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Your search keyword '"Vite, Gregory D."' showing total 4 results
Start Over Author "Vite, Gregory D." Publisher american association for cancer research
4 results on '"Vite, Gregory D."'

1. Abstract 1140: A novel MTA non-competitive PRMT5 inhibitor

Author

Malik, Rohit, primary, Park, Peter K., additional, Barbieri, Christopher M., additional, Blat, Yuval, additional, Sheriff, Steven, additional, Weigelt, Carolyn A., additional, Kopcho, Lisa M., additional, Celiktas, Muge, additional, Ruzanov, Max, additional, Naglich, Joseph G., additional, Price, Jennifer L., additional, Harner, Mary, additional, Omalley, Kevin M., additional, Deng, JIngjing, additional, Schmitz, William, additional, Li, Guo, additional, Ruan, Zheming, additional, Qin, Lan-ying, additional, Duke, Gerald J., additional, Rodrigo, Iyoncy, additional, Witmer, Mark R., additional, Harden, David G., additional, Demes, Shilpa, additional, Arey, Brian J., additional, Soars, Matt, additional, Fink, Brian E., additional, Gavai, Ashvinikumar V., additional, Vite, Gregory D., additional, and Voliva, Charles F., additional

Published
2021
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2. Abstract 5792: Preclinical antitumor activity of BMS-986158, an oral BET inhibitor, for the treatment of cancer

Author

Wee, Susan, primary, Jackson, Donald, additional, Desilva, Heshani, additional, Dajee, Maya, additional, Carman, Julie, additional, Ross-MacDonald, Petra, additional, Gan, Jinping, additional, Westhouse, Richard A., additional, Huang, Christine, additional, Yang, Zheng, additional, Poss, Michael, additional, Hunt, John T., additional, Vite, Gregory D., additional, and Gavai, Ashvinikumar V., additional

Published
2018
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3. Abstract 5417: The identification of BMS-595, an orally active imidazo[1,2-b]pyridazine CK2 inhibitor with in vivo anti-tumor activity

Author

Tarby, Christine M., primary, He, Liqi, additional, Fink, Brian E., additional, Nation, Andrew, additional, Zhao, Yufen, additional, Kim, Soong-Hoon, additional, Chen, Libing, additional, Tokarski, John S., additional, Yu, Chiang, additional, Pabalan, Jonathan G., additional, Roongta, Urvashi V., additional, Lippy, Jonathan, additional, Obermeier, Mary, additional, Elzinga, Paul A., additional, Fura, Aberra, additional, Henley, Benjamin, additional, Fargnoli, Joseph J., additional, Foster, William R., additional, Gavai, Ashvinikumar V., additional, Wong, Tai W., additional, Hunt, John T., additional, Vite, Gregory D., additional, Purandare, Ashok V., additional, and Rupnow, Brent A., additional

Published
2015
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4. Apoptotic and cytostatic farnesyltransferase inhibitors have distinct pharmacology and efficacy profiles in tumor models.

Author

Manne V, Lee FY, Bol DK, Gullo-Brown J, Fairchild CR, Lombardo LJ, Smykla RA, Vite GD, Wen ML, Yu C, Wong TW, and Hunt JT

Subjects
Animals, Antineoplastic Agents pharmacology, Cell Line, Tumor, Drug Screening Assays, Antitumor, Enzyme Activation, Enzyme Inhibitors pharmacology, Farnesyltranstransferase, Humans, MAP Kinase Kinase 4, Mice, Mitogen-Activated Protein Kinase Kinases metabolism, NIH 3T3 Cells, Rats, ras Proteins antagonists & inhibitors, Alkyl and Aryl Transferases antagonists & inhibitors, Apoptosis drug effects, Benzodiazepines pharmacology, Imidazoles pharmacology, JNK Mitogen-Activated Protein Kinases
Abstract

BMS-214662 and BMS-225975 are tetrahydrobenzodiazepine-based farnesyltransferase inhibitors (FTIs) that have nearly identical structures and very similar pharmacological profiles associated with farnesyltransferase (FT) inhibition. Despite their similar activity against FT in vitro and in cells, these compounds differ dramatically in their apoptotic potency and tumor-regressing activity in vivo. BMS-214662 is the most potent apoptotic FTI known and exhibits curative responses in mice bearing a variety of staged human tumor xenografts such as HCT-116 human colon tumor. By contrast, BMS-225975 does not cause tumor regression and at best causes partial tumor growth inhibition in staged HCT-116 human colon tumor xenografts. Lack of tumor regression activity in BMS-225975 was attributable to its relatively weak apoptotic potency, not to poor cell permeability or pharmacokinetics. Both compounds were equally effective in inhibiting Ras processing and causing accumulation of a variety of nonfarnesylated substrates of FT in HCT-116 cells. Because BMS-225975 has poor apoptotic activity compared with BMS-214662 but inhibits FT to the same extent as BMS-214662, it is very unlikely that FT inhibition alone can account for the apoptotic potency of BMS-214662. Clearly distinct patterns of sensitivities in a cell line panel were obtained for the apoptotic FTI BMS-214662 and the cytostatic FTI BMS-225975. Activation of the c-Jun-NH(2)-terminal kinase pathway was readily observed with BMS-214662 but not with BMS-225975. We developed a highly sensitive San-1 murine xenograft tumor model that is particularly useful for evaluating the in vivo activity of cytostatic FTIs such as BMS-225975.

Published
2004
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