Evidence map›Paper›PMID 28264064›Full record

ArticlePloS one2017

Ion channel expression patterns in glioblastoma stem cells with functional and therapeutic implications for malignancy.

Julia Pollak, Karan G Rai, Cory C Funk, Sonali Arora, Eunjee Lee, Jun Zhu, Nathan D Price, Patrick J Paddison, Jan-Marino Ramirez, Robert C Rostomily

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
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  11. Hyper-active RAS/MAPK introduces cancer-specific mitotic vulnerabilities.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Ion Channels in Cancer: Orchestrators of Electrical Signaling and Cellular Crosstalk.Reviews of physiology, biochemistry and pharmacology · 2022
    Review
  16. Review
  17. Electrotherapies for Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Review
  18. Cancers · 2021
    Article
  19. Article
  20. Review
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

10 authors at 5 institutions in 1 country.

Julia PollakCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, Washington, United States of America.
Karan G RaiCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, Washington, United States of America.
Cory C FunkInstitute for Systems Biology, Seattle, Washington, United States of America.
Sonali AroraHuman Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Eunjee LeeDepartment of Genetics and Genomic Sciences, Icahn Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Jun ZhuDepartment of Genetics and Genomic Sciences, Icahn Institute of Genomics and Multiscale Biology, Icahn School of Medicine at Mount Sinai, New York, New York, United States of America.
Nathan D PriceInstitute for Systems Biology, Seattle, Washington, United States of America.
Patrick J PaddisonHuman Biology Division, Fred Hutchinson Cancer Research Center, Seattle, Washington, United States of America.
Jan-Marino RamirezCenter for Integrative Brain Research, Seattle Children's Research Institute, Seattle, Washington, United States of America.
Robert C RostomilyDepartment of Neurosurgery, University of Washington, Seattle, Washington, United States of America.
Fred Hutch Cancer Center · USIcahn School of Medicine at Mount Sinai · USInstitute for Systems Biology · USHouston Methodist · USUniversity of Washington · US

Funding

MYC-dependent loss of splicing fidelity in Glioblastoma multiformeR01CA190957 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PADDISON, PATRICK · 2015 to 2019
$2.2M
Transforming Genomics with 5 PB Big Omics Data Engine Cray CS300-AC SupercomputerS10OD018522 · OD · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI KOVATCH, PATRICIA · 2014 to 2014
$1.9M
Therapeutically relevant targets of Twist1 dimers in gliomaR01NS091251 · NINDS · UNIVERSITY OF WASHINGTON · PI ROSTOMILY, ROBERT C · 2015 to 2020
$1.8M
Identification of Small Molecule Inhibitors of PHF5A for GlioblastomaR01CA193841 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI MHYRE, ANDREW J., OLSON, JAMES M · 2015 to 2017
$1.6M
Developing methods for curating multi-omics dataU01HG008451 · NHGRI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI ZHU, JUN · 2015 to 2017
$1.5M
Regulation of glioma stem cell malignancy by neural activity in the tumor nicheF32CA199717 · NCI · SEATTLE CHILDREN'S HOSPITAL · PI POLLAK, JULIA · 2015 to 2017
$148k
NCI NIH HHS F32 CA199717NCI NIH HHS R01 CA190957NCI NIH HHS R01 CA193841NHGRI NIH HHS U01 HG008451NIH HHS S10 OD018522NINDS NIH HHS R01 NS091251
6 · The paper itself

Abstract

Ion channels and transporters have increasingly recognized roles in cancer progression through the regulation of cell proliferation, migration, and death. Glioblastoma stem-like cells (GSCs) are a source of tumor formation and recurrence in glioblastoma multiforme, a highly aggressive brain cancer, suggesting that ion channel expression may be perturbed in this population. However, little is known about the expression and functional relevance of ion channels that may contribute to GSC malignancy. Using RNA sequencing, we assessed the enrichment of ion channels in GSC isolates and non-tumor neural cell types. We identified a unique set of GSC-enriched ion channels using differential expression analysis that is also associated with distinct gene mutation signatures. In support of potential clinical relevance, expression of selected GSC-enriched ion channels evaluated in human glioblastoma databases of The Cancer Genome Atlas and Ivy Glioblastoma Atlas Project correlated with patient survival times. Finally, genetic knockdown as well as pharmacological inhibition of individual or classes of GSC-enriched ion channels constrained growth of GSCs compared to normal neural stem cells. This first-in-kind global examination characterizes ion channels enriched in GSCs and explores their potential clinical relevance to glioblastoma molecular subtypes, gene mutations, survival outcomes, regional tumor expression, and experimental responses to loss-of-function. Together, the data support the potential biological and therapeutic impact of ion channels on GSC malignancy and provide strong rationale for further examination of their mechanistic and therapeutic importance.

Indexed as

Gene Expression Regulation, NeoplasticAntineoplastic AgentsBrain NeoplasmsCell Line, TumorCell SurvivalCluster AnalysisGap JunctionsGene Expression ProfilingGene Knockdown TechniquesGlioblastomaHumansIon ChannelsNeoplastic Stem CellsPrognosisSignal TransductionSurvival AnalysisAntineoplastic AgentsIon Channels

Identifiers

PMID28264064
PMCPMC5338779
OpenAlexW2592007843

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.