Cox Regression.

<p>Cox Regression.</p

An Individual Patient Data Meta-Analysis on Characteristics and Outcome of Patients with Papillary Glioneuronal Tumor, Rosette Glioneuronal Tumor with Neuropil-Like Islands and Rosette Forming Glioneuronal Tumor of the Fourth Ventricle

<div><p>Background and Purpose</p><p>In 2007, the WHO classification of brain tumors was extended by three new entities of glioneuronal tumors: papillary glioneuronal tumor (PGNT), rosette-forming glioneuronal tumor of the fourth ventricle (RGNT) and glioneuronal tumor with neuropil-like islands (GNTNI). Focusing on clinical characteristics and outcome, the authors performed a comprehensive individual patient data (IPD) meta-analysis of the cases reported in literature until December 2012.</p><p>Methods</p><p>PubMed, Embase and Web of Science were searched for peer-reviewed articles reporting on PGNT, RGNT, and GNTNI using predefined keywords.</p><p>Results</p><p>95 publications reported on 182 patients (PGNT, 71; GNTNI, 26; RGNT, 85). Median age at diagnosis was 23 years (range 4–75) for PGNT, 27 years (range 6–79) for RGNT, and 40 years (range 2–65) for GNTNI. Ninety-seven percent of PGNT and 69% of GNTNI were located in the supratentorial region, 23% of GNTNI were in the spinal cord, and 80% of RGNT were localized in the posterior fossa. Complete resection was reported in 52 PGNT (73%), 36 RGNT (42%), and 7 GNTNI (27%) patients. Eight PGNT, 3 RGNT, and 12 GNTNI patients were treated with chemo- and/or radiotherapy as the primary postoperative treatment. Follow-up data were available for 132 cases. After a median follow-up time of 1.5 years (range 0.2–25) across all patients, 1.5-year progression-free survival rates were 52±12% for GNTNI, 86±5% for PGNT, and 100% for RGNT. The 1.5-year overall-survival were 95±5%, 98±2%, and 100%, respectively.</p><p>Conclusions</p><p>The clinical understanding of the three new entities of glioneuronal tumors, PGNT, RGNT and GNTNI, is currently emerging. The present meta-analysis will hopefully contribute to a delineation of their diagnostic, therapeutic, and prognostic profiles. However, the available data do not provide a solid basis to define the optimum treatment approach. Hence, a central register should be established.</p></div

Clinical Characteristics of ….

<p>Clinical Characteristics of ….</p

Kaplan-Meier Plot OS.

<p>Kaplan-Meier Plot OS.</p

Limitation of this study - non-English articles.

<p>Note: n/s – not specified; y/n – yes/no.</p>a<p>Provided by title of the article or abstract if available.</p

Kaplan-Meier Plot PFS.

<p>Kaplan-Meier Plot PFS.</p

Initial symptoms and radiology features.

<p>Initial symptoms and radiology features.</p

Systematic literature search.

<p>Procedure of publication retrieval and in- and exclusion of cases is displayed in a PRISMA (preferred reporting items for systematic reviews and meta-analyses) flow chart.</p

Mutant GFP-Cln6 is rapidly degraded by proteasomes.

<p>BHK cells overexpressing murine wild-type or mutant p.R103PfsX62 GFP-Cln6 (mut) were labelled for 24 hours with [³⁵S]-methionine (75 µCi/ml) and either harvested or chased for 3 (lanes 1–4) and 24 hours (lanes 5–8) in the absence (–) or presence (+) of the proteasomal inhibitor epoxomicin (2 µM). GFP-Cln6 fusion proteins were immunoprecipitated, separated by SDS-PAGE (10% acrylamide) and revealed by fluorography. A representative experiment out of three is shown. The [³⁵S]-labelled bands of the presented experiment were excised from the gel, solubilized and counted. The values are given above the lanes.</p

Activation of microglia in <i>nclf</i> brain.

<p>Immunohistochemical stainings of sagittal mouse brain sections showed a prominent microgliosis as assessed by the microglial marker CD68 at 54 weeks of age in <i>nclf</i> and wild-type (wt) mice. Scale bars. 500 µm. In the right panel, higher magnification images of the areas marked by the black rectangles are shown.</p