Satdarshan (Paul) Singh Monga, MD, FAASLD, is an academic physician by training with an interest in furthering our understanding of many aspects of liver health and disease. After completing his medical training and internship in India, he did his post-doctoral training in Gastroenterology, Hepatology & Molecular Biology at the Department of Veterans Affairs Medical Center in Washington D.C., learning about liver development and signal transduction. He joined the University of Pittsburgh in the Department of Pathology in 1999 for his second postdoctoral fellowship where he trained in the areas of liver regeneration and liver tumors. He became faculty in 2001 and was appointed on tenure stream in 2003.
He currently is the UPMC Endowed Chair for Experimental Pathology, and Professor of Pathology and Medicine. He serves as the Vice Chair and Chief of the Division of Experimental Pathology (https://path.upmc.edu/Exp-Pathology/dep.htm). He is the founding director of the Pittsburgh Liver Research Center (PLRC), an NIDDK-funded Silvio O Conte Digestive Diseases Research Core Centers. This center of around 100 members is highly accomplished and well known for their continued fundamental, translational and clinical impact on the liver field. The members of the center study regenerative medicine, chronic liver injury and tumorigenesis. The center provides 4 research core services- cell and tissue imaging, clinical tissue biobanking, genomics and systems biology, and synthetic biology (https://livercenter.pitt.edu).
He is also the program director of a NIH-funded T32 predoctoral training grants on Regenerative Medicine and serves as the Assistant Dean and co-Director for the Medical Scientist Training Program (MSTP) at our institution.
For the last 20 years, Dr. Monga’s lab has been focused on elucidated the cellular and molecular underpinnings of hepatic pathophysiology especially of liver development, repair, and tumorigenesis. His research has been consistently funded by NIH and industry since 2003 and is PI/MPI of 4 R01s and 5 corporate research agreements. He has over 185 manuscripts and reviews in journals like Hepatotology, Gastroenterology, Journal of Hepatology, American Journal of Pathology, Cell Metabolism, Cell Reports and others. Major areas of his research include cellular and molecular underpinnings of hepatobiliary repair where his group is focusing on innovations in regenerative therapies and cellular reprogramming. His lab has deconvoluted the complex cell-molecule circuitry of pathways like Wnt/-catenin in liver physiology especially in metabolic zonation and regeneration, which may be of essence in promoting hepatic repair. Over 2 decades of work from his lab has identified the cell source, identity of Wnt proteins and the ensuing paracrine effect on hepatocytes at both baseline and after surgical insult to the liver. His studies have revealed the importance of Wnt2 and Wnt9b from endothelial cells in the process of metabolic zonation and after partial hepatectomy, in inducing -catenin activation in the hepatocytes.
His lab has also shown an advantage of -catenin activation in promoting or accelerating liver repair after injury demonstrating therapeutic potential of regenerative hepatology in acute liver injury and transplantation settings. Another major focus of his lab is to understand the basis of liver tumors especially hepatoblastoma (HB), hepatocellular cancer (HCC) and cholangiocarcinoma (CCA). Using molecular and bioinformatic information from clinical tumors, his group has generated innovative animal models to address biology and therapies with the goals of enabling precision medicine in liver tumor space. Several groups including industry are now collaborating with his laboratory to test novel therapeutic modalities to treat -catenin-active liver tumors using their highly relevant models. Additional studies from his group have yielded many important biological, diagnostic and therapeutic insights into various categories of liver tumors. Some key findings include the ability of -catenin gene mutations in HCC to induce mTORC1 activation demonstrating a unique role of mTOR inhibitors in treatment of the subsets of HCC with CTNNB1 mutations. Likewise, they have shown resistance of CTNNB1 mutant HCCs to immune checkpoint inhibitors.