Evidence map›Paper›PMID 32573857›Full record

ArticleGlia2020

ASCL1 regulates neurodevelopmental transcription factors and cell cycle genes in brain tumors of glioma mouse models.

Tou Yia Vue, Rahul K Kollipara, Mark D Borromeo, Tyler Smith, Tomoyuki Mashimo, Dennis K Burns, Robert M Bachoo, Jane E Johnson

Open access · hybridAbstract read
In one paragraph

Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-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

28 citing papers in PubMed, 49 citations in OpenAlex.

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  20. GZ17-6.02 Inhibits the Growth of EGFRvIII+ Glioblastoma.International journal of molecular sciences · 2022
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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

8 authors at 2 institutions in 1 country.

Tou Yia VueDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas, USA.ORCID 0000-0002-5903-9968
Rahul K KolliparaMcDermott Center for Human Growth and Development, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Mark D BorromeoDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Tyler SmithDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Tomoyuki MashimoDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Dennis K BurnsDepartment of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Robert M BachooDepartment of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Jane E JohnsonDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
The University of Texas Southwestern Medical Center · USSouthwestern Medical Center · US

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
REGULATION OF THE NEURAL DETERMINATION GENE MASH1R01NS032817 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI JOHNSON, JANE E · 1995 to 2016
$5.8M
Underlying Molecular Mechanisms of Gliogenesis and Gliomagenesis in the Central Nervous SystemK22NS092767 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI VUE, TOU YIA · 2015 to 2019
$886k
Role of Ascl1 in gliomaF32CA168330 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI VUE, TOU YIA · 2012 to 2014
$156k
NCI NIH HHS F32 CA168330NCI NIH HHS P30 CA118100NINDS NIH HHS K22 NS092767NINDS NIH HHS R01 NS032817
6 · The paper itself

Abstract

Glioblastomas (GBMs) are incurable brain tumors with a high degree of cellular heterogeneity and genetic mutations. Transcription factors that normally regulate neural progenitors and glial development are aberrantly coexpressed in GBM, conferring cancer stem-like properties to drive tumor progression and therapeutic resistance. However, the functional role of individual transcription factors in GBMs in vivo remains elusive. Here, we demonstrate that the basic-helix-loop-helix transcription factor ASCL1 regulates transcriptional targets that are central to GBM development, including neural stem cell and glial transcription factors, oncogenic signaling molecules, chromatin modifying genes, and cell cycle and mitotic genes. We also show that the loss of ASCL1 significantly reduces the proliferation of GBMs induced in the brain of a genetically relevant glioma mouse model, resulting in extended survival times. RNA-seq analysis of mouse GBM tumors reveal that the loss of ASCL1 is associated with downregulation of cell cycle genes, illustrating an important role for ASCL1 in controlling the proliferation of GBM.

Indexed as

Brain NeoplasmsGlioblastomaAnimalsBasic Helix-Loop-Helix ProteinsGene Expression Regulation, NeoplasticGenes, cdcMiceTranscription FactorsAscl1 protein, mouseBasic Helix-Loop-Helix ProteinsTranscription FactorsASCL1brain tumorglioma developmentmouse modeltranscription factor function

Identifiers

PMID32573857
PMCPMC7587013
OpenAlexW3038104382

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.