Rate My Professor Suming Huang

Suming Huang, PhD, MS, is Professor of Pediatrics and Pharmacology and Chair of the Four Diamonds Epigenetics and Gene Regulation Research Program in Pediatric Oncology in the Department of Pediatrics at Pennsylvania State University College of Medicine. Prior to his current roles, he was affiliated with the University of Florida. Dr. Huang's research specializations include epigenetic mechanisms governing gene expression in hematopoiesis and leukemia development. His laboratory investigates the roles of long noncoding RNAs (lncRNAs), such as HoxBlinc and HOTTIP, in reprogramming chromatin architecture, including topologically associating domains (TADs) independent of CTCF, to activate HOX gene clusters in leukemia. These studies elucidate how epigenetic dysregulation contributes to oncogenesis and stem cell maintenance in acute myeloid leukemia (AML) and T-cell acute lymphoblastic leukemia (T-ALL).

Dr. Huang has authored over 140 publications, accumulating more than 4,400 citations and an h-index reflecting substantial influence in epigenetics and oncology. Key publications encompass 'HoxBlinc lncRNA reprograms CTCF-independent TADs to mediate HOXA cluster activation in leukemia' (Journal of Clinical Investigation, 2025), 'Long noncoding RNAs: emerging regulators of normal and malignant hematopoiesis' (Blood, 2021), 'Gene mutations linked to worse leukemia outcomes in Hispanic and Latino children' (2021), 'Researchers uncover genetic bridge to leukemia development' (2022), and 'AML chemoresistance: The role of mutant TP53 subclonal expansion and therapy strategy' (2020). He has received major funding, including a National Cancer Institute grant of $520,285 for exploring HOTTIP/β-catenin-HOXA9/PRMT1 interactions in AML. Dr. Huang contributes to graduate education as a dissertation advisor and committee member, and participates in international conferences like the SCBA International Symposium. His research advances therapeutic strategies for pediatric cancers through insights into epigenetic vulnerabilities.