Bahri Karacay, Ph.D. (Full Member) Adjunct Assistant Professor, The University of Iowa
Research Interest
Dr. Karacay's research focuses on abnormalities in nervous system development. One of the projects focuses on development of gene therapy to provide a specific and effective treatment for neuroblastoma, a childhood cancer of the nervous system. Current efforts attempt to activate the internal death mechanism (apoptosis) by delivering death-inducing genes to tumor cells and by blocking anti-apoptotic mechanisms. The long-term goal of this project is to apply transcriptional and transductional targeting of therapeutic genes for the treatment of neuroblastoma, using adenoviral and lentiviral gene therapy vectors. The second project focuses on the adverse effects of alcohol on the developing brain (fetal alcohol syndrome, FAS). Neuronal death is one of the most important consequences of fetal alcohol exposure and underlies many of the behavioral deficits associated with FAS. Therefore, a principal goal is to identify neuroprotective agents that can ameliorate alcohol-induced death. The research utilizes animal models and in vitro systems to explore the role neuroprotective agents against alcohol toxicity. Adenoviral and lentiviral vectors are used to express or silence neuroprotective genes to study protective signaling pathways. The third project is aimed at developing an effective therapy for Alexander Disease, a disease of cerebral white matter that affects children. The disease is caused by an autosomal dominant mutation of the gene for glial fibrillar acidic protein (GFAP), a protein expressed exclusively in brain astrocytes. RNA interference (RNAi) is a powerful tool for selectively suppressing specific genes. Viral gene therapy vectors are being developed to deliver RNAi to astrocytes to silence the disease-causing mutant GFAP gene.
Selected Publications:
Ahter D. Sanlioglu, Turker Koksal, Mehmet Baykara, Guven Luleci, Bahri Karacay and Salih Sanlioglu. 2006. IKKb Dominant Negative Mutant Expression Inhibited NF-kB Signaling and Sensitized Advanced Prostate Carcinoma Cells to TRAIL-Induced Apoptosis Cancer Gene Therap, 13(1):21-31.
VanOsten, R.L., Moore, M.L., Vermeson, C.P., Karacay, B., and Griffith T.S. (2005). The Histone Deacetylase Inhibitors Sodium Butyrate and Trichostatin A Modulate Renal Cell Carcinoma Sensitivity to TRAIL-InducedApoptosis by Enhancing TAIL-R2 Expression. Cancer Biology and Therapy, 4 (10):1104-12; Commentary Cancer Biology and Therapy, 4 (10):74-76.
Karacay, B., Sanlioglu S., Griffith T., Sandler, A. and Bonthius DJ. (2004) Inhibition of the NF-kB pathway enhances TRAIL-mediated apoptosis in neuroblastoma cells. Cancer Gene Therapy (in press).
Sanlioglu S., Karacay B., Benson PK and Engelhardt JF. (2004). Novel approaches to augment adeno-associated virus type-2 endocytosis and transduction. Virus Research 104 (2004) 51?59.
Sanlioglu A.D., Koksal, Y., Baykara, M., Luleci,G., Karacay, B. and Sanlioglu S., (2004). Current progress in adenovirus mediated gene therapy for patients with prostate carcinoma. Gene Ther Mol Biol 7:113-133. Review.
