumor microenvironment responsible for tumor vascularity, invasion and progression of disease. Secondly, we hope to target key signaling molecules in ovarian cancer with novel inhibitors that can block angiogenesis, reactive inflammation and extend survival in ovarian tumor mice models.
Recently we have identified stromal-derived matrix metalloprotease-1 (MMP-1) as a novel protease agonist that can cleave and activate Protease activated receptor 1 (PAR1) in ovarian tumors. In this grant we test the hypothesis that metalloprotease-PAR1 signaling is a critical regulator of cancer-stromal communication, angiogenesis and tumorigenesis in ovarian cancer through its paracrine control of the endothelial chemokine receptors. This grant will explore whether matrix metalloprotease-1 induction of chemokines from ovarian cancer cells is PAR1-dependent and if these chemokines lead to cancer-endothelial cell communication in blood vessel formation. We hope that novel inhibitors against these receptors used with conventional therapy will help target pivotal disease pathways to halt the progression of this deadly disease.
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