Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
3R01CA051912-02S1
Application #
3196634
Study Section
Pathology B Study Section (PTHB)
Project Start
1990-12-01
Project End
1993-11-30
Budget Start
1992-03-04
Budget End
1992-11-30
Support Year
2
Fiscal Year
1992
Total Cost
Indirect Cost
Name
University of North Carolina Chapel Hill
Department
Type
Schools of Medicine
DUNS #
078861598
City
Chapel Hill
State
NC
Country
United States
Zip Code
27599
Jiang, X R; Jimenez, G; Chang, E et al. (1999) Telomerase expression in human somatic cells does not induce changes associated with a transformed phenotype. Nat Genet 21:111-4
Tlsty, T D (1998) Cell-adhesion-dependent influences on genomic instability and carcinogenesis. Curr Opin Cell Biol 10:647-53
Gualberto, A; Aldape, K; Kozakiewicz, K et al. (1998) An oncogenic form of p53 confers a dominant, gain-of-function phenotype that disrupts spindle checkpoint control. Proc Natl Acad Sci U S A 95:5166-71
White, A E; Livanos, E M; Tlsty, T D (1994) Differential disruption of genomic integrity and cell cycle regulation in normal human fibroblasts by the HPV oncoproteins. Genes Dev 8:666-77
Tlsty, T D; White, A; Livanos, E et al. (1994) Genomic integrity and the genetics of cancer. Cold Spring Harb Symp Quant Biol 59:265-75
Forrester, K; Kispert, J; Sanchez, J H et al. (1994) Clonal variation of tumorigenic potential in v-Ha-ras-transformed human bronchial epithelial cells: relationship to ras oncogene expression and CAD gene amplification. Mol Carcinog 11:34-41
Jonczyk, P; White, A; Lum, K et al. (1993) Amplification potential in preneoplastic and neoplastic Syrian hamster embryo fibroblasts transformed by various carcinogens. Cancer Res 53:3098-102
Schaefer, D I; Livanos, E M; White, A E et al. (1993) Multiple mechanisms of N-(phosphonoacetyl)-L-aspartate drug resistance in SV40-infected precrisis human fibroblasts. Cancer Res 53:4946-51
Livingstone, L R; White, A; Sprouse, J et al. (1992) Altered cell cycle arrest and gene amplification potential accompany loss of wild-type p53. Cell 70:923-35