Center for Interdisciplinary Research
in Environmental Exposures and Health
Main / The Sherr Lab

David H. Sherr, Ph.D.

Dr. Sherr received his B.A. from Brandeis University in 1973 and his Ph.D. from Cornell University in 1978. He conducted his postdoctoral studies at Harvard Medical School with Dr. Martin Dorf and Nobel Laureate Baruj Benacerraf from 1978 to 1981. After rising to the rank of Associate Professor at Harvard Medical School, Dr. Sherr was recruited into the Department of Environmental Health at the Boston University School of Public Health in 1994. He holds joint appointments in the Department of Environmental Health and in the Department of Pathology and Laboratory Medicine in the B.U. School of Medicine. With an active program in basic immunology, Dr. Sherr is also a member of the Boston University Immunology Training Program, the Hematology/Oncology Training Program, the Amyloid Treatment and Research Program, and the Women's Health Interdisciplinary Research Center (WHIRC). Dr. Sherr directs the Boston University Medical Campus Flow Cytometry Core Facility, which services over 300 users throughout the medical camplus, and he has published over 96 articles in peer-reviewed journals including The Journal of Immunology, The Journal of Experimental Medicine, Blood, Nature, Nature Genetics, Molecular Pharmacology, and Cancer Research. Professor Sherr has established a robust research program that combines immunobiology, toxicology, and cancer biology. (See below for more detail on the Sherr laboratory) Specifically, his laboratory studies the role of the aryl hydrocarbon receptor (an intracellular protein which is activated by environmental pollutants such as dioxins, polycyclic aromatic hydrocarbons/PAH, and polychlorinated biphenyls/PCBs) in the death of immature B lymphocytes and in the aberrant regulation of breast cancer cell growth. In translational studies, Dr. Sherr's laboratory also is attempting to generate vaccines predicted to be effective against a number of cancers including breast cancer and B cell malignancies (AL amyloidosis, myeloma, and lymphoma).

The Sherr Lab
The Sherr laboratory is located in the Department of Environmental Health at the Boston University School of Public Health in Boston's South End. Minutes from Boston's cultural and sports attractions, the laboratory employs state-of-the-art cellular and molecular technologies to research three specific areas of basic and applied science: 1) mechanisms through which environmental chemicals suppress the immune system (the Apoptosis team), 2) molecular signaling leading to environmental carcinogen-induced and spontaneous breast cancers (the Breast Cancer team), 3) development of vaccines for the treatment of cancer and primary amyloidosis (the Cancer/Amyloid Immunotherapy team). The common element in these 3 disciplines is the involvement of an environmental chemical receptor, the aryl hydrocarbon receptor (AhR), in the suppression of the immune system and in maintaining tumor cell growth. The Sherr laboratory occupies 3,300 square feet of newly renovated laboratory space in the Housman Research Building within the Boston University Medical Center and School of Medicine.

Relevant Publications

Hahn, M. E., L. L. Allan, and D. H. Sherr. 2009. Regulation of constitutive and inducible AHR signaling: complex interactions involving the AHR repressor. Biochem Pharmacol 77:485-497.

Karchner, S. I., M. J. Jenny, A. M. Tarrant, B. R. Evans, H. J. Kang, I. Bae, D. H. Sherr, and M. E. Hahn. 2009. The active form of human aryl hydrocarbon receptor repressor lacks exon 8 and its Pro185 and Ala185 variants repress both AHR and HIF. Mol Cell Biol.

Yang, X., S. Solomon, L. R. Fraser, A. F. Trombino, D. Liu, G. E. Sonenshein, E. V. Hestermann, and D. H. Sherr. 2008. Constitutive regulation of CYP1B1 by the aryl hydrocarbon receptor (AhR) in pre-malignant and malignant mammary tissue. J Cell Biochem 104:402-417.

Min, C., S. F. Eddy, D. H. Sherr, and G. E. Sonenshein. 2008. NF-kappaB and epithelial to mesenchymal transition of cancer. J Cell Biochem 104:733-744.

Bissonnette, S., J. Emberley, D. Sherr, and J. Schlezinger. 2008. Overlapping but distinct apoptosis signaling pathways induced by an environmental (MEHP) and an endogenous (15d-PGJ2) PPAR agonist. J. Immunol. In Press.

Evans, B. R., S. I. Karchner, L. L. Allan, R. S. Pollenz, R. L. Tanguay, M. J. Jenny, D. H. Sherr, and M. E. Hahn. 2008. Repression of aryl hydrocarbon receptor (AHR) signaling by AHR repressor: role of DNA binding and competition for AHR nuclear translocator. Mol Pharmacol 73:387-398.

Belguise, K., S. Guo, S. Yang, A. E. Rogers, D. C. Seldin, D. H. Sherr, and G. E. Sonenshein. 2007. Green tea polyphenols reverse cooperation between c-Rel and CK2 that induces the aryl hydrocarbon receptor, slug, and an invasive phenotype. Cancer Res 67:11742-11750.

Ahmadi T, F. A., Efebera, Y, Sherr DH 2007. CD40 ligand-activated, antigen-specific B Cells are comparable to mature dendritic cells in presenting protein antigens and MHC class I- and class II-binding peptides Immunology 124:129-140.

Schlezinger JJ, Emberley J, Bissonette S, and Sherr DH. 2007. An 1-tyrosine derivative and PPARg agonist, GW7845, activates a multi-faceted caspase cascade in bone marrow B cells. Toxicological Sciences. 98:125-136

Schlezinger JJ, Liu D., Farago M, Seldin DC, Belguise K, Sonenshein G, and Sherr DH. 2006. A role for the aryl hydrocarbon receptor in mammary gland tumorigenesis Biological Chemistry. 387:1175-87. Abstract

Schlezinger JJ, Emberley J, and Sherr DH. 2006. Activation of multiple MAP Kinases in pro/pre-B cells by GW7845, a PPARg agonist, and their contribution to GW7845-induced apoptosis. Toxicological Sciences. 92:433. Publication

Murray TJ, Yang X, and Sherr DH. 2006. Growth of a human mammary tumor cell line is blocked by galangin, a naturally occurring bioflavonoid, and is accompanied by down-regulation of cyclins D3, E, and A. Breast Cancer Res 8:R17. Publication

Allan LL, Schlezinger J, Shansab M, and Sherr DH. 2006. CYP1A1 in polycyclic aromatic hydrocarbon-induced B lymphocyte growth suppression. Biochem Biophys Res Commun. 342:227. Publication

Shin SR, Sanchez-Velar N, Sherr DH, and Sonenshein GE. 2006. 7,12-Dimethylbenz[a]Anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of NF-kB. Cancer Research. 66:2570. Publication

Schlezinger JJ, Emberley J, and Sherr DH. 2006. Activation of multiple MAP Kinases in pro/pre-B cells by GW7845, a PPAR agonist, and their contribution to GW7845-induced apoptosis. Toxicological Sciences. In Press. Abstract

Murray TJ, Yang X, and Sherr DH. 2006. Growth of a human mammary tumor cell line is blocked by galangin, a naturally occurring bioflavonoid, and is accompanied by down-regulation of cyclins D3, E, and A. Breast Cancer Res 8:R17. Publication

Allan LL, Schlezinger J, Shansab M, and Sherr DH. 2006. CYP1A1 in polycyclic aromatic hydrocarbon-induced B lymphocyte growth suppression. Biochem Biophys Res Commun 342:227. Abstract

Shin SR, Sanchez-Velar N, Sherr DH, and Sonenshein GE. 2006. 7,12-Dimethylbenz[a]Anthracene treatment of a c-rel mouse mammary tumor cell line induces epithelial to mesenchymal transition via activation of NF-eB. Cancer Research. 66:2570. Abstract

Currier N, Solomon S, Demicco E, Chang D, Farago M, Ying H, Dominguez I, Rogers AE, Sonenshein GE, Cardiff R, Xiao J, Sherr DH, and Seldin DC. 2005. Oncogenic signaling pathways activated in DMBA-induced mouse mammary tumors. Toxicologic Pathology.33:726.

Ryu H-Y, Emberley J, Schlezinger J, Allan LL, Na S, and Sherr DH. 2005. Environmental chemical-induced bone marrow B cell apoptosis: Death receptor-independent activation of a caspase-3 to caspase-8 pathway. Molecular Pharmacology. 68:1087. Abstract

Yang X, Murray TJ, Liu D, Mitchell GC, Hesterman EV, Karchner SI, Hahn ME and Sherr DH. 2005. The aryl hydrocarbon receptor/transcription factor constitutively represeses c-myc transcription in human mammary tumor cells. Oncogene. 24:7869. Abstract

Allan L and Sherr DH. 2005. Constitutive activation and environmental chemical induction of the aryl hydrocarbon receptor/transcription Factor (AhR) in activated human B lymphocytes. Mol. Pharmacol. 67:1740. Abstract

Schaefer KL, Senevich S, Ma C, Cooley SR, Nakajima A, Wada, K, Schlezinger JJ, Sherr DH, and Saubermann LJ. 2005. Intestinal anti-inflammatory effects of thiazolidenedione PPAR ligands on Th1 chemokine regulation include non-transcriptional control mechansisms. Inflammatory Bowel Diseases. 11:244. Abstract

Murray SA, Yang S, Demicco E, Ying H, Sherr DH, Hafer LJ, Rogers AE, Sonenshein GE, and Xiao Z-X J. 2005. Increased expression of MDM2, cyclin D1, and p27Kip1 in carcinogen-induced rat mammary tumors. J. Cell Biochem. 95:875. Abstract

Maecker B, von Bergwelt-Baildon MS, Sherr DH, Nadler LM, Schultze JL. Identification of a new HLA-A*0201 restricted cryptic epitope from CYP1B1. 2005. International Journal of Cancer. 115:333 Abstract

Tiwari, S, Felekkis K, Moon EY, Flies A, Sherr DH, and Lerner A. 2004. Among circulating hematopoietic cells, B-CLL uniquely expresses functional EPAC1, but EPAC1-mediated Rap1 activation does not account for PDE4 inhibitor-induced apoptosis. Blood. 103:2661. Abstract

Schlezinger, JJ, Hurst CH, Waxman DJ, Sherr DH. 2004.Environmental and Endogenous Peroxisome Proliferator-Activated Receptor {gamma} Agonists Induce Bone Marrow B Cell Growth Arrest and Apoptosis: Interactions between Mono(2-ethylhexyl)phthalate, 9-cis-Retinoic Acid, and 15-Deoxy-{Delta}12,14-prostaglandin J21. J. Immunol.173:3165. Abstract

Xiao, S, Zhang X, Mann KK, Jodo S, Sherr DH, Marshak-Rothstein A, and Ju S-T. 2004. Changes in sensitivity of peripheral lymphocytes of autoimmune gld mice to FasL-mediated apoptosis reveal a mechanism for the preferential deletion of CD4CD8B220+ T cells. Int. Immuno. 16:759 Abstract

Sherr DH. 2004. 2,3,7,8-Tetrachloro-p-dioxin (TCDD) and long term immunologic memory. Toxicol. Sci. 79:211 Abstract

Tiwari S, Felekkis K, Moon E, Flies A, Sherr DH, Lerner A. 2003. Among circulating hematopoeitic cells, B-CLL uniquely expresses functional EPAC1 bu tEPAC1-mediated Rap1 activation does not account for PDE4 inhibitor-induced apoptosis. Blood. 103(7):2661-7. Abstract

Jensen, BA, Leeman, RJ, Schlezinger, JJ, Sherr, DH. 2003. Aryl hydrocarbon receptor (AhR) agonists suppress interleukin-6 expression by bone marrow stromal cells. Env. Health. J. 2:16. Abstract

Allan, LL, Mann, KK, Schlezinger, JL, Sherr, DH. 2003. Bone Marrow Stromal-B Cell Interactions in Polycyclic Aromatic Hydrocarbon-Induced Pro/Pre-B Cell Apoptosis. Toxicol. Sci. 76:357. Abstract

Ryu-K-Y, Mann KK, Schlezinger JJ, Jensen B, Sherr, DH. 2003. Environmental Chemical-Induced Pro/Pre-B Cell Apoptosis: Analysis of c-Myc, p27Kip1, and p21WAF1 Reveals a Death Pathway Distinct from Clonal Deletion. J. Immunol. 170:4897-4904 Abstract

Maecker B, Sherr DH, Vonderheide RH, von Bergwelt-Baildon M, Hirano N, Anderson KS, Xia Z, Butler MO, Wucherpfennif KW, O'Hara C, Cole G, Ramstedt U, Tomlinson AJ, Chicz RM, Nadler LM, and Schultze JL. 2003. The shared tumor associated antigen cytochrome P450 1B1 is recognized by specific cytotoxic T cells. Blood. 102:3287. Abstract

Takai, Y., J. Canning, G. I. Perez, J. K. Pru, J. J. Schlezinger, Sherr, DH, R. N. Kolesnick, J. Yuan, R. A. Flavell, S. J. Korsmeyer, and J. L. Tilly. 2003. Bax, caspase-2, and caspase-3 are required for ovarian follicle loss caused by 4-vinylcyclohexene diepoxide exposure of female mice in vivo. Endocrinology 144:69-74. Abstract

Schlezinger JJ, Jensen BA, Mann KK, Ryu H-Y, Sherr DH. 2002. Peroxisome proliferator-activated receptor -mediated NF-B activation and apoptosis in pre-B cells. J.Immunol. 169:6831. Abstract

Matikainen, TM, Moriyama T, Morita Y, Perez, GI, Korsmeyer SJ, Sherr, DH, Tilly, JL. 2001. Ligand activation of the aromatic hydrocarbon receptor (AHR)-transcription factor drives Bax-dependent apoptosis in developing fetal ovarian germ cells. Endocrinology. 143:615-620 Abstract

Matikainen T, Perez, GI, Jurisicova A, Mann KK, Schlezinger JJ, Ryu H-Y, Sakai T, Korsmeyer SJ, Casper RF, Sherr DH, Tilly JT. 2001, Dioxin receptor-dependent bax gene transcription is required for ovarian failure caused by biohazardous environmental chemicals. Nature Genetics. 28:355-360.

Kavanagh KT, Hafer LJ, Kim DW, Mann KK, Sherr DH, Rogers AE, Sonenshein GE. 2001. Green tea extracts decrease carcinogen-induced mammary tumor burden in rats and rate of breast cancer cell proliferation in culture. J. Cell. Biochem. 82:387-398. Abstract

Mann KK, Doerre, S, Sherr DH, Quadri S. 2001. The role of NF-B as a survival factor in environmental chemical-induced preB cell apoptosis. Molec. Pharmacol. 59:302-309. Abstract

Jodo S, Hohlbaum A, Xiao S, Chan D, Strehlow D, Sherr DH, Marshak-Rothstein, M and Ju S-T. 2000. CD 95 ligand (FasL)-expressing vesicles display antibody-mediated, FcR-dependent enhancement of cytotoxicity. J. Immunol. 165:5487-5494. Abstract

Kim, DW, Gazourian, L, Quadri, SA, Sherr, DH, Sonenshein, GE. 2000. The aryl hydrocarbon receptor/transcriptiojn factor (AhR) and the Rel A nuclear factor-B subunit cooperate to transactivate the c-myc promoter. Oncogene. 19:5498-5506. Abstract

Quadri S, Qadri A, Hahn ME, Mann KK, Sherr DH. 2000. The bioflavonoid galangin blocks aryl hydrocarbon receptor (AhR) activation and polycyclic aromatic hydrocarbon-induced pre-B cell apoptosis. Molec. Pharmacol. 58:515-525. Abstract

Trombino AF, Near, RI, Matulka, RA, Yang S, Hafer, LJ, Toselli, PA, Kim D, Sovak, M, Rogers A, Sonenshein G, Sherr DH. 2000. Expression of the aryl hydrocarbon receptor/transcription Factor (AhR) and AhR-regulated CYP1 gene transcripts in a rat model of mammary tumorigenesis. Breast Cancer Research and Treatment, 62:117-131.

Robles, R, Morita, Y, Mann, KK, Perez, GI, Yang, S, Matikainen, T, Sherr, DH, Tilly, JL. 2000. The aryl hydrocarbon receptor, a basic helix-loop-helix trancription factor of the PAS gene family, is required for normal ovarian germ cell dynamics in the mouse. Endocrinology. 141:450-453. Abstract

Mann K., Matulka R, Lawrence BP, Kerkvliet, N, Trombino AF, Hahn M, and Sherr, DH. 1999. The role of polycyclic aromatic hydrocarbon metabolism in dimethylbenz[a]anthracene-induced pre-B lymphocyte apoptosis. Toxicol. Appl. Pharmacol. 161:10-22. Abstract

Near, R.I., Matulka, R.A., Mann, K.K., Shneider, A.M. Gogate, S.U., Trombino, A.F., and Sherr DH. 1999. Regulation of PreB Cell Apoptosis by Aryl Hydrocarbon Receptor/Transcription Factor-Expressing Stromal/AdherentCells. Proceedings of the Society for Experimental Biology and Medicine. 221:242-252 Abstract

Yamaguchi, K., Matulka, RA, Shneider A., Toselli, P., Trombino, AF, Yang, S, Hafer, LJ., Mann, KK., Tao, X-J., Tilly, JL., Near R., Sherr DH, 1997. Induction of preB cell apoptosis by 7,12 dimethylbenz[]anthracene in long term primary bone marrow cultures. Toxicology and Applied Pharmacology. 147: 190. Abstract

Yamaguchi K, Near R, Matulka R, Shneider A, Toselli, P, Trombino, A.F., and Sherr DH. 1997. Activation of the aryl hydrocarbon receptor/transcription factor and bone marrow stromal cell-dependent preB cell apoptosis. J. Immunol. 158: 2165 Abstract

Vaziri, C, Shneider, A., Sherr, DH., and Faller, D. 1996. Expression of the aryl hydrocarbon receptor is regulated by serum and mitogenic growth factors in murine 3T3 fibroblasts. J. Biol. chem. 271:25921. Abstract

Cui, H., Ju, S-T, and Sherr DH, 1996. Functional expression of Fas (CD95) protein in autoimmune lpr mice. Cell. Immunol. 174:35-41. Abstract

Wu M, Arsura M, Bellas, RE, FitzGerald, MJ, Lee H, Schauer SL, Sherr, DH and Sonenshein GE. 1996. Inhibition of c-myc expression induces apoptosis of WEHI 231 murine B cells. Molec. Cell. Biol. 16:5015. Abstract

Wu M, Lee H, Bellas RB, Schauer SL, Arsura M, Katz D, Fitzgerald MJ, Rothstein TL, Sherr DH, Sonenshein GE. 1996. Inhibition of NF-B/Rel induces apoptosis of murine B cells. EMBO. J. 15:101.

Yamaguchi K, Near R, Shneider A, Cui, H., Ju S-T, and Sherr DH. 1996. Fluoranthene mediated apoptosis in murine T cell hybridomas is aryl hydrocarbon receptor independent. Toxicol. and Appl. Pharmacol. 139:144. Abstract

Cui H, El-Khatib M, Sherr DH, Ettinger R, Sy M-S, Marshak-Rothstein A, Ju S-T. 1996. Characterization of LPR-derived T cell hybridomas:Fas-death deficient hybridomas are deathless, growth-arrested, and cytotoxic upon activation. Cell Immunol. 167:302.

Cui H, Sherr DH, El-Khatib M, Matsui K, Panka DJ, Marshak-Rothstein A, Ju S-T. 1996. Regulation of T-cell death genes: Selective inhibition of FasL- but not Fas-mediated function. Cell. Immunol.167:276

Ju S-T, Panka DJ, Cui H, Ettinger R, El-Khatib M, Sherr DH, Stanger BZ, and Marshak-Rothstein, A. 1995. Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation. Nature. 373:444. Abstract

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