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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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Scaffolds biomimicking macrophages for a glioblastoma NIR-Ib imaging guided photothermal therapeutic strategy by crossing Blood-Brain Barrier

TL;DR: Plasma membrane of macrophage camouflaged DSPE-PEG loaded near-infrared Ib fluorescence dye IR-792 nanoparticles (MDINPs) were designed to penetrate BBB and selectively accumulate at tumor site, and then could be used as NIR-Ib fluorescence probes for targeted tumor imaging.
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STAT3 Gene Silencing by Aptamer-siRNA Chimera as Selective Therapeutic for Glioblastoma

TL;DR: The objective of this study is to explore the use of nucleic acid aptamers as carriers to specifically drive a STAT3 siRNA to GBM cells in a receptor-dependent manner and reveals Gint4.T-STAT3 conjugate as a novel molecule with great translational potential for GBM therapy.
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Integrin Signaling in Glioma Pathogenesis: From Biology to Therapy.

TL;DR: An overview of the involvement of integrin signaling in glioma pathogenesis, formation of the tumor niche and brain tissue infiltration is provided and up-to-date therapeutic strategies for gliomas focused on interference with integrin ligand-receptor signaling are summarized.
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Frequent AKT1E17K mutations in skull base meningiomas are associated with mTOR and ERK1/2 activation and reduced time to tumor recurrence.

TL;DR: Patients with skull base meningiomas with AKT1E17K mutation might benefit from additional treatment targeting the mTOR pathway, and the PI3K-Akt-mTOR axis might be a potential target for kinase inhibitors in these tumors.
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.
Journal ArticleDOI

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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