E-051 The Role of Follow-up Imaging after Resection of Brain Arteriovenous Malformations in the Pediatric Patient: A Review

ObjectPediatric patients are at significant risk for recurrence of brain AVM after resection. While there is general consensus as to the importance of follow-up after surgical resection of an AVM, there is a lack of consistency in follow-up duration. The object of this systematic review is to examine the role of follow-up imaging in detecting AVM recurrence early and preventing AVM rupture.MethodsThis systematic review was carried out with articles obtained through a search of the literature according to PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines.ResultsSearch results revealed 1052 articles, of which 13 studies describing 31 cases of AVM recurrence met criteria for inclusion in this study. Patients receiving follow-up imaging experienced AVM detection significantly earlier (mean = 3.56 years, SD = 3.67) than patients with no follow-up (mean = 8.86 years, SD = 5.61; p = 0.0085). While 13.34% of patients that were not receiving follow-up imaging presented with rupture of recurrent AVM, 57.14% of patients that were receiving follow-up imaging presented with ruptured recurrence (p = 0.019).ConclusionsFollow-up imaging has an integral role after AVM resection and is sometimes not carried out for a sufficient period of time, leading to delayed detection of recurrence and increased likelihood of recurrent AVM rupture.DisclosuresJ. Jimenez: None. Z. Gersey: None. J. Wagner: None. B. Snelling: None. S. Ambekar: None. E. Peterson: None

Intracranial Langerhans cell Histiocytosis: A review

•LCH is a disease caused by the proliferation of antigen presenting cells in the skin.•LCH rarely affects the brain as primary or secondary focus.•Biopsy is required for diagnosis and exclusion of other intracranial lesions.•This review serves as a guide for previous efficacious therapies in intracranial LCH. Intracranial Langerhans Cell Histiocytosis (LCH) is a rare disease caused by the proliferation and dissemination of antigen presenting cells in the skin. Few cases have been reported on to date and there is a lack of consensus on the most effective means of diagnosis and treatment of these lesions. This paper will serve as a review of this malady. MeSH database search was performed to include all relevant studies on intracranial LCH. A total of 146 studies with 192 patients were included in our review. Men were more commonly affected and the average age of diagnosis was 31.6 and 28.0 in men and women respectively. CT and MRI were the most common imaging modalities. The majority of the case reports performed biopsies and the most common lesion location was the hypothalamus-pituitary axis. All studies used surgical resection, radiotherapy, chemotherapy or combination therapy as means of treatment, with resection plus chemotherapy being the most successful. 74 cases were successful in preventing recurrence. LCH rarely affects the brain as primary or secondary focus. Biopsy is required for precise diagnosis and exclusion of other intracranial lesions. There is no standard treatment for LCH of the central nervous system, but this review may serve as a guide to chronicle previous efficacious therapeutics strategies

The response of a spherical tissue-equivalent proportional counter to 56-Fe particles from 200-1000 MeV/nucleon

The radiation environment aboard the space shuttle and the International Space Station includes high-Z and high-energy (HZE) particles that are part of the galactic cosmic radiation (GCR) spectrum. Iron-56 is considered to be one of the most biologically important parts of the GCR spectrum. Tissue-equivalent proportional counters (TEPC) are used as active dosimeters on manned space flights. These TEPC's are further used to determine average quality factor for each space mission. A TEPC simulating a 1 micron diameter sphere of tissue was exposed as part of a particle spectrometer to iron-56 at energies from 200-1000 MeV/nucleon. The response of TEPC in terms of frequency-averaged lineal energy, dose-averaged lineal energy, as well as energy deposited at different impact parameters through detector was determined for six different incident energies of iron-56 in this energy range. Calculations determined that charged particle equilibrium was achieved for each of the six experiments. Energy depositions at different impact parameters were calculated using a radial dose distribution model and the results compared to experimental data

Investigating the therapeutic role and molecular biology of curcumin as a treatment for glioblastoma

Objectives: Despite the aggressive standard of care for patients with glioblastoma multiforme, survival rates typically do not exceed 2 years. Therefore, current research is focusing on discovering new therapeutics or rediscovering older medications that may increase the overall survival of patients with glioblastoma. Curcumin, a component of the Indian natural spice, turmeric, also known for its antioxidant and anti-inflammatory properties, has been found to be an effective inhibitor of proliferation and inducer of apoptosis in many cancers. The goal of this study was to investigate the expanded utility of curcumin as an antiglioma agent. Methods: Using the PubMed MeSH database, we conducted a systematic review of the literature to include pertinent studies on the growth inhibitory effects of curcumin on glioblastoma cell lines based on Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Results: A total of 19 in vitro and five in vivo studies were analyzed. All of the studies indicated that curcumin decreased glioblastoma cell viability through various pathways (i.e. decrease in prosurvival proteins such as nuclear factor κB, activator protein 1, and phosphoinositide 3 kinase, and upregulation of apoptotic pathways like p21, p53, and executor caspase 3). Curcumin treatment also increased animal survival compared with control groups. Conclusions: Curcumin inhibits proliferation and induces apoptosis in certain subpopulations of glioblastoma tumors, and its ability to target multiple signaling pathways involved in cell death makes it an attractive therapeutic agent. As such, it should be considered as a potent anticancer treatment. Further experiments are warranted to elucidate the use of a bioavailable form of curcumin in clinical trials

Curcumin decreases malignant characteristics of glioblastoma stem cells via induction of reactive oxygen species

Abstract Background Glioblastoma Multiforme (GBM) is the most common and lethal form of primary brain tumor in adults. Following standard treatment of surgery, radiation and chemotherapy, patients are expected to survive 12\u201314 months. Theorized cause of disease recurrence in these patients is tumor cell repopulation through the proliferation of treatment-resistant cancer stem cells. Current research has revealed curcumin, the principal ingredient in turmeric, can modulate multiple signaling pathways important for cancer stem cell self-renewal and survival. Methods Following resection, tumor specimens were dissociated and glioblastoma stem cells (GSCs) were propagated in neurosphere media and characterized via immunocytochemistry. Cell viability was determined with MTS assay. GSC proliferation, sphere forming and colony forming assays were conducted through standard counting methods. Reactive oxygen species (ROS) production was examined using the fluorescent molecular probe CM-H2DCFA. Effects on cell signaling pathways were elucidated by western blot. Results We evaluate the effects of curcumin on patient-derived GSC lines. We demonstrate a curcumin-induced dose-dependent decrease in GSC viability with an approximate IC 50 of 25\ua0\u3bcM. Treatment with sub-toxic levels (2.5\ua0\u3bcM) of curcumin significantly decreased GSC proliferation, sphere forming ability and colony forming potential. Curcumin induced ROS, promoted MAPK pathway activation, downregulated STAT3 activity and IAP family members. Inhibition of ROS with the antioxidant N-acetylcysteine reversed these effects indicating a ROS dependent mechanism. Conclusions Discoveries made in this investigation may lead to a non-toxic intervention designed to prevent recurrence in glioblastoma by targeting glioblastoma stem cells