Journal of Multiple Sclerosis

Biography

Dr. Jorge Kattah, received his M.D. degree in 1972 from the University of Rosario, Bogota, Colombia. Following completion of a Neurology Residency Program at Georgetown University Medical Center in Washington, DC, Dr. Kattah obtained his Fellowship in Neurophthalmology and Orbital Disease at the University of Pittsburgh Eye and Ear Hospital. Since completion of his residency program and fellowship, Dr. Kattah served on the faculty of Georgetown University for 20 years and obtained the rank of tenured Professor and Vice Chairman before being recruited to the Peoria area. He currently serves as Professor and Head of the Department of Neurology with the University of Illinois College of Medicine at Peoria. Dr. Kattah’s areas of clinical interest are Neurophthalmology and Neurovestibular Neurology.

Research Interest

• Neuronal differentiation of hiPSCs, particularly into Radial Glial cells • Onset of brain tumor formation • In-vivo brain tumor modeling • Nanotechnology - diagnostic mapping of Radial Glial cells in the human brain by MRI Hypoxia and neuroblastoma tumorigenesis Neuroblastoma is the most common pediatric solid tumor that arises from the sympathetic nervous system. Neuroblastoma tumors exhibit clinical and biological heterogeneity associated with certain genetic aberrations. Advanced stage neuroblastoma is refractory to all conventional therapeutic modalities and is associated with a dismal prognosis. The cure rate of children with high-risk stage IV neuroblastoma remains low, providing a compelling reason to better understand the molecular mechanisms that can be targeted to treat this disease. Neuroblastoma tumors present hypoxic areas and metastasize to sites such as bone and bone marrow. Hypoxia induces a multitude of biological responses in cells and also alters neuronal characteristics of human neuroblastoma cells. Hypoxia-inducible factors (HIFs) are transcriptional regulators that mediate the cellular response to low oxygen. Although HIF-1α is usually considered as the principal mediator of hypoxic adaptation, several tissues and different cell types express both HIF-1α and HIF-2α isoforms under hypoxia. HIFs are also implicated in the progression of several cancer forms including neuroblastoma. Transient hypoxia and subsequent reoxygenation is a common phenomenon occurring within most solid tumors. Intermittent hypoxic tumor cells have the potential to influence the in tumor response to therapy. In our laboratory, we study the effects of intermittent hypoxia/HIFs on tumor cell clonogenicity, differentiation and tumorigenicity using in vitro and in vivo approaches. These studies should generate major insights into the pathogenesis of intermittent hypoxia-induced alterations in neuroblastoma tumors and in turn should suggest novel targets for therapeutic interventions.

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