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The 2016 World Health Organization Classification of Tumors of the Central Nervous System: a summary.

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TLDR
The 2016 World Health Organization Classification of Tumors of the Central Nervous System is both a conceptual and practical advance over its 2007 predecessor and is hoped that it will facilitate clinical, experimental and epidemiological studies that will lead to improvements in the lives of patients with brain tumors.
Abstract
The 2016 World Health Organization Classification of Tumors of the Central Nervous System is both a conceptual and practical advance over its 2007 predecessor. For the first time, the WHO classification of CNS tumors uses molecular parameters in addition to histology to define many tumor entities, thus formulating a concept for how CNS tumor diagnoses should be structured in the molecular era. As such, the 2016 CNS WHO presents major restructuring of the diffuse gliomas, medulloblastomas and other embryonal tumors, and incorporates new entities that are defined by both histology and molecular features, including glioblastoma, IDH-wildtype and glioblastoma, IDH-mutant; diffuse midline glioma, H3 K27M-mutant; RELA fusion-positive ependymoma; medulloblastoma, WNT-activated and medulloblastoma, SHH-activated; and embryonal tumour with multilayered rosettes, C19MC-altered. The 2016 edition has added newly recognized neoplasms, and has deleted some entities, variants and patterns that no longer have diagnostic and/or biological relevance. Other notable changes include the addition of brain invasion as a criterion for atypical meningioma and the introduction of a soft tissue-type grading system for the now combined entity of solitary fibrous tumor / hemangiopericytoma-a departure from the manner by which other CNS tumors are graded. Overall, it is hoped that the 2016 CNS WHO will facilitate clinical, experimental and epidemiological studies that will lead to improvements in the lives of patients with brain tumors.

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Assessment of Glioblastoma Response in the Era of Bevacizumab: Longstanding and Emergent Challenges in the Imaging Evaluation of Pseudoresponse.

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Silencing LncRNA LOXL1-AS1 attenuates mesenchymal characteristics of glioblastoma via NF-κB pathway

TL;DR: It is demonstrated that silencing LncRNA LOXL1-AS1 was a new regulator of NF-κB signaling pathway through repressing RELB directly, resulting in increased marker genes of PN subtype and decreased those of MES.
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MGMT promoter methylation level in newly diagnosed low-grade glioma is a predictor of hypermutation at recurrence

TL;DR: These findings reveal a mechanistic basis for observed differences in patient susceptibility to TMZ-driven hypermutation and establish MGMT promoter methylation level as a potential biomarker to inform clinical management of LGG patients, including monitoring and treatment decisions, by predicting risk ofhypermutation at recurrence.
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Fatal correlation between YAP1 expression and glioma aggressiveness: clinical and molecular evidence.

TL;DR: The results showed that YAP1 could be a relevant prognostic biomarker and a potential therapeutic target in glioma and found that it may have prognostic significance for predicting patient survival, especially in low‐grade gliomas.
References
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Journal ArticleDOI

Comprehensive, Integrative Genomic Analysis of Diffuse Lower-Grade Gliomas.

Daniel J. Brat, +306 more
TL;DR: The integration of genomewide data from multiple platforms delineated three molecular classes of lower-grade gliomas that were more concordant with IDH, 1p/19q, and TP53 status than with histologic class.
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Somatic histone H3 alterations in pediatric diffuse intrinsic pontine gliomas and non-brainstem glioblastomas

TL;DR: To identify somatic mutations in pediatric diffuse intrinsic pontine glioma (DIPG), whole-genome sequencing of DNA from seven DIPGs and matched germline tissue and targeted sequencing of an additional 43 DIPG and 36 non-brainstem pediatric glioblastomas (non-BS-PGs) were performed.
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Population-based studies on incidence, survival rates, and genetic alterations in astrocytic and oligodendroglial gliomas.

TL;DR: Data is summarized on incidence rates, survival, and genetic alterations from population-based studies of astrocytic and oligodendrogliomas that were carried out in the Canton of Zurich, Switzerland to suggest that the acquisition of TP53 mutations in these glioblastoma subtypes may occur through different mechanisms.
Journal ArticleDOI

The Definition of Primary and Secondary Glioblastoma

TL;DR: IDH1 mutations are the earliest detectable genetic alteration in precursor low-grade diffuse astrocytomas and in oligodendrogliomas, indicating that these tumors are derived from neural precursor cells that differ from those of primary glioblastomas.
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