David H. Sherr, PhD

Professor, Environmental Health
David Sherr
(617) 638-6464dsherr@bu.edu
R Building


Since 1993, David Sherr’s laboratory has conducted research on how common environmental pollutants, such as dioxins, polycyclic aromatic hydrocarbons and PCBs, adversely affect the growth and behavior of several different types of normal and malignant cells. In previous work, the Sherr laboratory studied how environmental chemicals affect the development of the immune system. In specific, his laboratory demonstrated that aromatic hydrocarbons (generated by the combuston of any carbon source) compromise the function of bone marrow cells required for the development of antibody-forming cells. These cells are critical for immune protection against viruses and bacteria. This work had its orignis in Dr. Sherr’s graduate studies on the ontogeny of lymphocyte development. More recently, Dr. Sherr’s laboratory has focused on the molecular mechanisms that initiate and maintain breast cancer and on the effects of environmental chemicals on these processes. The laboratory has shown that a cellular protein receptor, referred to as the aryl hydrocarbon receptor (AhR), plays an important role in the initiation and progression of human breast cancer. The results explain, in part, the association between environmental chemical exposure and breast cancer risk. Perhaps most importantly, these studies demonstrate that the AhR drives human breast cancer cells to invade and, presumably, metastasize even in the absence of environmental chemicals. These observations have led to the development of AhR inhibitors which block AhR activity and prevent tumor cells from invading. One immediate goal of the laboratory, therefore, is the development of potent AhR inhibitors as novel, targeted therapeutics to be used for treatment of all breast cancers but especially for treatment of “triple negative” or chemotherapy-resistant breast cancers. Interestingly, preliminary studies suggest that these AhR inhibitors could be useful for treatment of several other cancer cell types. A new area of study in Dr. Sherr’s laboratory is the analysis of the role of the AhR in blood cell development. These studies are important from both an environmental science and medical science point of view. Studies performed to date suggest that the AhR plays an important roll in the normal development of blood cells. The results suggest the intriguing possibility that common environmental pollutants can alter normal blood cell development by interfering with AhR signaling. Dr. Sherr came to BUSPH from the faculty of Harvard Medical School, where he had earlier been a postdoctoral fellow in the department of Nobel Laureate Baruj Benacerraf. The Sherr Laboratory is funded by research grants from the National Institute of Environmental Health Sciences, the NIH Superfund Basic Research Program, and the Art BeCAUSE breast cancer foundation. Dr. Sherr is the Director of the Boston University Immunology Training Program, and a member of the Amyloid Treatment Research Program, the BU Cancer Center, the Hematology/Oncology Training Program, and the BU Hormone-dependent Cancer Center. He has trained 21 postdoctoral (M.D. or Ph.D.) and 11 predoctoral (M.D. and/or Ph.D.) fellows.

Other Positions:

  • Graduate Faculty (Primary Mentor of Grad Students), Boston University School of Medicine, Graduate Medical Sciences
  • Professor, Pathology & Laboratory Medicine, Boston University School of Medicine
  • Director, Superfund Research Program , Boston University
  • Director, Immunology Training Program, Boston University


  • Brandeis University, BA
  • Cornell University, PhD

Classes Taught

  • SPHEH713


  • Published on 7/24/2014

    Gusenleitner D, Auerbach SS, Melia T, Gómez HF, Sherr DH, Monti S. Genomic models of short-term exposure accurately predict long-term chemical carcinogenicity and identify putative mechanisms of action. PLoS One. 2014; 9(7):e102579.

    Read at: PubMed
  • Published on 2/3/2014

    Lowe MM, Mold JE, Kanwar B, Huang Y, Louie A, Pollastri MP, Wang C, Patel G, Franks DG, Schlezinger J, Sherr DH, Silverstone AE, Hahn ME, McCune JM. Identification of Cinnabarinic Acid as a Novel Endogenous Aryl Hydrocarbon Receptor Ligand That Drives IL-22 Production. PLoS One. 2014; 9(2):e87877.

    Read at: PubMed
  • Published on 1/1/2014

    Gusenleitner, D., S. Auerbach, H. Gomez, T. Meila, R. Tice, D. Sherr, and S. Monti. Genomics Model of Environmental and Chemical Hepatocarcinogenicity. PLOS One. 2014.

  • Published on 8/13/2013

    Sherr DH, Monti S. The role of the aryl hydrocarbon receptor in normal and malignant B cell development. Semin Immunopathol. 2013 Nov; 35(6):705-16.

    Read at: PubMed
  • Published on 8/1/2013

    Sherr DH. Blocking triple negative breast cancer. International Innovations. 2013.

  • Published on 8/1/2013

    Quintana FJ, Sherr DH. Aryl hydrocarbon receptor control of adaptive immunity. Pharmacol Rev. 2013; 65(4):1148-61.

    Read at: PubMed
  • Published on 5/30/2013

    Smith BW, Rozelle SS, Leung A, Ubellacker J, Parks A, Nah SK, French D, Gadue P, Monti S, Chui DH, Steinberg MH, Frelinger AL, Michelson AD, Theberge R, McComb ME, Costello CE, Kotton DN, Mostoslavsky G, Sherr DH, Murphy GJ. The aryl hydrocarbon receptor directs hematopoietic progenitor cell expansion and differentiation. Blood. 2013 Jul 18; 122(3):376-85.

    Read at: PubMed
  • Published on 6/28/2012

    Selmi C, Leung PS, Sherr DH, Diaz M, Nyland JF, Monestier M, Rose NR, Gershwin ME. Mechanisms of environmental influence on human autoimmunity: a National Institute of Environmental Health Sciences expert panel workshop. J Autoimmun. 2012 Dec; 39(4):272-84.

    Read at: PubMed
  • Published on 1/19/2012

    Lawrence BP, Sherr DH. You AhR what you eat? Nat Immunol. 2012 Feb; 13(2):117-9.

    Read at: PubMed
  • Published on 9/6/2011

    Flies A, Ahmadi T, Parks AJ, Prokaeva T, Weng L, Rolfe SS, Seldin DC, Sherr DH. Immunoglobulin light chain, Blimp-1 and cytochrome P4501B1 peptides as potential vaccines for AL amyloidosis. Immunol Cell Biol. 2012 May; 90(5):528-39.

    Read at: PubMed

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