Evidence map›Paper›PMID 31471491›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Comprehensive genomic profiling of glioblastoma tumors, BTICs, and xenografts reveals stability and adaptation to growth environments.

Yaoqing Shen, Cameron J Grisdale, Sumaiya A Islam, Pinaki Bose, Jake Lever, Eric Y Zhao, Natalie Grinshtein, Yussanne Ma, Andrew J Mungall, Richard A Moore and 14 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. 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
5.3field-weighted citation impact, top 4% 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, 61 citations in OpenAlex.

  1. Article
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  5. CDKN2A/B Homozygous Deletion Sensitizes IDH-Mutant Glioma to CDK4/6 Inhibition.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024
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  9. Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023
    Review
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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

24 authors at 5 institutions in 1 country.

Yaoqing ShenCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.
Cameron J GrisdaleCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.
Sumaiya A IslamCenter for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, BC, Canada V5Z 4H4.
Pinaki BoseDepartment of Biochemistry & Molecular Biology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 1N4.ORCID 0000-0002-8338-2838
Jake LeverCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.
Eric Y ZhaoCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.ORCID 0000-0003-1277-6335
Natalie GrinshteinProgram in Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada M5G 1X8.
Yussanne MaCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.
Andrew J MungallCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.
Richard A MooreCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.
Xueqing LunDepartment of Oncology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N2.ORCID 0000-0001-9728-2996
Donna L SengerDepartment of Oncology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N2.
Stephen M RobbinsDepartment of Oncology, Cumming School of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N2.
Alice Yijun WangHotchkiss Brain Institute, University of Calgary, Calgary, AB, Canada T2N 4N1.
Julia L MacIsaacCenter for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, BC, Canada V5Z 4H4.
Michael S KoborCenter for Molecular Medicine and Therapeutics, University of British Columbia, Vancouver, BC, Canada V5Z 4H4.
H Artee LuchmanClark H. Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada T2N 4Z6.
Samuel WeissClark H. Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada T2N 4Z6.
Jennifer A ChanArnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada T2N 4Z6.
Michael D BloughClark H. Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada T2N 4Z6.
David R KaplanProgram in Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, ON, Canada M5G 1X8.
J Gregory CairncrossClark H. Smith Brain Tumour Centre, Arnie Charbonneau Cancer Institute, University of Calgary, Calgary, AB, Canada T2N 4Z6.
Marco A MarraCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6.ORCID 0000-0001-7146-7175
Steven J M JonesCanada's Michael Smith Genome Sciences Centre, British Columbia Cancer Agency, Vancouver, BC, Canada V5Z 4S6; sjones@bcgsc.ca.
University of Calgary · CACanada's Michael Smith Genome Sciences Centre · CAUniversity of British Columbia · CAHospital for Sick Children · CAUniversity of Toronto · CA

Funding

CIHR FDN-143288
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is the most deadly brain tumor, and currently lacks effective treatment options. Brain tumor-initiating cells (BTICs) and orthotopic xenografts are widely used in investigating GBM biology and new therapies for this aggressive disease. However, the genomic characteristics and molecular resemblance of these models to GBM tumors remain undetermined. We used massively parallel sequencing technology to decode the genomes and transcriptomes of BTICs and xenografts and their matched tumors in order to delineate the potential impacts of the distinct growth environments. Using data generated from whole-genome sequencing of 201 samples and RNA sequencing of 118 samples, we show that BTICs and xenografts resemble their parental tumor at the genomic level but differ at the mRNA expression and epigenomic levels, likely due to the different growth environment for each sample type. These findings suggest that a comprehensive genomic understanding of in vitro and in vivo GBM model systems is crucial for interpreting data from drug screens, and can help control for biases introduced by cell-culture conditions and the microenvironment in mouse models. We also found that lack of

Indexed as

Gene Expression Regulation, NeoplasticAdultAgedAged, 80 and overAnimalsApoptosisBiomarkers, TumorBrain NeoplasmsCase-Control StudiesCell ProliferationDNA MethylationDrug Resistance, NeoplasmFemaleGene Expression ProfilingGenomicsGlioblastomaBiomarkers, TumorBTICsgenomeglioblastomatherapytranscriptome

Identifiers

PMID31471491
PMCPMC6754609
OpenAlexW2971157179

What OpenQuestion holds

Textmetadata
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.