- Medical/Professional School:
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Johns Hopkins University School of Medicine, Baltimore
- Residency:
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University of Washington, Seattle, Pediatrics
- Fellowship:
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University of Washington, SeattleUniversity of Washington, Seattle, Adolescent Medicine
- Description of Research:
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Human papillomavirus (HPV) is the most common sexually transmitted infection, affecting more than 75percent of the adult population. HPV is categorized as high-risk or low-risk, based on its association with cancer. Through dysregulation of normal cellular function, high-risk HPV blocks signals for DNA damage, programmed cell death, and cellular arrest, all as a part of its viral life cycle. I am studying the mechanism by which high-risk HPV activates telomerase, and enzyme found normally in stem cells and almost categorically activated in cancers, in order to understand how HPV drives cells to become malignant.
- Key Publications:
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UB Kaiser, RA Katzenellenbogen, PM Conn, WW Chin. Evidence that signalling pathways by which Thyrotropin-Releasing Hormone and Gonadotropin-Releasing Hormone act are both common and distinct. Molec. Endocrinol. 8: 1038-1048, 1994.
UB Kaiser, E Sabbagh, RA Katzenellenbogen, PM Conn, WW Chin. A mechanism for the differential regulation of gonadotropins by different Gonadotropin-Releasing Hormone pulse frequencies. Proc. Natl. Acad. Sci. USA 92: 12280-12284, 1995.
RA Katzenellenbogen, SB Baylin, JG Herman. Hypermethylation of DAP-Kinase CpG island is a common alteration in B-Cell malignancies. Blood 93: 4347-4353, 1999.
DA Galloway, L Gewin, H Myers, W Luo, C Grandori, RA Katzenellenbogen, JK McDougall. Telomerase regulation by HPV. Cold Spring Harbor Symposia on Quantitative Biology 70: 209-215, 2005.
RA Katzenellenbogen, E Egelkrout, P Vliet-Gregg, L Gewin, P Gafken, DA Galloway. NFX1-123 and Poly(A) Binding Proteins Synergistically Augment Activation of Telomerase in HPV 16E6 Expressing Cells. Journal of Virology 81: 3786-3796, 2007.