Evidence map›Paper›PMID 32699356›Full record

ArticleNature communications2020

Murine models of IDH-wild-type glioblastoma exhibit spatial segregation of tumor initiation and manifestation during evolution.

Yinghua Li, Bo Li, Wei Li, Yuan Wang, Seçkin Akgül, Daniel M Treisman, Kevin A Heist, Brianna R Pierce, Benjamin Hoff, Cheng-Ying Ho and 6 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

16 citing papers in PubMed, 42 citations in OpenAlex.

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  16. Alterations inNeuro-oncology advances
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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

16 authors at 3 institutions in 2 countries.

Yinghua Li *Gilbert Family Neurofibromatosis Institute, Children's National Hospital, Washington, DC, 20010, USA.ORCID http://orcid.org/0000-0001-9837-9634
Bo Li *Department of Human Genetics, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Wei Li *Center for Genetic Medicine Research, Children's National Hospital, Washington, DC, 20010, USA.
Yuan WangGilbert Family Neurofibromatosis Institute, Children's National Hospital, Washington, DC, 20010, USA.ORCID http://orcid.org/0000-0002-6324-6134
Seçkin AkgülGilbert Family Neurofibromatosis Institute, Children's National Hospital, Washington, DC, 20010, USA.ORCID http://orcid.org/0000-0003-1263-8557
Daniel M TreismanGilbert Family Neurofibromatosis Institute, Children's National Hospital, Washington, DC, 20010, USA.ORCID http://orcid.org/0000-0002-1692-2857
Kevin A HeistDepartment of Radiology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Brianna R PierceGilbert Family Neurofibromatosis Institute, Children's National Hospital, Washington, DC, 20010, USA.
Benjamin HoffDepartment of Radiology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Cheng-Ying HoCenter for Genetic Medicine Research, Children's National Hospital, Washington, DC, 20010, USA.
David O FergusonDepartment of Pathology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Alnawaz RehemtullaDepartment of Radiation Oncology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Siyuan ZhengGreehey Children's Cancer Research Institute, The University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.ORCID http://orcid.org/0000-0002-1031-9424
Brian D RossDepartment of Radiology, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.
Jun Z LiDepartment of Human Genetics, University of Michigan Medical School, Ann Arbor, MI, 48109, USA.ORCID http://orcid.org/0000-0001-6727-0812
Yuan ZhuGilbert Family Neurofibromatosis Institute, Children's National Hospital, Washington, DC, 20010, USA. yzhu@childrensnational.org.ORCID http://orcid.org/0000-0002-6173-0627
Children's National · USUniversity of Michigan · USThe University of Texas Health Science Center at San Antonio · US

Funding

QUANTITATION OF HUMAN BRAIN TUMOR THERAPY RESPONSE BY MRP01CA085878 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROSS, BRIAN D. · 2001 to 2017
$31.9M
Imaging of Hematologic and Oncologic DisordersR35CA197701 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROSS, BRIAN D. · 2016 to 2022
$5.9M
Cellular and molecular basis of malignant astrocytomaR01NS053900 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ZHU, YUAN · 2006 to 2010
$1.6M
NCI NIH HHS P01 CA085878NCI NIH HHS R35 CA197701NINDS NIH HHS R01 NS053900
6 · The paper itself

Abstract

Recent characterization of spatiotemporal genomic architecture of IDH-wild-type multifocal glioblastomas (M-GBMs) suggests a clinically unobserved common-ancestor (CA) with a less aggressive phenotype, generating highly genetically divergent malignant gliomas/GBMs in distant brain regions. Using serial MRI/3D-reconstruction, whole-genome sequencing and spectral karyotyping-based single-cell phylogenetic tree building, we show two distinct types of tumor evolution in p53-mutant driven mouse models. Malignant gliomas/GBMs grow as a single mass (Type 1) and multifocal masses (Type 2), respectively, despite both exhibiting loss of Pten/chromosome 19 (chr19) and PI3K/Akt activation with sub-tetraploid/4N genomes. Analysis of early biopsied and multi-segment tumor tissues reveals no evidence of less proliferative diploid/2N lesions in Type 1 tumors. Strikingly, CA-derived relatively quiescent tumor precursors with ancestral diploid/2N genomes and normal Pten/chr19 are observed in the subventricular zone (SVZ), but are distantly segregated from multi focal Type 2 tumors. Importantly, PI3K/Akt inhibition by Rictor/mTORC2 deletion blocks distant dispersal, restricting glioma growth in the SVZ.

Indexed as

Clonal EvolutionEvolution, MolecularAnimalsBiopsyBrainBrain NeoplasmsCarcinogenesisDisease Models, AnimalDNA Copy Number VariationsGene Expression Regulation, NeoplasticGlioblastomaHumansIsocitrate DehydrogenaseKaryotypingMagnetic Resonance ImagingMechanistic Target of Rapamycin Complex 2Isocitrate DehydrogenaseMechanistic Target of Rapamycin Complex 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouseRapamycin-Insensitive Companion of mTOR Proteinrictor protein, mouse

Identifiers

PMID32699356
PMCPMC7376246
OpenAlexW3044270971

What OpenQuestion holds

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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.