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Research Clinical Services Education |
The Scope | Grand Rounds | Research In Progress Schedule | RIP Presentation | RIP Archive RESEARCH IN PROGRESS PRESENTATION "Examining EB 1089's Ability to Promote
MCF-7 breast tumor cells exposed to fractionated
radiation (5 X 2 Gy) alone undergo a senescence-like
growth arrest succeeded by rapid recovery of
proliferative capacity. Exposure to the
1á,25(OH)2Vitamin D3 analog EB 1089 (100nM) prior to
irradiation converts the initial growth arrest response to cell death in part through the promotion
of apoptosis and delayed radiation-induced senescence.
EB 1089 also profoundly reduces the rate of recovery
following fractionated irradiation. EB 1089 reduces
the doubling time of the proliferating cell population
after fractionated radiation treatment by 50%,
translating to a 95% reduction in relative cell number
within 9-10 days. Radiation suppresses the expression
of both myc and cdc2, two proteins associated with the
induction of senescence. Prior exposure to EB 1089
interferes with the suppression of these proteins,
suggesting that myc and cdc2 may be factors in
conversion of the response from senescence to cell death. The importance of apoptotic versus
non-apoptotic cell death in the radio-sensitizing
effects of EB 1089 is currently being investigated in
MCF-7 cells transfected with caspase 3. Although EB
1089 increases the amount of radiation-induced
apoptosis in MCF-7 cells expressing caspase 3,
non-apoptotic cell death may prove to play a more
substantial role in radio-sensitization than
apoptosis. For more information contact Gerald DeMasters at gademast@vcu.edu or visit the Pharmacology and Toxicology web page. For more information about VCU Pathology
Research in Progress presentations contact Updated December 6, 2004 |
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