Muzhou Wu, PhD

IMG_8722

Research Assistant Professor of Dermatology

Boston University School of Medicine

Administrative Office

Boston University School of Medicine

609 Albany Street, Boston, MA 02118
Tel: 617-358-9743
Fax: 614-358-9709

Education

2004 B.S. University of Science and Technology of China, Hefei, Anhui
2009 Ph.D. Stony Brook University, Stony Brook, NY
2009-2012 Neuroscience Postdoctoral Fellow Mount Sinai School of Medicine, New York, NY
2014-2017 Dermatology Postdoctoral Associate Boston University School of Medicine, Boston, MA

Research Interests

  • Biomarker Epigenetic cancer therapy
  • Novel therapy for melanoma
  • Melanoma biomarker
  • Melanoma immunotherapy

Summary

Dr. Muzhou Wu’s research interests involve identifying the molecular basis for epigenetic alternations in melanoma development and progression using novel pharmacological inhibitors targeting specific epigenetic proteins. The experimental approaches include both in vitro cell-based assays and preclinical animal models of human disease, including melanoma xenograft model and PDX model. Dr. Wu is also seeking to develop quantitative tools utilizing critical molecular biomarkers, to predict patient responses to targeted epigenetic therapies, which will help to optimize therapeutic decision-making for a personalized approach to treatment of patients with advanced melanoma.

 

Selected Publications

  • Hanly A, Gibson F, Kuang K, Kalin J, Nocco S, Alani RM, Wu M (2020) Drugging the epigenome: overcoming resistance to targeted and immunotherapy in advanced melanoma. Pending
  • Wu M, Hanly A, Gibson F, Kuang K, Kalin J, Nocco S, Collard M, Cole M, Chen A, Agus F, Labadorf A, Cole PA, Alani RM (2020) A novel selective CoREST inhibitor mediates phenotype switching and overcomes therapy resistance in melanoma. Pending
  • Anastas JN, Zee BM, Kalin JH, Kim M, Guo R, Alexandrescu S, Blanco MA, Wu M, Nocco S, Bernstein BE, Alani R, Golub TR, Cole PA, Filbin MG, Shi Y Re-programing Chromatin with a Bifunctional LSD1/HDAC Inhibitor Induces Therapeutic Differentiation in DIPG. (2019) Cancer Cell. Nov 11;36(5):528-544 PMID: 31631026
  • Kim E, Zucconi B, Wu M, Nocco SE, Meyers DJ, McGee J, Venkatesh S, Cohen DL, Gonzalez EC, Ryu B, Cole PA and Alani RM (2019) MITF Expression Predicts Therapeutic Vulnerability to p300 Inhibition in Human Melanoma. Cancer Research May 15;79(10):2649-2661. PMID: 30910803
  • Wu M⌠, Kalin J⌠, Das J, Panova I, Chung HJ, Kim E, Roberts HJ, Roberts JM, Prusevich P, Jeliazkov JR, Burman SSR, Fairall L, Milano C, Eroglu A, Proby CM, Dinkova-Kostova AT, Hancock WW, Gray JJ, Bradner JE, Valente S, Hu Y, Schwabe J, Alani RM, Cole PA. (⌠ equal contribution) (2018) Targeting the CoREST Complex with Dual Histone Deacetylase and Demethylase Inhibitors. Nature Communication. Jan 4;9(1):53 PMID: 29302039
  • Eisenstein A, Chen E, Raghunathan R, Xu X, Wu M, McLean M, McGee J, Ryu B, Alani RM. (2018) Emerging Biomarkers in Cutaneous Melanoma. Molecular Diagnosis & Therapy. Apr;22(2):203-218. PMID: 29411301
  • Magri L, Gacias-Monserrat M, Wu M, Swiss V, Phillips GR, Casaccia P. (2013) Myc-dependent transcriptional regulation of cell cycle and nucleosomal histones during oligodendrocyte differentiation. Neuroscience, special Issue “The secrets of CNS white matter”. PMID: 24502923
  • Wu M, Hernandez M, Shen S, Kelkar D, Wang J, O’Leary R, Phillips GR, Sabo JK, Cate HS, Casaccia P. (2012) Differential modulation of the oligodendrocyte transcriptome by sonic hedgehog and bone morphogenetic protein 4 via opposing effects on histone acetylation. Journal of Neuroscience, May 9; 32(19): 6651-64. PMID: 22573687
  • Wu M, Nissen JC, Chen EI, Tsirka SE (2012) Tuftsin promotes an anti-inflammatory switch and attenuates symptoms in experimental autoimmune encephalomyelitis. PLoS One, 7(4): e34933. PMID: 22529957
  • Wu M, Tsirka SE. (2009) Endothelial NOS-deficient mice reveal dual roles for nitric oxide during experimental autoimmune encephalomyelitis, Glia, 57, 1204-1215. PMID: 19170181
  • Bhasin M, Wu M, Tsirka SE. (2007) Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis, BMC Immunology, 8: 10 PMID: 17634104