The UAB Division of Neurological Oncology consists of a multidisciplinary team of neuro-oncologists, neurosurgeons, radiation oncologists, neuroradiologists and neuropathologists, all devoted to the care and treatment of patients with brain tumors and neurologic complications of systemic cancers. This includes conventional chemotherapy as well as the use of novel, experimental therapies designed to destroy tumors unable to be removed by surgery or radiation therapy. Neuro-oncologists oversee this process, as well as treating the medical and neurological issues many patients with brain tumors develop, including seizures, infections and emotional difficulties.
Through the Division of Neuro-Oncology, the UAB Comprehensive Cancer Center is part of several national efforts focused on brain cancer. One is the highly prestigious SPORE (Specialized Program of Research Excellence) grant, led by Yancey Gillespie, Ph.D., and James Markert, M.D, Ph.D., which are designed to quickly and safely move research findings from the laboratory bench to the patient bedside. The division is also a member of the Adult Brain Tumor Consortium, a National Cancer Institute-funded consortium of 10 institutions conducting early phase brain cancer research.
Dr. Markert’s research team has found that a genetically engineered herpes simplex virus known as G207 is safe when used in conjunction with low doses radiation in the treatment of malignant gliomas. The virus infects and kills tumor cells and is genetically modified to reproduce only in tumor cells, which lack the stronger antiviral defense mechanisms of healthy brain cells. Early results have been extremely promising, and UAB researchers are currently preparing further studies in this area.
Assistant Professor Susan Nozell, Ph.D., is investigating the various genetic factors that increase the risk for gliomas and that impact survival after diagnosis. She is exploring the role of a molecular protein called NF-kB that consistently correlates with patient prognosis by impacting a specific population of glioma stem cells. Defects in this particular protein mediate cell growth, migration, invasion, blood vessel formation and cell death. Research has identified a novel gene, microRNA-31, that reduces the activity level of not only this molecular protein, but other proteins that specifically promote tumor growth. Investigating the interaction between molecular proteins and microRNA-31 has yielded promising results, but more research is needed to fully understand the functionality of microRNA-31. Pinpointing this correlation may provide valuable information that not only improves patient prognosis and survival, but paves the way for future glioma research.
Postdoctoral fellow Braden McFarland, Ph.D., is focused on the role of chemical signaling through cell membranes in gliomas. Normal cell signaling enables cells to perceive and correctly respond to routine growth and tissue repair commands. However, miscommunication between certain cells can lead to the development of gliomas. Studies of these signaling pathways have greatly increased understanding of the biology and clinical behavior of glioma formation. Dr. McFarland is currently completing preclinical investigations of an inhibitor that stabilizes chemical signaling between cells with hopes of moving this research into human clinical trials in the near future.