Gang Huang, PhD

Member, Division of Experimental Hematology & Cancer Biology

Assistant Professor, UC Department of Pediatrics

Phone 513-636-3214

Fax 513-636-3768


Research in Dr. Huang’s laboratory focuses on genetic and epigenetic regulations of blood cell normal development and leukemia. We first demonstrated that AML1/CBFβ (a hetero-dimer transcription factor) and Mixed-Lineage Leukemia (MLL) protein (an enzyme which methylates lysine 4 of histone H3 tails), form a regulatory complex, which is important for normal blood development and acts as a tumor suppressor in leukemia. Mutations in either one of these three genes account for majority of acute myelogenous leukemia (AML), acute lymphoblastic leukemia (ALL) and myelodysplastic syndromes (MDS).

We also found that the AML1/CBFβ/MLL complex regulates another transcription factor, PU.1, through the upstream regulatory region of the PU.1 gene and that the epigenetic changes of the histone tails occurring in the PU.1 regulatory region correlate with the PU.1 expression level. PU.1 expression level changes are critical for blood cell differentiation and dysregulation of PU.1 dosages leading to leukemia.

This research will provide new insight into the interplay between genetics and epigenetics in normal blood development and leukemia. It will also help to develop generic drugs for most of the AML, ALL and MDS, which will benefit the future clinical treatments.
BS: Peking University, College of Science, Beijing, P.R. China, 1991.

MS: Inner Mongolia University, Graduate School of Science, Huhhort, P.R. China, 1994.

PhD: Kyoto University, Graduate School of Medicine, Kyoto, Japan, 2001.

View PubMed Publications

Staber PB, Zhang P, Ye M, Welner R, Nombela-Arrieta C, Bach C, Kerenyi M, Bartholdy BA, Zhang H, Alberich-Jorda M, Lee S, Yang H, Ng F, Zhang J, Leddin M, Silberstein LE, Hoefler G, Orkin S, Gottgens B, Rosenbauer F, Huang G, Tenen DG. Sustained PU.1 Levels Balance Cell Cycle Regulators to Prevent Exhaustion of Adult Hematopoietic Stem Cells. Mol Cell. 2013.

Hirai H, Kamio N, Huang G, Matsusue A, Ogino S, Kimura N, Satake S, Ashihara E, Imanishi J, Tenen MD, DG, Maekawa T. Cyclic AMP Responsive Element Binding proteins are involved in “emergency” granulopoiesis through the upregulation of CCAAT/Enhancer Binder Protein. PlosONE. 2013

Zhang Y, Chen A, Yan XM, Huang G. Disordered epigenetic regulation in MLL-related leukemia. Int J Hematol. 2012 Oct;96(4):428-37.

Zhang Y, Yan XM, Sashida G, Zhao XH, Rao YL, Goyama S, Whitman SP, Zorko N, Bernot K, Conway R, Witte D, Wang QF, Tenen DG, Xiao ZJ, Marcucci G, Mulloy J, Grimes HL, Caligiuri MA, Huang G. Mll partial tandem duplication (Mll-PTD) causes abnormal hematopoiesis in mice by reprogramming, enhancing self-renewal, lineage skewing and blocking myeloid differentiation. Blood. 2012 Aug 2;120(5):1118-29.

Zorko N, Bernot KS, Whitman SP, Siebenaler RF, Ahmed E, Marcucci GG, Yanes DA, McConnell KK, Mao C. Kalu C, Zhang XL, Jarjoura D, Dorrance AM, Lee BH, Huang G, Marcucci G, Caligiuri MA. Mll Partial Tandem Duplication and Flt3-Internal Tandem Duplication in a Double Knock-in Mouse Recapitulates Features of Counterpart Human Acute Myeloid Leukemias. Blood. 2012 Aug 2;120(5):1130-6.

Huang G, Zhao XH, Wang L, Elf S, Xu H, Zhao XY, Sashida G, Zhang Y, Liu Y, Lee J, Menendez S, Yang YY, Yan XM, Zhang P, Tenen DG, Osato M, Hsieh JDJ, Nimer SD. The ability of MLL to bind RUNX1 and methylate H3K4 at PU.1 regulatory regions is impaired by MDS/AML-associated RUNX1/AML1 mutations. Blood. 2011;118(25):6544-52.

Wang L, Gural A, Sun XJ, Zhao X, Perna F, Huang G, Hatlen MA, Vu L, Liu F, Xu H, Asai T, Xu H, Deblasio T, Menendez S, Voza F, Jiang Y, Cole PA, Zhang J, Melnick A, Roeder RG, Nimer SD. The leukemogenicity of AML1-ETO is dependent on site-specific lysine Acetylation. Science. 2011;333(6043):765-9.

Huang G, Zhang P, Hirai H, Elf S, Yan XM, Chen Z, Koschmieder S, Okuno Y, Dayaram T, Growney JD, Shivdasani RA, Gilliland DG, Speck NA, Nimer SD, Tenen DG. PU.1 is a major downstream target of AML1/RUNX1 in adult hematopoiesis. Nat Genet. 2008;40:51-60.