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Author |
Fogel, O.; Richard-Miceli, C.; Tost, J. |
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Title |
Epigenetic Changes in Chronic Inflammatory Diseases |
Type |
Journal Article |
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Year |
2017 |
Publication |
Advances in Protein Chemistry and Structural Biology |
Abbreviated Journal |
Adv Protein Chem Struct Biol |
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Volume  |
106 |
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Pages |
139-189 |
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Keywords |
Behcet's disease; Crohn's disease; DNA methylation; Ewas; Epigenetics; Histone modifications; Inflammatory bowel disease; Psoriasis; Spondyloarthritis; Ulcerative colitis |
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Abstract |
The number of people diagnosed with chronic inflammatory diseases has increased noteworthy in the last 40 years. Spondyloarthritis (SpA), inflammatory bowel diseases (IBD), and psoriasis are the most frequent chronic inflammatory diseases, resulting from a combination of genetic predisposition and environmental factors. Epigenetic modifications include DNA methylation, histone modifications, and small and long noncoding RNAs. They are influenced by environmental exposure, life-style, and aging and have recently been shown to be altered in many complex diseases including inflammatory diseases. While epigenetic modifications have been well characterized in other diseases such as cancer and autoimmune diseases, knowledge on changes in inflammatory diseases is lagging behind with some disease-specific differences. While the DNA methylation profile of different cell types in patients with IBD has been relatively well described, less is known on changes implicated in psoriasis, and no systematic genome-wide studies have so far been performed in SpA. In this chapter, we review in detail the reported changes in patterns of DNA methylation and posttranslational histone modifications in chronic inflammatory diseases highlighting potential connections between disease-associated pathophysiological changes such as the dysbiosis of the microbiome or genetic variations associated with disease susceptibility and the epigenome. We also discuss important parameters of meaningful epigenetic studies such as the use of well defined, disease-relevant cell populations, and elude on the potential future of engineering of the epigenome in inflammatory diseases. |
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Laboratory for Epigenetics and Environment, Centre National de Genotypage, CEA-Institut de Genomique, Evry, France. Electronic address: tost@cng.fr |
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1876-1623 |
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PMID:28057210 |
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ref @ user @ |
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96374 |
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Author |
Behling, F.; Kaltenstadler, M.; Noell, S.; Schittenhelm, J.; Bender, B.; Eckert, F.; Tabatabai, G.; Tatagiba, M.; Skardelly, M. |
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Title |
The Prognostic Impact of Ventricular Opening in Glioblastoma Surgery: A Retrospective Single Center Analysis |
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Journal Article |
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Year |
2017 |
Publication |
World Neurosurgery |
Abbreviated Journal |
World Neurosurg |
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Volume |
106 |
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Pages |
615-624 |
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Keywords |
Extent of resection; Glioblastoma; Hydrocephalus; Overall survival; Prognosis; Tumor volume; Ventricle opening |
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Abstract |
OBJECTIVE: Ventricular opening during glioblastoma (GBM) resection is controversial. Sufficient evidence regarding its prognostic role is missing. We investigated the impact of ventricular opening on overall survival (OS), hydrocephalus development, and postoperative morbidity in patients with GBM. METHODS: Patients who underwent primary GBM resection between 2006 and 2013 were assessed retrospectively. Established predictors for overall survival (age, Karnofsky Performance Status, extent of resection, O-6-methylguanine-DNA methyltransferase promoter methylation status, isocitrate dehydrogenase mutation status) and further clinical data (postoperative status, further treatment, preoperative tumor volume, proximity to the ventricle) were included in univariate and multivariate analyses. RESULTS: Thirteen (5.7%) of 229 patients developed a hydrocephalus. Multivariate logistic regression showed that neither ventricular opening, tumor size, proximity to the ventricle, nor extent of resection were significant risk factors for hydrocephalus. Ventricular opening did not delay postoperative therapy and was not associated with neurological morbidity. Kaplan-Meier analysis demonstrated that patients who underwent ventricular opening (n = 114) exhibited a median OS of 14.3 months (12.9-16.5), whereas patients who did not undergo ventricular opening (n = 115) exhibited a median OS of 18.6 months (16.1-20.8). However, multivariate Cox regression (n = 134) did not confirm ventricular opening as an independent negative predictor of OS (risk ratio 1.09, P = 0.77). Instead, it showed that a greater preoperative tumor volume >22.8 cm3 was a negative predictor of OS (risk ratio 1.76, P = 0.02). CONCLUSIONS: Because extent of resection is a strong independent predictor of OS and ventricular opening is safe, neurosurgeons should consider ventricular opening to achieve maximal tumor resection. |
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Department of Neurosurgery, University Hospital Tuebingen, Eberhard Karls University, Tuebingen, Germany; Center for CNS Tumors, Comprehensive Cancer Center Tuebingen Stuttgart, University Hospital Tuebingen, Eberhard Karls University, Tuebingen, Germany |
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1878-8750 |
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PMID:28729143 |
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Call Number |
ref @ user @ |
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96576 |
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Author |
Alshehri, M.M.; Robbins, S.M.; Senger, D.L. |
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Title |
The Role of Neurotrophin Signaling in Gliomagenesis: A Focus on the p75 Neurotrophin Receptor (p75NTR/CD271) |
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Journal Article |
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Year |
2017 |
Publication |
Vitamins and Hormones |
Abbreviated Journal |
Vitam Horm |
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104 |
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367-404 |
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Brain tumor; Cd271; Cancer stem cells; Glioblastoma; Glioma invasion; Nerve growth factor; Neurotrophin; p75(NTR) |
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Abstract |
The p75 neurotrophin receptor (p75NTR, a.k.a. CD271), a transmembrane glycoprotein and a member of the tumor necrosis family (TNF) of receptors, was originally identified as a nerve growth factor receptor in the mid-1980s. While p75NTR is recognized to have important roles during neural development, its presence in both neural and nonneural tissues clearly supports the potential to mediate a broad range of functions depending on cellular context. Using an unbiased in vivo selection paradigm for genes underlying the invasive behavior of glioma, a critical characteristic that contributes to poor clinical outcome for glioma patients, we identified p75NTR as a central regulator of glioma invasion. Herein we review the expanding role that p75NTR plays in glioma progression with an emphasis on how p75NTR may contribute to the treatment refractory nature of glioma. Based on the observation that p75NTR is expressed and functional in two critical glioma disease reservoirs, namely, the highly infiltrative cells that evade surgical resection, and the radiation- and chemotherapy-resistant brain tumor-initiating cells (also referred to as brain tumor stem cells), we propose that p75NTR and its myriad of downstream signaling effectors represent rationale therapeutic targets for this devastating disease. Lastly, we provide the provocative hypothesis that, in addition to the well-documented cell autonomous signaling functions, the neurotrophins, and their respective receptors, contribute in a cell nonautonomous manner to drive the complex cellular and molecular composition of the brain tumor microenvironment, an environment that fuels tumorigenesis. |
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Arnie Charbonneau Cancer Centre, University of Calgary, Calgary, AB, Canada. Electronic address: senger@ucalgary.ca |
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0083-6729 |
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PMID:28215302 |
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Call Number |
ref @ user @ |
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96606 |
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Roh, T.H.; Park, H.H.; Kang, S.-G.; Moon, J.H.; Kim, E.H.; Hong, C.-K.; Ahn, S.S.; Choi, H.J.; Cho, J.; Kim, S.H.; Lee, S.K.; Kim, D.S.; Kim, S.H.; Suh, C.-O.; Lee, K.S.; Chang, J.H. |
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Title |
Long-term outcomes of concomitant chemoradiotherapy with temozolomide for newly diagnosed glioblastoma patients: A single-center analysis |
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Journal Article |
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Year |
2017 |
Publication |
Medicine |
Abbreviated Journal |
Medicine (Baltimore) |
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Volume |
96 |
Issue |
27 |
Pages |
e7422 |
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Keywords |
Adult; Aged; Aged, 80 and over; Antineoplastic Agents, Alkylating/*therapeutic use; Brain Neoplasms/diagnosis/genetics/metabolism/*therapy; *Chemoradiotherapy; DNA Methylation; DNA Modification Methylases/genetics/metabolism; DNA Repair Enzymes/genetics/metabolism; Dacarbazine/*analogs & derivatives/therapeutic use; Disease-Free Survival; Female; Follow-Up Studies; Glioblastoma/diagnosis/genetics/metabolism/*therapy; Humans; Male; Middle Aged; Prognosis; Promoter Regions, Genetic; Retrospective Studies; Treatment Outcome; Tumor Suppressor Proteins/genetics/metabolism; Young Adult |
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The present study analyzed outcomes of surgery followed by concomitant chemoradiotherapy (CCRT) with temozolomide (TMZ) in patients with newly diagnosed glioblastoma (GBM) at a single institution. Outcomes were retrospectively reviewed in 252 consecutive patients with newly diagnosed GBM who underwent surgery followed by CCRT with TMZ at the authors' institution between 2005 and 2013. At initial operation, 126 (50.0%), 55 (21.8%), 45 (17.9%), and 26 (10.3%) patients underwent gross total resection (GTR), subtotal resection, partial resection (PR), and biopsy, respectively. Their median overall survival (OS) was 20.8 months (95% confidence interval [CI] 17.7-23.9 months) and their median progression-free survival was 12.7 months (95% CI 11.2-14.2 months). The O-methylguanine-DNA methyltransferase (MGMT) promoter was methylated in 78 (34.1%) of the 229 patients assayed, and an isocitrate dehydrogenase 1 mutation was detected in 7 (6.6%) of the 106 patients analyzed. Univariate analyses showed that patient age, involvement of eloquent areas, involvement of the subventricular zone, presence of leptomeningeal seeding, Karnofsky Performance Status, extent of resection (EOR), MGMT promoter methylation, and presence of an oligodendroglioma component were prognostic of OS. Multivariate analysis showed that age, involvement of eloquent areas, presence of leptomeningeal seeding, EOR, and MGMT promoter methylation were significantly predictive of survival. OS in patients with GBM who undergo surgery followed by CCRT with TMZ is enhanced by complete resection. Other factors significantly prognostic of OS include that age, involvement of eloquent areas, presence of leptomeningeal seeding, and MGMT promoter methylation. |
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aYonsei University Graduate School, Seoul bDepartment of Neurosurgery, Ajou University Hospital, Ajou University School of Medicine, Suwon cDepartment of Neurosurgery dDepartment of Radiology eDepartment of Medical Oncology fDepartment of Radiation Oncology gDepartment of Pathology, Yonsei University College of Medicine hBrain Tumor Center, Severance Hospital, Yonsei University Health System iBrain Research Institute, Yonsei University College of Medicine, Seoul, Republic of Korea |
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0025-7974 |
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PMID:28682902 |
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Call Number |
ref @ user @ |
Serial |
96578 |
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Author |
Pinsky, I.; Noto, A.R.; Botequio de Moraes, M.C.; Lucas Dos Santos, E.; Sparks, R.; O'Brien, K. |
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Title |
Alcohol Industry Sponsorship of University Student Sports Clubs in Brazil |
Type |
Journal Article |
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Year |
2017 |
Publication |
Journal of Studies on Alcohol and Drugs |
Abbreviated Journal |
J Stud Alcohol Drugs |
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Volume |
78 |
Issue |
2 |
Pages |
306-312 |
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Keywords |
Alcohol Drinking/*economics; Brazil; Commerce; Humans; Marketing/*economics; Perception; *Sports; Students; *Universities |
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OBJECTIVE: The university sport environment represents an important target for alcohol industry marketing. This study investigated the nature of relationships between the alcohol industry and university student sports clubs (USSCs). METHOD: Semi-structured interviews were conducted with board members from 60 active USSCs in the city of Sao Paulo, Brazil. Interviews were transcribed and subjected to content analysis using NVivo10. RESULTS: All invited USSCs participated in the study. Most (n = 53; 88%) reported having signed contracts with the alcohol industry (breweries, in every case) to have their sports events and parties sponsored. The most common sponsorship arrangement involved the supply of discounted beer for sport and student events. T-shirts, beer freezers, and stereo systems were also frequently provided by the alcohol industry to support alcohol-related sports events. In addition, the alcohol industry event promoters helped market the events and products. In return, the USSCs agreed to exclusively sell the sponsors' brand of beer and/or order and sell a quota of beer at their events. Forty-nine interviewees (81%) reported agreements with alcohol companies whereby open bars (free alcohol events) would also be provided. Despite reporting a range of alcohol harms, participants did not perceive there to be a high risk of harm from the alcohol sponsorship arrangements. CONCLUSIONS: Most USSCs in Sao Paulo, Brazil, have formalized contracts with the alcohol industry that promote the marketing, sale, and consumption of alcohol at parties and university games. A critical review of the impacts of these practices and university policies on alcohol industry sponsorship that can take account of the role of such arrangements in student drinking is warranted. |
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School of Social Sciences, Monash University, Melbourne, Australia |
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1937-1888 |
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PMID:28317512 |
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Call Number |
ref @ user @ |
Serial |
97333 |
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