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Waziri A.,Inova Neuroscience Institute | Curry W.T.,Harvard University
Journal of Neuro-Oncology

Over the 30 years since the formation of the AANS/CNS Section on Tumors, the breadth and scope of our activities have continued to expand. An initial focus on education and collaboration between those members of the neurosurgical community dedicated to the care of patients with neurological tumors has broadened to include development of international relationships, participation in clinical trials and efforts to define standards of care and quality metrics. As we navigate the rapidly changing environment of health care, the Section on Tumors will occupy a central role in promoting advocacy, establishing collaboration, providing education, and supporting research for the community of neurosurgeons dedicated to the care of patients with neurological tumors. This article will provide an update and status report on the development of the Section on Tumors, followed by a brief discussion of the challenges and opportunities emerging at the onset of our fourth decade of service. © 2014, Springer Science+Business Media New York. Source

Lipsky R.H.,Inova Neuroscience Institute
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience

A balance between rapid, short lived, neuronal responses and prolonged ones fulfill the biochemical and cellular requirements for creating a molecular memory. I provide an overview of epigenetic mechanisms in the brain and discuss their impact on synaptic plasticity, cognitive functions, and discuss a recent example of how they can contribute to neurodegeneration and the cognitive decline associated with Alzheimer's disease. Copyright © 2012 ISDN. Published by Elsevier Ltd. All rights reserved. Source

See A.P.,Brigham and Womens Hospital | Parker J.J.,University of Colorado at Denver | Waziri A.,Inova Neuroscience Institute
Journal of Neuro-Oncology

Cell-mediated suppression of anti-tumor immunity is multifactorial in patients with cancer, and recent studies have focused on several distinct cellular agents that are associated with this phenomenon. This review will focus on the potential role of regulatory T cells (Tregs) and microglia in the suppression of cellular immunity observed in patients with glioblastoma. We discuss the ontogeny, basic biology, evidence for activity, and potential clinical options for targeting Tregs and microglia as part of immunotherapy in affected patients. © 2015, Springer Science+Business Media New York. Source

Griesinger A.M.,University of Colorado at Denver | Birks D.K.,Childrens Hospital Colorado | Birks D.K.,University of Colorado at Denver | Donson A.M.,University of Colorado at Denver | And 7 more authors.
Journal of Immunology

Despite increasing evidence that antitumor immune control exists in the pediatric brain, these findings have yet to be exploited successfully in the clinic. A barrier to development of immunotherapeutic strategies in pediatric brain tumors is that the immunophenotype of these tumors' microenvironment has not been defined. To address this, the current study used multicolor FACS of disaggregated tumor to systematically characterize the frequency and phenotype of infiltrating immune cells in the most common pediatric brain tumor types. The initial study cohort consisted of 7 pilocytic astrocytoma (PA), 19 ependymoma (EPN), 5 glioblastoma (GBM), 6 medulloblastoma (MED), and 5 nontumor brain (NT) control samples obtained from epilepsy surgery. Immune cell types analyzed included both myeloid and T cell lineages and respective markers of activated or suppressed functional phenotypes. Immune parameters that distinguished each of the tumor types were identified. PA and EPN demonstrated significantly higher infiltrating myeloid and lymphoid cells compared with GBM, MED, or NT. Additionally, PA and EPN conveyed a comparatively activated/classically activated myeloid cell-skewed functional phenotype denoted in particular by HLA-DR and CD64 expression. In contrast, GBM and MED contained progressively fewer infiltrating leukocytes and more muted functional phenotypes similar to that of NT. These findings were recapitulated using whole tumor expression of corresponding immune marker genes in a large gene expression microarray cohort of pediatric brain tumors. The results of this crosstumor comparative analysis demonstrate that different pediatric brain tumor types exhibit distinct immunophenotypes, implying that specific immunotherapeutic approaches may be most effective for each tumor type. Copyright © 2013 by The American Association of Immunologists, Inc. Source

Xu K.,Yale University | Lipsky R.H.,Inova Neuroscience Institute | Lipsky R.H.,George Mason University
Experimental Biology and Medicine

For more than 40 years following its approval by the Food and Drug Administration (FDA) as an anesthetic, ketamine, a non-competitive N-methyl-d-aspartic acid (NMDA) receptor antagonist, has been used as a tool of psychiatric research. As a psychedelic drug, ketamine induces psychotic symptoms, cognitive impairment, and mood elevation, which resemble some symptoms of schizophrenia. Recreational use of ketamine has been increasing in recent years. However, little is known of the underlying molecular mechanisms responsible for ketamine-associated psychosis. Recent animal studies have shown that repeated ketamine administration significantly increases NMDA receptor subunit gene expression, in particular subunit 1 (NR1 or GluN1) levels. This results in neurodegeneration, supporting a potential mechanism where up-regulation of NMDA receptors could produce cognitive deficits in chronic ketamine abuse patients. In other studies, NMDA receptor gene variants are associated with addictive behavior. Here, we focus on the roles of NMDA receptor gene subunits in ketamine abuse and ketamine psychosis and propose that full sequencing of NMDA receptor genes may help explain individual vulnerability to ketamine abuse and ketamine-associated psychosis. © 2014 by the Society for Experimental Biology and Medicine. Source

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