Shannon C. Kenney, M.D.
Wattawa Bascom
Professor in Cancer Research
Professor of Oncology and Medicine
B.A., 1975, Geology, Yale University
M.D., 1979, Medicine, Yale School of
Medicine
Residency: Medicine/Pediatrics, Univ. of
North Carolina Hospitals
Postdoctoral research: NIH and Univ. of
North Carolina Hospitals
Office: 611A McArdle
Laboratory
Telephone: Office - (608) 265-0533; Lab -
(608) 261-1196
Email: skenney@wisc.edu
Research Interests: Understanding the molecular regulation and pathogenesis of the human herpesvirus, Epstein-Barr virus (EBV)
Research Description: Dr.
Kenney’s research effort has been focused upon
understanding the molecular regulation and pathogenesis of
the human herpesvirus, Epstein-Barr virus (EBV). Her
work in EBV spans a broad range of topics, including viral
gene regulation, the effects of the virus on the host
immune response, and the development of novel, EBV-targeted
therapies for EBV-positive tumors. She has
extensively studied the mechanisms by which both EBV
immediate-early proteins, BZLF1 and BRLF1, activate the
lytic form of viral infection. Her group discovered
that BZLF1 preferentially binds to, and transcriptionally
activates, the methylated form of its downstream target
promoter, suggesting a unique and unexpected mechanism by
which EBV overcomes the inhibitory effect of viral genome
methylation. Her group has also shown how the
two EBV immediate-early proteins alter the host cell
environment in multiple different ways, including usurping
control of the host cell cycle, activating a variety of
signal transduction pathways, inhibiting p53 function,
dispersing PML nuclear bodies, and attenuating the host
innate immune response. Dr. Kenney is now translating
the results of these basic molecular studies into the
development of new, EBV-targeted therapies for EBV-positive
tumors. Her group is also developing a new small animal
model to study EBV pathogenesis in vivo.
Selected recent publications
Bhatia, N., Xiao, T. Z., Rosenthal, K. A., Siddiqui, I. A., Thiyagarajan, S., Smart, B., Meng, Q., Zuleger, C. L., Mukhtar, H., Kenney, S. C., Albertini, M. R., and Longley, B. J. MAGE-C2 Promotes Growth and Tumorigenicity of Melanoma Cells, Phosphorylation of KAP1, and DNA Damage Repair. J. Invest. Dermatol., 133(3): 759-767, 2013.
Raver, R. M., Panfil, A. R., Hagemeier, S. R., and Kenney, S. C. The B-Cell Specific Transcription Factor and Master Regulator, Pax5, Promotes EBV Latency by Negatively Regulating the Viral Immediate Early Protein, BZLF1. J. Virol., in press, 2013 [Epub ahead of print May 15 2013].
Wille, C. K., Nawandar, D. M., Panfil, A. R., Ko, M. M., Hagemeier, S. R., and Kenney, S. C. Viral Genome Methylation Differentially Affects the Ability of BZLF1 versus BRLF1 To Activate Epstein-Barr Virus Lytic Gene Expression and Viral Replication. J. Virol., 87(2): 935-950, 2013.
Hagemeier, S. R., Barlow, E. A., Meng, Q., and Kenney, S. C. The Cellular Ataxia Telangiectasia-Mutated Kinase Promotes Epstein-Barr Virus Lytic Reactivation in Response to Multiple Different Types of Lytic Reactivation-Inducing Stimuli. J. Virol., 86: 13360-13370, 2012.
Hoebe, E. K., Wille, C., Hopmans, E. S., Robinson, A. R., Middeldorp, J. M., Kenney, S. C., and Greijer, A. E. Epstein-Barr Virus Transcription Activator R Upregulates BARF1 Expression by Direct Binding To Its Promoter, Independent of Methylation. J. Virol., 86: 11322-11332, 2012.
Ma, S.-D., Yu, X., Mertz, J. E., Gumperz, J. E., Reinheim, E., Zhou, Y., Tang, W., Burlingham, W. J., Gulley, M. L., and Kenney, S. C. An Epstein-Barr Virus (EBV) Mutant with Enhanced BZLF1 Expression Causes Lymphomas with Abortive Lytic EBV Infection in a Humanized Mouse Model. J. Virol., 86: 7976-7987, 2012.
Robinson, A. R., Kwek, S. S., and Kenney, S. C. The B-Cell Specific Transcription Factor, Oct-2, Promotes Epstein-Barr Virus Latency by Inhibiting the Viral Immediate-Early Protein, BZLF1. PLoS Pathog., 8(2):e1002516, 2012.
Ryan, J. L., Shen, Y.-J., Morgan, D. R., Thorne, L. B., Kenney, S. C., Dominguez, R. L., and Gulley, M. L. Epstein-Barr Virus Infection Is Common in Inflamed Gastrointestinal Mucosa. Dig. Dis. Sci., 57: 1887-1898, 2012.
Hagemeier, S. R., Barlow, E. A., Kleman, A. A., and Kenney, S. C. The Epstein-Barr Virus BRRF1 Protein, Na, Induces Lytic Infection in a TRAF2- and p53-Dependent Manner. J. Virol., 85: 4318-4329, 2011.
Hegde, S., Lockridge, J. L., Becker, Y. A., Ma, S., Kenney, S. C., and Gumperz, J. E. Human NKT Cells Direct the Differentiation of Myeloid APCs That Regulate T Cell Responses via Expression of Programmed Cell Death Ligands. J. Autoimmun., 37: 28-38, 2011.
Ma, S.-D., Hegde, S., Young, K. H., Sullivan, R., Rajesh, D., Zhou, Y., Jankowska-Gan, E., Burlingham, W. J., Sun, X., Gulley, M. L., Tang, W., Gumperz, J. E., and Kenney, S. C. A New Model of Epstein-Barr Virus Infection Reveals an Important Role for Early Lytic Viral Protein Expression in the Development of Lymphomas. J. Virol., 85: 165-177, 2011.
Robinson, A. R., Kwek, S. S., Hagemeier, S. R., Wille, C. K., and Kenney, S. C. Cellular Transcription Factor Oct-1 Interacts with the Epstein-Barr Virus BRLF1 Protein To Promote Disruption of Viral Latency. J. Virol., 85: 8940-8953, 2011.
Shaffer, D. R., Savoldo, B., Yi, Z., Chow, K. K. H., Kakarla, S., Spencer, D. M., Dotti, G., Wu, M.-F., Liu, H., Kenney, S., and Gottschalk, S. T Cells Redirected Against CD70 for the Immunotherapy of CD70-Positive Malignancies. Blood, 117: 4304-4314, 2011.