Numsen Hail, Jr., M.S., Ph.D.
Assistant Professor, Department of Pharmaceutical Sciences
Mailing address:
4200 E. 9th Ave, C238
Denver, CO 80262
Telephone:
School of Pharmacy, Room 221
Voice: 303-315-0004
Email: Numsen.Hail@uchsc.edu
Training and Education:
B.S., Texas A&M University (Biology/Biochemistry)
M.S., The University of Texas/Houston (Environmental Sciences/Toxicology)
Ph.D., The University of Texas/Houston (Toxicology)
Postdoctoral Fellow, The University of Texas M.D. Anderson Cancer Center (Cancer Chemoprevention and Cell Death Regulation)
Research Interest:
Cancer chemoprevention uses natural or synthetic agents to slow the progression of, reverse, or inhibit carcinogenesis, thereby lowering the risk of developing invasive or clinically significant disease. We are currently investigating the mechanistic aspects of apoptosis induction by several putative cancer chemopreventive agents in transformed human epithelial cells. We hypothesize that certain changes in cellular bioenergetic and/or redox processes may dictate sensitivity to certain types of chemopreventive agents (e.g., phenoloic compounds, selenium compounds, and vitamin E analogues). Also, in addition to genetic changes, epigenetic changes like reactive oxygen production and oxidative stress are emerging as key players in tumorigenesis at various sites in the human body. We hope to look at ways to modulate these epigenetic changes, perhaps resulting in apoptosis induction in the transformed cells, as a means of preventing malignancies in humans.
Recent Publications
1. Hail, N., Jr., and Lotan, R. Celecoxib. Encyclopedia of Cancer, Second Edition, M. Schwab, Editor. Springer Science and Business Media, In Press, 2007. 2. Hail, N., Jr. Differences in Mitochondrial Reactive Oxygen Species Production Affect Sensitivity to Curcumin-induced Apoptosis. Free Radical Biology and Medicine, In Press, 2007. 3. Hail, N., Jr., and Lotan, R. Cancer chemoprevention and mitochondria: targeting apoptosis in transformed cells via the disruption of mitochondrial bioenergetics/redox state. Molecular Nutrition and Food Research, In Press, 2007. 4. Leroux, M.E., Auzenne, E., Evans, R., Hail, N., Jr., Spohn, W., Ghosh, S., Farquhar, D., McDonnell, T. J., and Klostergaard, J. Sphingolipids and the Sphingosine Kinase Inhibitor, SKI II, Induce BCL-2- Independent Apoptosis in Human Prostatic Adenocarcinoma Cells. Prostate, 67: 1699-717, 2007. 5. Hail, N., Jr., Kim, H. J., and Lotan, R. Mechanisms of fenretinide-induced apoptosis. Apoptosis, 11: 1677-1694, 2006. 6. Zeng, Z., Samudio, I.Z., Zhang, W., Estrov, Z., Pelicano, H.,Harris, D., Frolova, O., Hail, N., Jr., Chen, W., Kornblau, S.M., Huang, P., Mills, G.B., Andreeff, M., and Konopleva, M. Simultaneous inhibition of PDK1/AKT and FLT3 signaling by a small-molecule KP372-1 induces mitochondrial dysfunction and apoptosis in AML. Cancer Research, 66: 3737-3746, 2006. 7. Hail, N., Jr., Carter, B.Z., Konopleva, M., and Andreeff, M. Apoptosis effector mechanisms: A requiem performed in different keys. Apoptosis, 11: 889–904, 2006. 8. Samudio, I.J., Konopleva, M., Hail, N., Jr., Shi, X.Y., McQueen, T., Hsu, T., Evans, R., Honda, T., Gribble, G.W., Sporn, M., Gilbert, H.F., Safe, S., and Andreeff, M. 2-Cyano-3,12 dioxooleana-1,9 diene-28-imidazolide (CDDO-Im) directly targets mitochondrial glutathione to induce apoptosis in pancreatic cancer. Journal of Biological Chemistry, 280: 36273-36282, 2005. 9. Hail, N., Jr., Mitochondria: a novel target for the chemoprevention of cancer. Apoptosis, 8: 687-705 2005.
Last updated: 1/14/08