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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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Neuropathology of Alzheimer's Disease.

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The role of hypoxia and SRC tyrosine kinase in glioblastoma invasiveness and radioresistance

TL;DR: The role of the hypoxic microenvironment and SRC proto-oncogene non-receptor tyrosine kinase in the activation of radioresistance and invasion pathways of glioblastoma is described, providing updated evidences on the involvement of SRC in these processes.
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Treatment of Glioblastoma in Older Adults.

TL;DR: There is evidence that elderly patients with glioblastoma can benefit from a more aggressive and safe resection, from hypofractionated radiation treatments, and from adjuvant temozolomide.
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Non-invasive detection of 2-hydroxyglutarate in IDH-mutated gliomas using two-dimensional localized correlation spectroscopy (2D L-COSY) at 7 Tesla

TL;DR: The ability of 2D L-COSY to unambiguously detect 2HG in addition to other neuro metabolites is demonstrated, which may aid in establishing2HG as a biomarker of malignant progression as well as for disease monitoring in IDH-mutated 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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