Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Project (R01)
Project #
5R01CA056075-04
Application #
2097076
Study Section
Hematology Subcommittee 2 (HEM)
Project Start
1992-03-04
Project End
1998-02-28
Budget Start
1995-03-01
Budget End
1998-02-28
Support Year
4
Fiscal Year
1995
Total Cost
Indirect Cost
Name
University of California San Diego
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
077758407
City
La Jolla
State
CA
Country
United States
Zip Code
92093
Schoppmeyer, K; Norris, P S; Haas, M (1999) Inhibition of T-cell acute lymphoblastic leukemia proliferation in vivo by re-expression of the p16INK4a tumor suppressor gene. Neoplasia 1:128-37
Costanzi-Strauss, E; Strauss, B E; Naviaux, R K et al. (1998) Restoration of growth arrest by p16INK4, p21WAF1, pRB, and p53 is dependent on the integrity of the endogenous cell-cycle control pathways in human glioblastoma cell lines. Exp Cell Res 238:51-62
Vogt, M; Haggblom, C; Yeargin, J et al. (1998) Independent induction of senescence by p16INK4a and p21CIP1 in spontaneously immortalized human fibroblasts. Cell Growth Differ 9:139-46
Norris, P S; Jepsen, K; Haas, M (1998) High-titer MSCV-based retrovirus generated in the pCL acute virus packaging system confers sustained gene expression in vivo. J Virol Methods 75:161-7
Hsiao, M; Tse, V; Carmel, J et al. (1997) Intracavitary liposome-mediated p53 gene transfer into glioblastoma with endogenous wild-type p53 in vivo results in tumor suppression and long-term survival. Biochem Biophys Res Commun 233:359-64
Norris, P S; Haas, M (1997) A fluorescent p53GFP fusion protein facilitates its detection in mammalian cells while retaining the properties of wild-type p53. Oncogene 15:2241-7
Hsiao, M; Tse, V; Carmel, J et al. (1997) Functional expression of human p21(WAF1/CIP1) gene in rat glioma cells suppresses tumor growth in vivo and induces radiosensitivity. Biochem Biophys Res Commun 233:329-35
Strauss, B E; Haas, M (1995) The region 3' to the major transcriptional start site of the MDR1 downstream promoter mediates activation by a subset of mutant P53 proteins. Biochem Biophys Res Commun 217:333-40
Hsiao, M; Wu, C Y; Low, J et al. (1995) Dissemination and tissue invasiveness in murine acute leukemia associated with acquisition of p53 mutation and loss of wild-type p53. Mol Carcinog 13:112-21
Strauss, B E; Shivakumar, C; Deb, S P et al. (1995) The MDR1 downstream promoter contains sequence-specific binding sites for wild-type p53. Biochem Biophys Res Commun 217:825-31

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