) The general goal of this program is to investigate the molecular mechanisms by which betaIFN modulates the repair capacity and increases the radiation sensitivity of human lung and brain tumor cells. Recent studies in their laboratory and others have shown that betaIFN increases the duration of radiation-induced G2/M delay. This delay is accompanied by a temporary loss of DNA binding activity of Ku 70/80. Since Ku 70/80 has been suggested to be involved in the repair of DNA strand breaks, the possible roles of Ku 70/80 and DNA-dependent protein kinase (DNA-PK) in the betaIFN induced radiation sensitivity will be examined. In addition, the roles of p34 kinase, and cyclin B in the G2/M delay induced by interferon and radiation will be determined. The central hypothesis to be tested in this program is that betaIFN either directly (DNA-PK/Ku 70/80 activity) or indirectly (cell cycle regulation) modulates the repair capacity of irradiated human lung and brain tumor cells.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
5P01CA011051-29
Application #
6563660
Study Section
Project Start
2002-02-01
Project End
2003-07-31
Budget Start
1997-10-01
Budget End
1998-09-30
Support Year
29
Fiscal Year
2002
Total Cost
$157,506
Indirect Cost
Name
University of Rochester
Department
Type
DUNS #
208469486
City
Rochester
State
NY
Country
United States
Zip Code
14627
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Liang, Li; Hu, Dongping; Liu, Weimin et al. (2003) Celecoxib reduces skin damage after radiation: selective reduction of chemokine and receptor mRNA expression in irradiated skin but not in irradiated mammary tumor. Am J Clin Oncol 26:S114-21
Williams, Jacqueline; Chen, Yuhchyau; Rubin, Philip et al. (2003) The biological basis of a comprehensive grading system for the adverse effects of cancer treatment. Semin Radiat Oncol 13:182-8
Chen, Yuhchyau; Williams, Jacqueline; Ding, Ivan et al. (2002) Radiation pneumonitis and early circulatory cytokine markers. Semin Radiat Oncol 12:26-33

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