Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Research Project (R01)
Project #
5R01GM051827-03
Application #
2190567
Study Section
Radiation Study Section (RAD)
Project Start
1995-08-10
Project End
1998-07-31
Budget Start
1996-08-01
Budget End
1997-07-31
Support Year
3
Fiscal Year
1996
Total Cost
Indirect Cost
Name
University of Washington
Department
Radiation-Diagnostic/Oncology
Type
Schools of Medicine
DUNS #
135646524
City
Seattle
State
WA
Country
United States
Zip Code
98195
Schwartz, J L; Jordan, R; Sun, J et al. (2000) Dose-dependent changes in the spectrum of mutations induced by ionizing radiation. Radiat Res 153:312-7
Schwartz, J L; Jordan, R; Kaufmann, W K et al. (2000) Evidence for the expression of radiation-induced potentially lethal damage being a p53-dependent process. Int J Radiat Biol 76:1037-43
Schwartz, J L; Russell, K J (1999) The effect of functional inactivation of TP53 by HPV-E6 transformation on the induction of chromosome aberrations by gamma rays in human tumor cells. Radiat Res 151:385-90
Schwartz, J L; Rasey, J; Wiens, L et al. (1999) Functional inactivation of p53 by HPV-E6 transformation is associated with a reduced expression of radiation-induced potentially lethal damage. Int J Radiat Biol 75:285-91
Schwartz, J L; Murnane, J; Weichselbaum, R R (1999) The contribution of DNA ploidy to radiation sensitivity in human tumour cell lines. Br J Cancer 79:744-7
Schwartz, J L (1998) Alterations in chromosome structure and variations in the inherent radiation sensitivity of human cells. Radiat Res 149:319-24
Schwartz, J L; Jordan, R (1997) Selective elimination of human lymphoid cells with unstable chromosome aberrations by p53-dependent apoptosis. Carcinogenesis 18:201-5
Schwartz, J L; Hsie, A W (1997) Genetic and cytogenetic markers of exposure to high-linear energy transfer radiation. Radiat Res 148:S87-92
Kaufmann, W K; Schwartz, J L; Hurt, J C et al. (1997) Inactivation of G2 checkpoint function and chromosomal destabilization are linked in human fibroblasts expressing human papillomavirus type 16 E6. Cell Growth Differ 8:1105-14