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Open AccessJournal ArticleDOI

An Integrative Model of Cellular States, Plasticity, and Genetics for Glioblastoma

TLDR
It is found that malignant cells in glioblastoma exist in four main cellular states that recapitulate distinct neural cell types, are influenced by the tumor microenvironment, and exhibit plasticity.
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This article is published in Cell.The article was published on 2019-08-08 and is currently open access. It has received 1189 citations till now. The article focuses on the topics: Cell Plasticity.

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Reconstructing and Reprogramming the Tumor-Propagating Potential of Glioblastoma Stem-like Cells

TL;DR: This study identifies a core set of neurodevelopmental TFs (POU3F2, SOX2, SALL2, and OLIG2) essential for GBM propagation and reconstructs a network model that highlights critical interactions and identifies candidate therapeutic targets for eliminating TPCs.
References
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Journal ArticleDOI

RSEM: accurate transcript quantification from RNA-Seq data with or without a reference genome

TL;DR: It is shown that accurate gene-level abundance estimates are best obtained with large numbers of short single-end reads, and estimates of the relative frequencies of isoforms within single genes may be improved through the use of paired- end reads, depending on the number of possible splice forms for each gene.
Journal ArticleDOI

The 2007 WHO Classification of Tumours of the Central Nervous System

TL;DR: The fourth edition of the World Health Organization (WHO) classification of tumours of the central nervous system, published in 2007, lists several new entities, including angiocentric glioma, papillary glioneuronal tumour, rosette-forming glioneurs tumour of the fourth ventricle, Papillary tumourof the pineal region, pituicytoma and spindle cell oncocytoma of the adenohypophysis.
Journal ArticleDOI

Glioma stem cells promote radioresistance by preferential activation of the DNA damage response

TL;DR: This work shows that cancer stem cells contribute to glioma radioresistance through preferential activation of the DNA damage checkpoint response and an increase in DNA repair capacity, and suggests that CD133-positive tumour cells could be the source of tumour recurrence after radiation.
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