Photo of Baochun Zhang,  MD, PhD

Baochun Zhang, MD, PhD

Dana-Farber Cancer Institute

Dana-Farber Cancer Institute
Phone: (617) 582-7590


Baochun_Zhang@dfci.harvard.edu

Baochun Zhang, MD, PhD

Dana-Farber Cancer Institute

EDUCATIONAL TITLES

  • Assistant Professor, Medicine, Harvard Medical School
  • Assistant Professor, Medical Oncology, Dana-Farber Cancer Institute

DF/HCC PROGRAM AFFILIATION

Research Abstract

In our laboratory, we use genetically modified mice to study the molecular pathogenesis of human diffuse large B cell lymphoma and EBV-associated B cell lymphomas in immunosuppressed patients. We also use these mouse models to study the roles of adaptive immune cells in tumor surveillance, in order to develop new immunotherapies.

Publications

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  • 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. PubMed
  • Sander S, Calado DP, Srinivasan L, Köchert K, Zhang B, Rosolowski M, Rodig SJ, Holzmann K, Stilgenbauer S, Siebert R, Bullinger L, Rajewsky K. Synergy between PI3K signaling and MYC in Burkitt lymphomagenesis. Cancer Cell 2012; 22:167-79. PubMed
  • 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; 148:739-51. PubMed
  • 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-虜B activation cooperates with disruption of BLIMP1 in the pathogenesis of activated B cell-like diffuse large cell lymphoma. Cancer Cell 2010; 18:580-9. PubMed
  • 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; 176:2646-57. PubMed
  • 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; 139:573-86. PubMed
  • Sasaki Y,Calado DP,Derudder E,Zhang B,Shimizu Y,Mackay F,Nishikawa S,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 U S A 2008; 105:10883-8. PubMed
  • Wang Z, Zhang B, Yang L, Ding J, Ding HF. Constitutive production of NF-kappaB2 p52 is not tumorigenic but predisposes mice to inflammatory autoimmune disease by repressing Bim expression. J Biol Chem 2008; 283:10698-706. PubMed
  • 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; 9:405-14. PubMed
  • Zhang B, Wang Z, Li T, Tsitsikov EN, Ding HF. NF-kappaB2 mutation targets TRAF1 to induce lymphomagenesis. Blood 2007; 110:743-51. PubMed
  • Zhang B, Wang Z, Ding J, Peterson P, Gunning WT, Ding HF. NF-kappaB2 is required for the control of autoimmunity by regulating the development of medullary thymic epithelial cells. J Biol Chem 2006; 281:38617-24. PubMed