Jian Huang, MD, PhD

Associate Professor
Senior Scientist for Stem Cell Biology and Gene Engineering

I trained in medicine at Peking University Health Science Center of China, started my research career at State University of New York Downstate Medical Center as a PhD student, did my postdoc training at University of Pennsylvania School of Medicine. As a faculty member, I started my independent laboratory with a K99/R00 career award from NHLBI/NIH at Temple University, School of Medicine in 2013. I am currently a Senior Scientist for Stem Cell Biology and Gene Engineering at the Coriell Institute for Medical Research.

My laboratory studies signal transduction pathways regulate hematopoietic stem cell (HSC) self-renewal and differentiation as well as drug resistance of hematological malignancies. Specifically, our research focuses on three main topics: 1. Understanding the roles of GSK3 and PPAR-d/mitophagy signaling in the regulation of HSCs self-renewal, and the contribution to leukemogenesis; 2. Identifying new targets in leukemia therapy with a multiplexed genome editing CRISPR screening platform; 3. Investigating the role of epigenetic regulation especially DNA methylation in HSC function and homeostasis.

HSCs are able to self-renew and differentiate into all blood cell lineages. Several decades of successful HSC transplantations have demonstrated the therapeutic importance of HSC. Hematopoietic stem cell transplantation (HSCT) is a life-saving procedure for treatment of malignant and non-malignant disorders and is usually a last resort for those with no other treatment options available. Although HSCs are the most well-characterized tissue-specific stem cells, our understanding of the molecular pathways that control HSC maintenance and function is still limited. A better understanding of the complex signaling network regulating the balance between HSC self-renewal and differentiation will allow us to manipulate HSCs to enhance their therapeutic efficacy. Our recent work identified a new connection between GSK3 and PPAR-δ/mitophagy pathway, which will provide new insights into the mechanisms of the regulation of HSC activity and may improve the therapy of many hematopoietic disorders.

As an effort to understand hematological malignancies, we also developed a new research direction that focuses on drug resistance of Acute Myeloid Leukemia (AML) The drug resistance of AML contributes to the relapse of the disease. We carried out an unbiased CRISPR-based screen for genes whose loss confers drug resistance. In the screen, we identified SPRY3 and GSK3 as the leading hits. SPRY3 and GSK3 are key negative regulators of Ras/MAPK and Wnt signaling, respectively. Accordingly, we discovered that re-activation of these signaling pathways in AML are a major mechanism that confer resistance to Quizartinib (AC220). Remarkably, we also confirmed our findings in primary AML patient samples and discovered that the expression of SPRY3 and GSK3 is dramatically reduced in AC220 resistant AML patient samples. Next, we plan to further explore the detailed mechanisms underlying resistance to Tyrosine kinase inhibitor (TKI) in FLT3ITD+ AML.


Postdoctoral Fellow, University of Pennsylvania Perelman School of Medicine

Ph.D, State University of New York Downstate Medical Center

MD, Peking University Health Science Center

BS, Peking University Health Science Center



PubMed - My Bibliography