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Baochun Zhang, MD, PhD

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  • Adjunct, Department of Cancer Immunology and Virology
  • Assistant Professor of Medicine, Harvard Medical School

Contact Information

  • Office Phone Number617-582-7590


After studying Medicine in China, Dr. Zhang pursued Ph.D study at the Medical University of Ohio, where he used genetic mouse models to study the physiological role of NF-kB2 signaling in immune tolerance and the pathogenic function of NF-kB2 mutation in B cell lymphomagenesis. Dr. Zhang then had his postdoctoral training with Dr. Klaus Rajewsky and Dr. Frederick Alt at the Immune Disease Institute and Children’s Hospital Boston, Harvard Medical School, where he focused on understanding the pathogenesis of diffuse large B cell lymphoma, and immune surveillance against Epstein-Barr virus-associated B cell lymphomas. Dr. Zhang is now an Assistant Professor at the Division of Hematologic Neoplasia of DFCI, and Harvard Medical School. His research group currently focuses on two areas: understanding the biology of normal and malignant B cells; revealing immune surveillance mechanism in B cell malignancies and developing new immunotherapy strategies.

Recent Awards:

  • Fellowship, Leukemia and Lymphoma Society 2008
  • Scholar, American Society of Hematology 2014


Molecular pathogenesis and immune control of B cell lymphomas

Our research effort proceeds along two directions. 1) Using genetically modified mice to study the molecular pathogenesis of diffuse large B cell lymphoma (DLBCL) and Epstein-Barr virus-associated B cell lymphoma. Lymphomas derive from B cells acquiring multiple oncogenic events. Genetically engineered mice, carrying conditional gain- and/or loss-of-function mutants, allow us to assess the causal role of each individual mutational event, the cooperation of multiple such events in lymphomagenesis, and to follow up disease dynamics in vivo. These studies form the basis for identification/validation of therapeutic targets, and rational design of combinatory therapies. 2) Using our mouse models to reveal the surveillance mechanism of immune system on B cell lymphomas, with particular focuses on tumor-killing CD4+ T cells and their regulation by CD8+ regulatory T cells. This work should guide us to develop new immunotherapy strategies for B cell malignancies, and possibly other cancers as well.

Yasuda T, Wirtz T, Zhang B, Wunderlich T, Schmidt-Supprian M, Sommermann T, Rajewsky K. Studying Epstein-Barr Virus Pathologies and Immune Surveillance by Reconstructing EBV Infection in Mice. Cold Spring Harb Symp Quant Biol. 2013, 78: 259-63.


Zhang B*, Kracker S*, Yasuda T*, Casola S*, Vanneman M, Hömig-Hölzel C, Wang Z, Derudder E, Li S, Chakraborty T, Cotter SE, Koyama S, Currie T, Freeman GJ, Kutok JL, Rodig SJ, Dranoff G, Rajewsky K. Immune Surveillance and Therapy of Lymphomas Driven by Epstein-Barr-Virus Protein LMP1 in a Mouse Model. Cell. 2012, 148(4): 739-51.


Sander S, Calado, DP, Srinivasan L, Kochert K, Zhang B, Rosolowski M, Rodig S, Holzmann K, Stilgenbauer S, Siebert R, Bullinger L, Rajewsky K. Synergy between PI3K Signalling and MYC in Burkitt Lymphomagenesis. Cancer Cell. 2012, 22(2): 167-79.


Yang L, Cui H, Wang Z, Zhang B, Ding J, Liu L, Ding HF. Loss of Negative Feedback Control of Nuclear Factor-kappaB2 Activity in Lymphocytes Leads to Fatal Lung Inflammation. Am J Pathol. 2010, 176(6): 2646-57.


Calado DP*, Zhang B*, Srinivasan L, Sasaki Y, Seagal J, Unitt C, Rodig S, Kutok J, Tarakhovsky A, Schmidt-Supprian M, Rajewsky K. Constitutive canonical NF-kB activation cooperates with disruption of Blimp1 in the pathogenesis of activated B cell-like diffuse large cell lymphoma. Cancer Cell. 2010, 18(6): 580-9.


Srinivasan L, Sasaki Y, Calado DP, Zhang B, Paik JH, DePinho RA, Kutok JL, Kearney JF, Otipoby KL, Rajewsky K. PI3 kinase signals BCR-dependent mature B cell survival. Cell. 2009, 139(3): 573-86.


Xiao C, Srinivasan L, Calado DP, Patterson HC, Zhang B, Wang J, Henderson JM, Kutok JL, Rajewsky K. Lymphoproliferative disease and autoimmunity in mice with increased miR-17-92 expression in lymphocytes. Nat Immunol. 2008, 9(4): 405-14.


Wang Z*, Zhang B*, Yang L, Ding J, Ding HF. Constitutive production of NF-kB2 p52 is not tumorigenic but predisposes mice to inflammatory autoimmune disease by repressing Bim expression. J Biol Chem. 2008, 283(16): 10698-706.


Sasaki Y, Calado DP, Derudder E, Zhang B, Shimizu Y, Mackay F, Nishikawa SI, Rajewsky K, Schmidt-Supprian M. NIK-overexpression amplifies, whereas ablation of its TRAF3-binding domain replaces BAFF:BAFF-R-mediated survival signals in B cells. Proc Natl Acad Sci USA. 2008, 105(31): 10883-8.


Zhang B, Wang Z, Li T, Tsitsikov EN, Ding HF. NF-kB2 mutation targets TRAF1 to induce lymphomagenesis. Blood. 2007, 110(2): 743-51.


Zhang B*, Wang Z*, Ding J, Peterson P, Gunning WT, Ding HF. NF-kB2 is required for the control of autoimmunity by regulating the development of medullary thymic epithelial cells. J Biol Chem. 2006, 281(50): 38617-24.



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