Evidence map›Paper›PMID 31588023›Full record

ArticleMolecular cell2019

Histone Variant and Cell Context Determine H3K27M Reprogramming of the Enhancer Landscape and Oncogenic State.

Surya Nagaraja, Michael A Quezada, Shawn M Gillespie, Marlene Arzt, James J Lennon, Pamelyn J Woo, Volker Hovestadt, Madhuri Kambhampati, Mariella G Filbin, Mario L Suva and 2 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed
13.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

106 citing papers in PubMed, 183 citations in OpenAlex.

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46 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Surya NagarajaDepartment of Neurology, Stanford University School of Medicine, Stanford, CA, USA; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Michael A QuezadaDepartment of Neurology, Stanford University School of Medicine, Stanford, CA, USA.
Shawn M GillespieDepartment of Neurology, Stanford University School of Medicine, Stanford, CA, USA.
Marlene ArztDepartment of Neurology, Stanford University School of Medicine, Stanford, CA, USA.
James J LennonDepartment of Neurology, Stanford University School of Medicine, Stanford, CA, USA.
Pamelyn J WooDepartment of Neurology, Stanford University School of Medicine, Stanford, CA, USA.
Volker HovestadtDepartment of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Klarman Cell Observatory, Broad Institute of Harvard and Massachusetts Institute of Technology (MIT), Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.
Madhuri KambhampatiResearch Center for Genetic Medicine, Children's National Health System, Washington, DC, USA.
Mariella G FilbinBroad Institute of Harvard and MIT, Cambridge, MA 02142, USA; Department of Pediatric Oncology, Dana-Farber/Boston Children's Cancer and Blood Disorder Center and Harvard Medical School, Boston, MA, USA.
Mario L SuvaDepartment of Pathology and Center for Cancer Research, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA; Klarman Cell Observatory, Broad Institute of Harvard and Massachusetts Institute of Technology (MIT), Cambridge, MA 02142, USA; Broad Institute of Harvard and MIT, Cambridge, MA 02142, USA.
Javad NazarianResearch Center for Genetic Medicine, Children's National Health System, Washington, DC, USA; Department of Integrative Systems Biology, George Washington University School of Medicine and Health Sciences, Washington, DC, USA; Department of Oncology, University Children's Hospital, Zurich, Switzerland.
Michelle MonjeDepartment of Neurology, Stanford University School of Medicine, Stanford, CA, USA; Stanford Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, CA, USA; Stanford Cancer Institute, Stanford University School of Medicine, Stanford, CA, USA; Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA; Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA, USA; Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA. Electronic address: mmonje@stanford.edu.
Stanford University · USBroad Institute · USChildren's National · USStanford Medicine · US

Funding

Glioma Circuitry: Bridging Systems Neuroscience and CancerDP1NS111132 · NINDS · STANFORD UNIVERSITY · PI MONJE-DEISSEROTH, MICHELLE · 2018 to 2022
$5.7M
Neuronal activity-regulated mechanisms of glioma growthR01NS092597 · NINDS · STANFORD UNIVERSITY · PI MONJE-DEISSEROTH, MICHELLE · 2016 to 2021
$2.1M
NINDS NIH HHS DP1 NS111132NINDS NIH HHS R01 NS092597
6 · The paper itself

Abstract

Development of effective targeted cancer therapies is fundamentally limited by our molecular understanding of disease pathogenesis. Diffuse intrinsic pontine glioma (DIPG) is a fatal malignancy of the childhood pons characterized by a unique substitution to methionine in histone H3 at lysine 27 (H3K27M) that results in globally altered epigenetic marks and oncogenic transcription. Through primary DIPG tumor characterization and isogenic oncohistone expression, we show that the same H3K27M mutation displays distinct modes of oncogenic reprogramming and establishes distinct enhancer architecture depending upon both the variant of histone H3 and the cell context in which the mutation occurs. Compared with non-malignant pediatric pontine tissue, we identify and functionally validate both shared and variant-specific pathophysiology. Altogether, we provide a powerful resource of epigenomic data in 25 primary DIPG samples and 5 rare normal pediatric pontine tissue samples, revealing clinically relevant functional distinctions previously unidentified in DIPG.

Indexed as

BrainBrain NeoplasmsCellular ReprogrammingDiffuse Intrinsic Pontine GliomaEnhancer Elements, GeneticEpigenesis, GeneticEpigenomicsGene Expression ProfilingGene Expression Regulation, NeoplasticGliomaHistonesHumansLysineMutationPonsSignal TransductionHistonesLysineactive enhancersDIPGgliomaH3.3H3K27AcH3K27MH3K27me3histone variantoligodendrocyte precursor cellPRC2

Identifiers

PMID31588023
PMCPMC7104854
OpenAlexW2978540141

What OpenQuestion holds

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LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.