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David Symer
David Symer, M.D., Ph.DHuman Cancer Genetics Program Departments of Molecular Virology, Immunology and Medical Genetics, Internal Medicine, and Biomedical Informatics The Ohio State University Comprehensive Cancer Center Tzagournis Research Facility, Room 440 420 West 12th Avenue Columbus, Ohio 43210 (614) 292 0885 office (614) 292 6108 fax (614) 292 6486 lab david.symer@osumc.edu Education and Training A.B., Mathematics, 1984, Dartmouth College M.D., Ph.D., 1993, laboratory of Dr. Howard M. Dintzis, Department of Biophysics and Biophysical Chemistry, The Johns Hopkins University School of Medicine Clinical internship and residency, 1995, Department of Medicine, Brigham and Women’s Hospital (Harvard Medical School) Clinical fellowship in Hematology and Oncology, 1996, Brigham and Women’s Hospital (Harvard Medical School) Clinical fellowship in Hematology and Oncology, 2002, The Johns Hopkins Medical Institutions Research postdoctoral fellowship, 2002, laboratory of Dr. Jef D. Boeke, Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine Positions and Appointments 2002-2009 Principal Investigator, Center for Cancer Research, National Cancer Institute 2009- Assistant Professor, Human Cancer Genetics Program, and Departments of Molecular Virology, Immunology and Medical Genetics, Internal Medicine, and Biomedical Informatics, The Ohio State University Comprehensive Cancer Center Honors and Awards 1984-1993 Medical Scientist Training Program, The Johns Hopkins University School of Medicine 1992 W. Barry Wood student research award 1997-2000 Howard Hughes Medical Institute, Physician Postdoctoral Research Fellowship award Research Interests The recent completion of the human and mouse genome sequence assemblies has highlighted the astonishing fact that almost half of our DNA — and that of other mammals -- is made up of retrotransposons. In addition, several labs have demonstrated that retrotransposons even now can move from one chromosomal location to another, sometimes resulting in human diseases including cancers. Perhaps because of their potential to cause various forms of damage, these mobile genetic elements are a prime target for various epigenetic controls that can regulate them. The Symer research group studies mammalian retrotransposons, their epigenetic controls, and resulting functional variation. The group aims to understand some of the causes and consequences of changing epigenetic states upon the transposons, the genes and transcripts they affect, and on genomic stability. In particular, specific examples of transcriptional and phenotypic variation that are due to existing or de novo endogenous retrotransposon integrants and due to the epigenetic controls that regulate them are being identified and characterized. Since in most cases the molecular basis for phenotypic variation between individuals or between different tissues is not known, these questions are centrally important. The Symer lab group uses a range of modern molecular and bioinformatics tools to study the movement, the epigenetic controls and the consequences of retrotransposons in normal development and aging and in certain cancers. Publications Repasky, E.A., Symer, D.E. and Bankert, R.B.: Spectrin immunofluorescence distinguishes a population of naturally capped lymphocytes in situ. J. Cell Biol. 99: 350-355, 1984. Slezak, S., Symer, D.E. and Shin, H.S.: Platelet-mediated cytotoxicity. Role of antibody and C3, and localization of the cytotoxic system in membranes. J. Exp. Med. 166: 489-505, 1987. Nishijima, J. Wright, T.M., Hoffman, R.D., Liao, F., Symer, D.E. and Shin, H.S.: Lysophosphatidylcholine metabolism to 1,2-diacylglycerol in lymphoblasts: involvement of a phosphatidylcholine-hydrolyzing phospholipase C. Biochemistry 28: 2902-2909, 1989. Diamond, D.J., Szalay, P., Symer, D., Hao, P., Shin, H.S., Dintzis, R.Z., Dintzis, H.M., Reinherz, E. and Siliciano, R.F.: Major histocompatibility complex independent T cell receptor-antigen interaction: functional analysis using fluorescein derivatives. J. Exp. Med. 174: 229-241, 1991. Symer, D.E., Dintzis, R.Z., Diamond, D.J., and Dintzis, H.M.: Inhibition or activation of human T cell receptor transfectants is controlled by defined, soluble antigen arrays. J. Exp. Med. 176: 1421-1430, 1992. Symer, D.E., Paznekas, W.A., and Shin, H.S.: A requirement for membrane-associated phospholipase A2 in platelet cytotoxicity activated by receptors for IgG and complement. J. Exp. Med. 177: 937-947, 1993. Dintzis, H.M., Symer, D.E., Dintzis, R.Z., Zawadzke, L.E., and Berg, J.M.: A comparison of the immunogenicity of a pair of protein enantiomers. Proteins. 16: 306-308, 1993. Symer, D.E., Reim, J., Dintzis, R.Z., Voss, E.W., Jr., and Dintzis, H.M.: Durable elimination of high affinity, T cell-dependent antibodies by low molecular weight antigen arrays in vivo. J. Immunol. 155: 5608-5616, 1995. Reim, J., Symer, D.E., Watson, D.C., Dintzis, R.Z. and Dintzis, H.M.: Low molecular weight antigen arrays delete high affinity memory B cells without affecting specific T cell help. Mol. Immunol. 33: 1377-1388, 1996. Gillison, M.L., Koch, W., Capone, R.B., Spafford, M., Westra, W., Wu, L., Daniel, R., Symer D.E., Shah, K.V. and Sidransky, D.: Evidence for a causal association between human papillomavirus and a subset of head and neck cancers. J. Natl. Can. Inst. 92: 709-720, 2000. Symer, D.E., Connelly, C., Szak, S.T., Caputo, E.M., Cost, G.J., Parmigiani, G. and Boeke, J. D.: Human L1 retrotransposition is associated with genetic instability in vivo. Cell 110: 327-338, 2002. * Akagi, K., Li, J., Stephens, R.M., Volfovsky, N. and Symer, D.E.: Extensive variation between inbred mouse strains due to endogenous L1 retrotransposition. Genome Research 18: 869-880, 2008. * Van Duyne, R., Easley, R., Wu, W., Berro, R., Pedati, C., Klase, Z., Kehn-Hall, K., Flynn, E. K., Symer, D. E., and Kashanchi, F. (2008) Lysine methylation of HIV-1 Tat decreases transcriptional activation of the viral LTR. Retrovirology 5: 40 doi:10.1186/1742-4690-5-40, 2008. Agarwal, Y., Koch, W. M., Xiao, W., Westra, W., Trivett, A. L., Symer, D. E., and Gillison, M. L. Oral human papillomavirus infection before and after treatment for human papillomavirus 16-positive and human papillomavirus 16-negative head and neck squamous cell carcinoma. Clin. Canc. Res. 14: 7143-7150, 2008. * denotes cover article |
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