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Shannon C. Kenney, M.D.

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Shannon C Kenney, MD 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

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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

Iempridee, T., Reusch, J. A., Riching, A., Johannsen, E. C., Dovat, S., Kenney, S. C., and Mertz, J. E.  Epstein-Barr Virus Utilizes Ikaros in Regulating Its Latent-Lytic Switch in B Cells.  J. Virol., 88(9): 4811-4827, 2014.

Kenney, S. C., and Mertz, J. E.  Regulation of the Latent-Lytic Switch in Epstein-Barr Virus.  Semin. Cancer Biol., in press, 2014 [Epub ahead of print Jan 20 2014].

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.

Lockridge, J. L., Zhou, Y., Becker, Y. A., Ma, S., Kenney, S. C., Hematti, P., Capitini, C. M., Burlingham, W. J., Gendron-Fitzpatrick, A., and Gumperz, J. E.  Mice Engrafted with Human Fetal Thymic Tissue and Hematopoietic Stem Cells Develop Pathology Resembling Chronic Graft-versus-Host Disease.  Biol. Blood Marrow Transplant., 19(9): 1310-1322, 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 Epstein-Barr Virus Latency by Negatively Regulating the Viral Immediate Early Protein BZLF1.  J. Virol., 87(14): 8053-8063, 2013.

Sun, X.,  Bristol, J. A., Iwahori, S., Hagemeier, S. R., Meng, Q., Barlow, E. A., Fingeroth, J. D., Tarakanova, V. L., Kalejta, R. F., and Kenney, S. C.  Hsp90 Inhibitor 17-DMAG Decreases Expression of Conserved Herpesvirus Protein Kinases and Reduces Virus Production in Epstein-Barr Virus-Infected Cells.  J. Virol., 87(18): 10126-10138, 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.

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