Abstract

This research program is aimed at understanding the regulation of expression of viral and cellular genes in normal and transformed cells, as well as the mechanisms by which viral or altered cellular gene expression leads to alterations of growth behavior. The project consists of seven parts: 1. The study of the control of gene expression in normal and polyoma virus transformed cells. 2. The study of the mechanisms regulating gene expression during the cell cycle and in response to growth factors. 3. The study of the biochemical properties and functions of the p53 cellular protein, which is induced in a variety of transformed cells. 4. The study of the rearrangements of the c-myc and c-myb proto oncogenes in human neoplasias and of the effects of such rearrangements on the expression of these genes. 5. The molecular and cytogenetic analysis of murine lymphomas induced by radiation and chemical carcinogens, with emphasis on the cellular oncogenes which are activated in this process. 6. The study of the role of human papilloma viruses in neoplastic lesions of the genital area, and of the expression of these viral genomes in tumors and in vitro. 7. The role of RNA helix destabilizing proteins in the process of transcription of eukaryotic genes.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
2P01CA016239-12
Application #
3092693
Study Section
Cancer Special Program Advisory Committee (CAK)
Project Start
1977-12-01
Project End
1990-11-30
Budget Start
1986-03-01
Budget End
1986-11-30
Support Year
12
Fiscal Year
1986
Total Cost
Indirect Cost

  Institution

Name
New York University
Department
Type
Schools of Medicine
DUNS #
004514360
City
New York
State
NY
Country
United States
Zip Code
10012

  Publications

Fontoura, B M; Sorokina, E A; David, E et al. (1992) p53 is covalently linked to 5.8S rRNA. Mol Cell Biol 12:5145-51
Morgan, D M; Pecoraro, G; Rosenberg, I et al. (1992) Transformation by human papillomavirus type 16 (HPV16) DNA but not HPV6b DNA is enhanced by addition of the human cytomegalovirus enhancer. Virology 189:687-94
Szer, W; Sierakowska, H; Szer, I S (1991) Antinuclear antibody profile in juvenile rheumatoid arthritis. J Rheumatol 18:401-8
Donti, E; Lanfrancone, L; Pelicci, P G et al. (1991) Loss of amplification and appearance of a novel translocation site of the c-myc oncogene in HL-60 leukemia cells. Cancer Genet Cytogenet 56:57-64
Sloan, S R; Pellicer, A (1991) Staging of T-cell receptor beta chain gene rearrangements and ras oncogene mutations in the development of murine thymic lymphomas. Cancer Res 51:1627-31
Pecoraro, G; Lee, M; Morgan, D et al. (1991) Evolution of in vitro transformation and tumorigenesis of HPV16 and HPV18 immortalized primary cervical epithelial cells. Am J Pathol 138:1-8
Samad, A; Carroll, R B (1991) The tumor suppressor p53 is bound to RNA by a stable covalent linkage. Mol Cell Biol 11:1598-606
Zuklys, K L; Szer, I S; Szer, W (1991) Autoantibodies to DNA topoisomerase II in juvenile rheumatoid arthritis. Clin Exp Immunol 84:245-9
Corominas, M; Leon, J; Kamino, H et al. (1991) Oncogene involvement in tumor regression: H-ras activation in the rabbit keratoacanthoma model. Oncogene 6:645-51
Lacal, J C; Cuadrado, A; Jones, J E et al. (1990) Regulation of protein kinase C activity in neuronal differentiation induced by the N-ras oncogene in PC-12 cells. Mol Cell Biol 10:2983-90

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