Evidence map›Paper›PMID 32642717›Full record

ArticleNeuro-oncology advances

Overexpression of HGF/MET axis along with p53 inhibition induces de novo glioma formation in mice.

Yuan Qin, Anna Musket, Jianqun Kou, Johanna Preiszner, Barbara R Tschida, Anna Qin, Craig A Land, Ben Staal, Liang Kang, Kirk Tanner and 4 more

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

Article in Neuro-oncology advances. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

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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

14 authors at 4 institutions in 1 country.

Yuan QinDepartment of Biomedical Science, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
Anna MusketDepartment of Biomedical Science, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
Jianqun KouDepartment of Biomedical Science, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
Johanna PreisznerDepartment of Pathology, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
Barbara R TschidaDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.
Anna QinDepartment of Biomedical Science, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
Craig A LandDepartment of Biomedical Science, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
Ben StaalCenter for Cancer and Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan, USA.
Liang KangCenter for Cancer and Cell Biology, Van Andel Research Institute, Grand Rapids, Michigan, USA.
Kirk TannerNational Brain Tumor Society, Newton, Massachusetts, USA.
Yong JiangDepartment of Biomedical Science, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
John B SchweitzerDepartment of Pathology, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
David A LargaespadaDepartment of Pediatrics, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota, USA.
Qian XieDepartment of Biomedical Science, Quillen College of Medicine, East Tennessee State University, Johnson City, Tennessee, USA.
East Tennessee State University · USUniversity of Minnesota Medical Center · USVan Andel Institute · USNational Brain Tumor Society · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAberrant MET receptor tyrosine kinase (RTK) activation leads to invasive tumor growth in different types of cancer. Overexpression of MET and its ligand hepatocyte growth factor (HGF) occurs more frequently in glioblastoma (GBM) than in low-grade gliomas. Although we have shown previously that HGF-autocrine activation predicts sensitivity to MET tyrosine kinase inhibitors (TKIs) in GBM, whether it initiates tumorigenesis remains elusive.

methodsUsing a well-established Sleeping Beauty (SB) transposon strategy, we injected human

resultsMixed injection of SB-hHgf.Met.ShP53 plasmids induced de novo glioma formation with invasive tumor growth accompanied by HGF and MET overexpression. While glioma stem cells (GSCs) are considered as the tumor-initiating cells in GBM, both SB-hHgf.Met.ShP53 tumor sections and glioma spheres harvested from these tumors expressed GSC markers nestin, GFAP, and Sox 2. Moreover, specific MET TKIs significantly inhibited tumor spheres' proliferation and MET/MAPK/AKT signaling.

conclusionsOverexpression of the HGF/MET axis along with p53 attenuation may transform neural stem cells into GSCs, resulting in GBM formation in mice. These tumors are primarily driven by the MET RTK pathway activation and are sensitive to MET TKIs. The SB-hHgf.Met.ShP53 spontaneous mouse glioma model provides a useful tool for studying GBM tumor biology and MET-targeting therapeutics.

Indexed as

genetically engineered mouse modelglioblastomaglioma initiating cellsHGF/MET signalingtargeted therapy

Identifiers

PMID32642717
PMCPMC7332240
OpenAlexW3033183994

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.