Evidence map›Paper›PMID 28434841›Full record

ArticleCancer cell2017

Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma.

Surya Nagaraja, Nicholas A Vitanza, Pamelyn J Woo, Kathryn R Taylor, Fang Liu, Lei Zhang, Meng Li, Wei Meng, Anitha Ponnuswami, Wenchao Sun and 6 more

Open access · bronzeAbstract read
In one paragraph

Article in Cancer cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 242 papers.

0numbers the graph read from it
0cells of the map it votes in
242citing papers in PubMed
16.1field-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

242 citing papers in PubMed, 397 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 4 countries.

Surya NagarajaDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA.
Nicholas A VitanzaDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA.
Pamelyn J WooDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA.
Kathryn R TaylorDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA.
Fang LiuKey Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, P.R. China.
Lei ZhangKey Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, P.R. China.
Meng LiKey Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, P.R. China.
Wei MengDepartment of Pediatric Neurosurgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China.
Anitha PonnuswamiDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA.
Wenchao SunDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA.
Jie MaDepartment of Pediatric Neurosurgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China.
Esther HullemanDepartment of Pediatric Oncology, VU University Medical Center, 1081 HV Amsterdam, the Netherlands.
Tomek SwigutDepartment of Chemical and Systems Biology, Stanford University, Palo Alto, CA 94305, USA.
Joanna WysockaDepartment of Chemical and Systems Biology, Stanford University, Palo Alto, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Palo Alto, California 94305, USA; Department of Developmental Biology, Stanford University, Palo Alto, California 94305, USA; Howard Hughes Medical Institute, Stanford School of Medicine, Stanford University, Palo Alto, California 94305, USA.
Yujie TangDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA; Key Laboratory of Cell Differentiation and Apoptosis of National Ministry of Education, Department of Pathophysiology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, P.R. China; Department of Pediatric Neurosurgery, Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200092, P.R. China. Electronic address: yujietang@shsmu.edu.cn.
Michelle MonjeDepartment of Neurology, Stanford University, Palo Alto, CA 94305, USA; Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Palo Alto, California 94305, USA. Electronic address: mmonje@stanford.edu.
Palo Alto University · USShanghai Jiao Tong University · CNAmsterdam UMC Location Vrije Universiteit Amsterdam · NLHoward Hughes Medical Institute · USStanford University · US

Funding

Translational Oncology Research Program (Project-005)P30CA124435 · NCI · STANFORD UNIVERSITY · PI Melinda L. Telli · 2007 to 2026
$71.4M
Neuronal activity-regulated mechanisms of glioma growthR01NS092597 · NINDS · STANFORD UNIVERSITY · PI MONJE-DEISSEROTH, MICHELLE · 2016 to 2021
$2.1M
Mechanisms of enhancer activation in early developmentR01GM112720 · NIGMS · STANFORD UNIVERSITY · PI WYSOCKA, JOANNA · 2015 to 2018
$1.2M
Howard Hughes Medical InstituteNCI NIH HHS P30 CA124435NIGMS NIH HHS R01 GM112720NINDS NIH HHS R01 NS092597
6 · The paper itself

Abstract

Diffuse intrinsic pontine glioma (DIPG) is a fatal pediatric cancer with limited therapeutic options. The majority of cases of DIPG exhibit a mutation in histone-3 (H3K27M) that results in oncogenic transcriptional aberrancies. We show here that DIPG is vulnerable to transcriptional disruption using bromodomain inhibition or CDK7 blockade. Targeting oncogenic transcription through either of these methods synergizes with HDAC inhibition, and DIPG cells resistant to HDAC inhibitor therapy retain sensitivity to CDK7 blockade. Identification of super-enhancers in DIPG provides insights toward the cell of origin, highlighting oligodendroglial lineage genes, and reveals unexpected mechanisms mediating tumor viability and invasion, including potassium channel function and EPH receptor signaling. The findings presented demonstrate transcriptional vulnerabilities and elucidate previously unknown mechanisms of DIPG pathobiology.

Indexed as

AnimalsAntineoplastic Combined Chemotherapy ProtocolsAzepinesBrain Stem NeoplasmsBromodomain Containing ProteinsCell Cycle ProteinsCell ProliferationChromatin Assembly and DisassemblyCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesDose-Response Relationship, DrugDrug Resistance, NeoplasmDrug SynergismFemaleGene Expression Regulation, NeoplasticGliomaAzepinesBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsCyclin-Dependent Kinase-Activating KinaseCyclin-Dependent KinasesHistone Deacetylase InhibitorsHistonesHydroxamic AcidsIndoles(+)-JQ1 compoundNuclear ProteinsPanobinostatPhenylenediaminesProtein Kinase InhibitorsPyrimidinesReceptors, Eph FamilyTHZ1 compoundTranscription FactorsTriazolesBRD4CDK7DIPGEPHoligodendrocyte precursor cellpotassium channelsuper-enhancer

Identifiers

PMID28434841
PMCPMC5462626
OpenAlexW2606835938

What OpenQuestion holds

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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.