David H. Sherr, PhD
Boston University School of Public Health
Dept of Environmental Health

PhD, Cornell University

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.

Graduate Faculty (Primary Mentor of Grad Students)
Boston University School of Medicine, Division of Graduate Medical Sciences

Boston University School of Medicine
Pathology & Laboratory Medicine

Boston University
Superfund Research Program

Boston University
Immunology Training Program

2014-2016 Avon Foundation: Research Award

Research Training in Immunology
09/01/2014 - 08/31/2018 (PI of Sub-Project / SP)
PI: Thomas Kepler, PhD
NIH/National Institute of Allergy & Infe

Superfund Research Program at Boston University
08/01/2017 - 03/31/2018 (PI)
NIH/National Institute of Environmental

Defining the role of the AHR in Blood Cell Specification
01/01/2016 - 11/30/2017 (PI)
NIH/National Institute of Environmental

Receptor-based Developmental and Reproductive Toxicity of Superfund Chemicals
04/01/2016 - 07/31/2017 (PI)
NIH/National Institute of Environmental

The Role of an Environmental Chemical Receptor in Development and Popagation of Cancer Stem Cells in Triple Negative and Inflammatory Breast Cancer
03/01/2016 - 04/20/2017 (PI)
Avon Breast Cancer Crusade, LLC.

Epidemiology of Immunotoxicant Exposure in Children
07/01/2011 - 02/28/2017 (PI)
President and Fellows of Harvard College NIH NIEHS

Receptor-based Developmental and Reproductive Toxicity of Superfund Chemicals
09/20/2012 - 03/31/2016 (PI)
NIH/National Institute of Environmental

The Role of an Environmental Chemical Receptor in Development and Propagation of Cancer Stem Cells in Triple Negative and Inflammatory Breast Cancer
07/01/2014 - 02/29/2016 (PI)
Avon Foundation

Stress Granules and the Biology of TDP-43
03/01/2012 - 12/31/2015 (SP Co-PI of Sub-Project / SP)
PI: Benjamin Wolozin, MD, PhD
NIH/National Institute of Environmental

Signaling Pathways in Stages of Mammary Tumorigenesis:Project1
01/01/2010 - 06/30/2015 (PI)
Trustees of Tufts College, Inc NIH NIEHS

Showing 10 of 28 results. Show All Results

Yr Title Project-Sub Proj Pubs
2018 Defining the Role of the AHR in Blood Cell Specifications 5R01ES025409-03 1
2017 Defining the Role of the AHR in Blood Cell Specifications 5R01ES025409-02 1
2017 Superfund Research Program at Boston University 2P42ES007381-21 314
2017 Core A: Administrative Core 2P42ES007381-21-8619 314
2017 Core-005 2P42ES007381-21-6458 314
2016 Defining the Role of the AHR in Blood Cell Specifications 1R01ES025409-01A1 1
2016 Receptor-based developmental and reproductive toxicity of Superfund chemicals 4P42ES007381-20 314
2015 Receptor-based developmental and reproductive toxicity of Superfund chemicals 5P42ES007381-19 314
2015 Receptor-based developmental and reproductive toxicity of Superfund chemicals 3P42ES007381-19S2 314
2015 Research Training in Immunology 5T32AI007309-27 46
Showing 10 of 58 results. Show All Results
Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Faculty can login to make corrections and additions.

  1. Shashar M, Belghasem ME, Matsuura S, Walker J, Richards S, Alousi F, Rijal K, Kolachalama VB, Balcells M, Odagi M, Nagasawa K, Henderson JM, Gautam A, Rushmore R, Francis J, Kirchhofer D, Kolandaivelu K, Sherr DH, Edelman ER, Ravid K, Chitalia VC. Targeting STUB1-tissue factor axis normalizes hyperthrombotic uremic phenotype without increasing bleeding risk. Sci Transl Med. 2017 Nov 22; 9(417).View Related Profiles. PMID: 29167396; DOI: 10.1126/scitranslmed.aam8475;.
  2. Ash PEA, Stanford EA, Al Abdulatif A, Ramirez-Cardenas A, Ballance HI, Boudeau S, Jeh A, Murithi JM, Tripodis Y, Murphy GJ, Sherr DH, Wolozin B. Dioxins and related environmental contaminants increase TDP-43 levels. Mol Neurodegener. 2017 05 05; 12(1):35.View Related Profiles. PMID: 28476168; DOI: 10.1186/s13024-017-0177-9;.
  3. Mulas F, Li A, Sherr DH, Monti S. Network-based analysis of transcriptional profiles from chemical perturbations experiments. BMC Bioinformatics. 2017 Mar 23; 18(Suppl 5):130.View Related Profiles. PMID: 28361664; DOI: 10.1186/s12859-017-1536-9;.
  4. Wang Z, Monti S, Sherr DH. The diverse and important contributions of the AHR to cancer and cancer immunity. 2017; 2:102-107.
  5. Novikov O, Wang Z, Stanford EA, Parks AJ, Ramirez-Cardenas A, Landesman E, Laklouk I, Sarita-Reyes C, Gusenleitner D, Li A, Monti S, Manteiga S, Lee K, Sherr DH. An Aryl Hydrocarbon Receptor-Mediated Amplification Loop That Enforces Cell Migration in ER-/PR-/Her2- Human Breast Cancer Cells. Mol Pharmacol. 2016 Nov; 90(5):674-688.View Related Profiles. PMID: 27573671.
  6. Chen HR, Sherr DH, Hu Z, DeLisi C. A network based approach to drug repositioning identifies plausible candidates for breast cancer and prostate cancer. BMC Med Genomics. 2016 Jul 30; 9(1):51. PMID: 27475327; PMCID: PMC4967295; DOI: 10.1186/s12920-016-0212-7;.
  7. Stanford EA, Ramirez-Cardenas A, Wang Z, Novikov O, Alamoud K, Koutrakis P, Mizgerd JP, Genco CA, Kukuruzinska M, Monti S, Bais MV, Sherr DH. Role for the Aryl Hydrocarbon Receptor and Diverse Ligands in Oral Squamous Cell Carcinoma Migration and Tumorigenesis. Mol Cancer Res. 2016 Aug; 14(8):696-706.View Related Profiles. PMID: 27130942; PMCID: PMC4987205; DOI: 10.1158/1541-7786.MCR-16-0069;.
  8. Smith BW, Stanford EA, Sherr DH, Murphy GJ. Genome Editing of the CYP1A1 Locus in iPSCs as a Platform to Map AHR Expression throughout Human Development. Stem Cells Int. 2016; 2016:2574152.View Related Profiles. PMID: 27148368; DOI: 10.1155/2016/2574152;.
  9. Stanford EA, Wang Z, Novikov O, Mulas F, Landesman-Bollag E, Monti S, Smith BW, Seldin DC, Murphy GJ, Sherr DH. The role of the aryl hydrocarbon receptor in the development of cells with the molecular and functional characteristics of cancer stem-like cells. BMC Biol. 2016 Mar 16; 14:20.View Related Profiles. PMID: 26984638; PMCID: PMC4794823; DOI: 10.1186/s12915-016-0240-y;.
  10. Grandjean P, Barouki R, Bellinger DC, Casteleyn L, Chadwick LH, Cordier S, Etzel RA, Gray KA, Ha EH, Junien C, Karagas M, Kawamoto T, Paige Lawrence B, Perera FP, Prins GS, Puga A, Rosenfeld CS, Sherr DH, Sly PD, Suk W, Sun Q, Toppari J, van den Hazel P, Walker CL, Heindel JJ. Life-Long Implications of Developmental Exposure to Environmental Stressors: New Perspectives. Endocrinology. 2015 Oct; 156(10):3408-15. PMID: 26241067; PMCID: PMC4588822; DOI: 10.1210/EN.2015-1350;.
Showing 10 of 123 results. Show More

This graph shows the total number of publications by year, by first, middle/unknown, or last author.

Bar chart showing 115 publications over 34 distinct years, with a maximum of 8 publications in 1996

In addition to these self-described keywords below, a list of MeSH based concepts is available here.

Aryl hydrocarbon receptor
Breast cancer and the environment
Contact for Mentoring:

72 E. Concord St Housman (R)
Boston MA 02118
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