Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
3R01CA061319-02S1
Application #
2102065
Study Section
Special Emphasis Panel (SRC (54))
Project Start
1993-12-22
Project End
1996-11-30
Budget Start
1994-12-01
Budget End
1995-11-30
Support Year
2
Fiscal Year
1995
Total Cost
Indirect Cost
Name
New York University
Department
Public Health & Prev Medicine
Type
Schools of Medicine
DUNS #
004514360
City
New York
State
NY
Country
United States
Zip Code
10012
Rossman, T G; Goncharova, E I (1998) Spontaneous mutagenesis in mammalian cells is caused mainly by oxidative events and can be blocked by antioxidants and metallothionein. Mutat Res 402:103-10
Rossman, T G; Goncharova, E I; Nadas, A et al. (1997) Chinese hamster cells expressing antisense to metallothionein become spontaneous mutators. Mutat Res 373:75-85
Nadas, A; Goncharova, E I; Rossman, T G (1996) Mutations and infinity: improved statistical methods for estimating spontaneous rates. Environ Mol Mutagen 28:90-9
Goncharova, E I; Nadas, A; Rossman, T G (1996) Serum deprivation, but not inhibition of growth per se, induces a hypermutable state in Chinese hamster G12 cells. Cancer Res 56:752-6
Nadas, A; Goncharova, E I; Rossman, T G (1996) Maximum likelihood estimation of spontaneous mutation rates from large initial populations. Mutat Res 351:9-17
Rossman, T G; Goncharova, E I; Nadas, A (1995) Modeling and measurement of the spontaneous mutation rate in mammalian cells. Mutat Res 328:21-30
Goncharova, E I; Rossman, T G (1994) A role for metallothionein and zinc in spontaneous mutagenesis. Cancer Res 54:5318-23