FACULTYOPINIONS . COM {}

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We began analyzing https://archive.connect.h1.co/article/727120897/, but it redirected us to https://archive.connect.h1.co/article/727120897/. The analysis below is for the second page.

Title[redir]:
Adaptive chromatin remodeling driv ... | Article | H1 Connect
Description:
Glioblastoma, the most common and aggressive malignant brain tumor, is propagated by stem-like cancer cells refractory to existing therapies. Understanding

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Keywords {🔍}

stem, cells, glioblastoma, drug, latest, recommendation, cell, finding, cancer, target, good, therapeutics, faculty, resistance, induction, biology, nuclear, structure, function, apr, jun, dec, teaching, plasticity, show, brent, cochran, population, persister, pdgfr, state, pathway, drugresistant, regulation, hkme, kdmb, neural, stat, interesting, molecular, neurooncology, haupt, opinions, collections, reviews, connecting, world, doctors, search, page,

Topics {✒️}

neuro-oncology cancer cell subpopulations cancer stem cells cell stem cell tumour cell plasticity drug-resistant cells mesenchymal stem cell glioblastoma stem cells drug target establishment cell cycle genes human glioblastoma reveals cells induces chemoresistance drug target drug target 1 repressive h3k27me3 mark h3k27me3 demethylase kdm6a/ neural gene induction stem cells drug resistance drug tolerance aberrant regulation glioblastoma multiforme faculty opinions teaching cellular state h1 company 2012 latest recommendation 07 latest recommendation 2016 latest recommendation glioblastoma stem doctors search liau bb e7 https paper builds evidence showing traditional chemotherapy population inhibitor treatment notch pathway neurodevelopmental programs global reduction h3k27 methylation common pathway sharma sv differentially expressed lang mf lathia jd jensen ss circadian clock

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ScholarlyArticle:
      context:https://schema.org
      headline:Adaptive chromatin remodeling drives glioblastoma stem cell plasticity and drug tolerance.
      abstract:Glioblastoma, the most common and aggressive malignant brain tumor, is propagated by stem-like cancer cells refractory to existing therapies. Understanding the molecular mechanisms that control glioblastoma stem cell (GSC) proliferation and drug resistance may reveal opportunities for therapeutic interventions. Here we show that GSCs can reversibly transition to a slow-cycling, persistent state in response to targeted kinase inhibitors. In this state, GSCs upregulate primitive developmental programs and are dependent upon Notch signaling. This transition is accompanied by widespread redistribution of repressive histone methylation. Accordingly, persister GSCs upregulate, and are dependent on, the histone demethylases KDM6A/B. Slow-cycling cells with high Notch activity and histone demethylase expression are present in primary glioblastomas before treatment, potentially contributing to relapse. Our findings illustrate how cancer cells may hijack aspects of native developmental programs for deranged proliferation, adaptation, and tolerance. They also suggest strategies for eliminating refractory tumor cells by targeting epigenetic and developmental pathways.<br><br>Copyright © 2017 Elsevier Inc. All rights reserved.
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WebPage:
      id:https://connect.h1.co/article/727120897

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