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Showing 1–10 of 10 results
Advanced filters: Author: William A Flavahan Clear advanced filters

  • High-grade glioblastomas survive glucose-poor environments by becoming more stem cell–like. Increased glucose uptake by the transporter Glut3, a new biomarker of poor clinical outcome, drives this enhanced malignant progression.

    • Shirin Ilkhanizadeh
    • William A Weiss
    News & Views
    Nature Neuroscience
    Volume: 16, P: 1359-1361

  • Third-generation sequencing can reveal information beyond the simple sequence of bases, but fulfilling this potential requires complex reference sets for training. Here, the authors present an approach to generate these reference sets and present various use cases for such multidimensional sequencing.

    • Serena S. David
    • Brendan A. Pacheco
    • William A. Flavahan
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-15

  • Gastrointestinal stromal tumours can be initiated by gain-of-function mutations of the KIT or PDGFRA oncogenes but also by loss of the metabolic complex succinate dehydrogenase (SDH), which leads to DNA hypermethylation; this study shows that in SDH-deficient tumours, displacement of CTCF insulators by DNA methylation activates oncogene expression, illustrating how epigenetic alterations can drive oncogenic signalling in the absence of kinase mutations.

    • William A. Flavahan
    • Yotam Drier
    • Bradley E. Bernstein
    Research
    Nature
    Volume: 575, P: 229-233

  • The role of CTCF-bound insulator elements in enhancer-gene interactions and transcriptional regulation remains poorly understood. Here, the authors investigate multiple epigenome editing strategies for perturbing individual CTCF-bound insulators, and evaluate their effects on genome topology and transcription.

    • Daniel R. Tarjan
    • William A. Flavahan
    • Bradley E. Bernstein
    ResearchOpen Access
    Nature Communications
    Volume: 10, P: 1-8

  • Glioblastomas contains stem-like tumor cells that display differential metabolic profiles. Here the authors show that brain tumor initiating cells contain fragmented mitochondria owing to activation of the key mediator of mitochondrial fission, DRP1, controlled by a competitive CDK5–CAMK2 axis. Targeting DRP1 activity attenuates growth of stem-like tumor cells, and activated DRP1 informs poor patient prognosis.

    • Qi Xie
    • Qiulian Wu
    • Jeremy N Rich
    Research
    Nature Neuroscience
    Volume: 18, P: 501-510

  • An epigenetic mechanism in which gain-of-function IDH mutations promote gliomagenesis by disrupting chromosomal topology is presented, with IDH mutations causing the binding sites of the methylation-sensitive insulator CTCF to become hypermethylated; disruption of a CTCF boundary near the glioma oncogene PDGFRA allows a constitutive enhancer to contact and activate the oncogene aberrantly.

    • William A. Flavahan
    • Yotam Drier
    • Bradley E. Bernstein
    Research
    Nature
    Volume: 529, P: 110-114

  • Brain tumor initiating cells (BTICs) are self-renewing, tumorigenic cells that often reside in a necrotic and hypoxic niche in the brain. Here the authors show that BTICs can become more tumorigenic upon glucose restriction and compensate for this cellular stress by upregulating their capacity to take up glucose.

    • William A Flavahan
    • Qiulian Wu
    • Anita B Hjelmeland
    Research
    Nature Neuroscience
    Volume: 16, P: 1373-1382

  • Brain tumor initiating cells (BTICs) utilize high-affinity glucose uptake, which is normally active in neurons to maintain energy demands and self-renew. Leveraging metabolomic and genomic analyses, Wang et al. report that de novo purine biosynthesis reprograms BTIC metabolism, revealing a potential point of fragility amenable to targeted cancer therapy.

    • Xiuxing Wang
    • Kailin Yang
    • Jeremy N Rich
    Research
    Nature Neuroscience
    Volume: 20, P: 661-673

  • An in vivo RNA interference screening strategy in glioblastoma enabled the identification of a host of epigenetic targets required for glioblastoma cell survival that were not identified by parallel standard screening in cell culture, including the transcription pause–release factor JMJD6, and could be a powerful tool to uncover new therapeutic targets in cancer.

    • Tyler E. Miller
    • Brian B. Liau
    • Jeremy N. Rich
    Research
    Nature
    Volume: 547, P: 355-359