Dipak Panigrahy, M.D.
Assistant Professor of Pathology
Beth Israel Deaconess Medical Center
Harvard Medical School

330 Brookline Avenue, RN-220
Boston, MA 02215
Office: 617-667-0577
Fax: 617-667-2913


Dr. Panigrahy was accepted into medical school at Boston University at age 17. He trained in surgery with Dr. Roger Jenkins, who performed the first liver transplant in New England. Over the past decade, Dr. Panigrahy led angiogenesis and cancer animal modeling in the Judah Folkman laboratory. Dr. Panigrahy joined the Beth Israel Deaconess Medical Center in 2013, and in 2014 was appointed Assistant Professor of Pathology and currently has a laboratory in the Center for Vascular Biology Research.

Research Interests: Bioactive Lipids in Cancer

Basic Research: Our laboratory has a longstanding interest in lipid autacoid mediators (also called eicosanoids) and their pathophysiologic roles in cancer biology. While exploring the mechanism by which PPAR pathways control tumor growth, we became interested in the cytochrome P450-derived arachidonic acid products called epoxyeicosatrienoic acids (EETs). These eicosanoids are down-regulated following PPAR activation. We recently demonstrated the endothelium and certain stromal cells secrete EETs, and that these lipid autacoids stimulate multi-organ metastasis and escape from tumor dormancy. Furthermore, we have found that EETs play a critical role in both normal processes [such as wound healing and organ regeneration] and disease processes. We also collaborate closely with Professor Charles Serhan (Brigham & Women’s Hospital), to study the role endogenous anti-inflammatory lipid autacoids such as the omega-3 fatty acid-derived resolvins and their role in inflammation resolution. In addition, we collaborate with industry (e.g. Inception Sciences, San Diego) to study eicosanoid modulating drugs in experimental cancer models.

Over the past decade we have collaborated closely with Professor Sui Huang (Institute of Systems Biology) on various animal models to study cancer control via the diet. Our studies may provide important insight regarding the outcomes of dramatically increasing omega-3 lipids such as DHA and EPA in the U.S. diet. We also collaborate with Professor Bruce Hammock (University of California, Davis) and Dr. Guodong Zhang (Univ of Massachusetts) on a novel approach to targeting cancer treatment via dual COX2-sEH inhibition. Our laboratory focuses on lipid autacoids that are ideally suited for translation into the clinic for the treatment of cancer patients. We work closely with Dr. Mark Kieran at Boston Children’s Hospital/Dana-Farber Cancer Institute, who leads several international clinical trials in brain tumors, to translate our scientific discoveries to treat children with various types of brain cancer, including medulloblastoma.

New and Noteworthy Publications:

Panigrahy D, Singer S, Shen LQ, Butterfield CE, Freedman DA, Moses MA, Kilroy S, Duensing S, Fletcher C, Fletcher JA, Hlatky L, Hahnfeldt P, Folkman J, Kaipainen A. PPARγ Ligands Inhibit Primary Tumor Growth and Metastasis by Inhibiting Angiogenesis. The Journal of Clinical Investigation. 2002;110(7):923-932. (cover) These studies demonstrated that the nuclear receptor PPARgamma is highly expressed in tumor endothelium and is activated by FDA approved ligands such as rosiglitazone in cultured endothelial cells.  These results demonstrate that PPARgamma ligands may be useful in treating angiogenic diseases such as cancer by inhibiting angiogenesis.

Panigrahy D, Edin ML, Lee CR, Huang S, Bielenberg DR, Butterfield CE, Barnés CM, Mammoto A, Mammoto T, Luria A, Benny O, Chaponis DM, Dudley AC, Greene ER, Vergilio J, Pietramaggiori G, Scherer-Pietramaggiori SS, Short SM, Seth M, Lih FB, Tomer KB, Yang J, Schwendener RA, Hammock, BD, Falck JR, Manthati VL, Ingber DE, Kaipainen A, D’Amore PA, Kieran MW, Zeldin DC. Epoxy-eicosanoids stimulate multi-organ metastasis and tumor dormancy escape in mice. The Journal of Clinical Investigation 2012, 122(1):178-191. PMID:22182838 (Featured with related commentary in The Journal of Clinical Investigation: Wang D, Dubois RN. Epoxyeicosatrienoic acids: a double-edged sword in cardiovascular diseases and cancer 2012, 122(1):19-22.) These studies showed that epoxyeicosatrienoic acids (EETs) induce multi-organ metastasis and tumor dormancy escape in a variety of transplantable and genetically engineered cancer models. These results pave the path for a new strategy for the prevention and treatment of metastatic disease – i.e. inhibition of EET bioactivity.

Zhang G, Panigrahy D, Mahakian L, Yang J, Liu J, Lee K, Wettersten H, Ulu A, Hu X, Tam S, Hwang S, Ingham E, Kieran MW, Weiss RH, Ferrara KW, and Hammock BD. Epoxy metabolites of docosahexaenoic acid (DHA) inhibit angiogenesis, tumor growth, and metastasis. Proceedings of the National Academy of Sciences. 2013, April 3. These results designate EDPs as unique endogenous mediators of an angiogenic switch to regulate tumorigenesis and implicate a unique mechanistic linkage between omega-3 and omega-6 fatty acids and cancers.

Panigrahy D, Kalish BT, Huang S, Bielenberg DR, Le HD, Yang J, Edin ML, Lee CR, Benny O, Mudge DK, Butterfield CE, Mammoto A, Mammoto T, Inceoglu B, Jenkins RL, Simpson M, Akino T, Lih FB, Tomer KB, Ingber DE, Hammock BD, Falck JR, Manthati VL, Kaipainen A, Amore PA,, Puder M, Zeldin DC, Kieran MW. Epoxyeicosanoids Promote Organ and Tissue Regeneration. Proceedings of the National Academy of Sciences. 2013 Aug 13:110(33):13528-33. These studies demonstrated that epoxyeicosatrienoic acids (EETs) stimulate organ regeneration in three different models (liver, lung and kidney) and are up-regulated both in mice and human patients undergoing partial liver resection. This provided in vivo demonstration that pharmacological modulation of EETs can affect organ regeneration.

Zhang G, Panigrahy D, Hwang SH, Yang J, Mahakian LM, Wettersten HI, Liu JY, Wang Y, Ingham ES, Tam S, Kieran MW, Weiss RH, Ferrara KW, Hammock BD. Dual inhibition of cyclooxygenase-2 and soluble epoxide hydrolase synergistically suppresses primary tumor growth and metastasis. Proceedings of the National Academy of Sciences. 2014 Jul 14: pii 201410432 These studies show that dual inhibition of COX-2 and sEH synergistically inhibits primary tumor growth and metastasis by suppressing tumor angiogenesis. These results demonstrate a critical interaction of these two lipid metabolism pathways on tumorigenesis and suggest dual inhibition of COX-2 and sEH as a potential therapeutic strategy for cancer therapy.