Evidence map›Paper›PMID 27723576›Full record

ArticleIEEE transactions on bio-medical engineering2017

Multiscale Modeling of Glioblastoma Suggests that the Partial Disruption of Vessel/Cancer Stem Cell Crosstalk Can Promote Tumor Regression Without Increasing Invasiveness.

Huaming Yan, Monica Romero-Lopez, Hermann B Frieboes, Christopher C W Hughes, John S Lowengrub

Abstract read
In one paragraph

Article in IEEE transactions on bio-medical engineering, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
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  8. Editorial: Special Section on Multiscale Cancer Modeling.IEEE transactions on bio-medical engineering · 2017
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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

5 authors at 2 institutions in 1 country.

Huaming Yan
Monica Romero-Lopez
Hermann B Frieboes
Christopher C W Hughes
John S Lowengrub
University of California, Irvine · USUniversity of Louisville · US

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Christine Hui · 1994 to 2026
$57.9M
Uncover Strategies Used By Biological SystemsP50GM076516 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI LANDER, ARTHUR D · 2007 to 2016
$25.1M
TRANS-NETWORK PROJECTSU54CA143907 · NCI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KESSELMAN, CARL · 2009 to 2013
$15.2M
MOLECULAR APPROACHES TARGETED ON BLOCKING ANGIOGENESISR01HL060067 · NHLBI · UNIVERSITY OF CALIFORNIA-IRVINE · PI HUGHES, CHRISTOPHER C. W. · 1999 to 2013
$3.1M
NCI NIH HHS P30 CA062203NCI NIH HHS U54 CA143907NHLBI NIH HHS R01 HL060067NIGMS NIH HHS P50 GM076516
6 · The paper itself

Abstract

objectiveIn glioblastoma, the crosstalk between vascular endothelial cells (VECs) and glioma stem cells (GSCs) has been shown to enhance tumor growth. We propose a multiscale mathematical model to study this mechanism, explore tumor growth under various initial and microenvironmental conditions, and investigate the effects of blocking this crosstalk.

methodsWe develop a hybrid continuum-discrete model of highly organized vascularized tumors. VEC-GSC crosstalk is modeled via vascular endothelial growth factor (VEGF) production by tumor cells and by secretion of soluble factors by VECs that promote GSC self-renewal and proliferation.

resultsVEC-GSC crosstalk increases both tumor size and GSC fraction by enhancing GSC activity and neovascular development. VEGF promotes vessel formation, and larger VEGF sources typically increase vessel numbers, which enhances tumor growth and stabilizes the tumor shape. Increasing the initial GSC fraction has a similar effect. Partially disrupting the crosstalk by blocking VEC secretion of GSC promoters reduces tumor size but does not increase invasiveness, which is in contrast to antiangiogenic therapies, which reduce tumor size but may significantly increase tumor invasiveness. SIGNIFICANCE: Multiscale modeling supports the targeting of VEC-GSC crosstalk as a promising approach for cancer therapy.

Indexed as

Cell CommunicationModels, BiologicalAnimalsCell ProliferationCell SurvivalComputer SimulationEndothelial CellsGlioblastomaHumansNeoplasm InvasivenessNeoplasm Regression, SpontaneousNeoplastic Stem CellsNeovascularization, PathologicSignal TransductionVascular Endothelial Growth Factor AVascular Endothelial Growth Factor A

Identifiers

PMID27723576
PMCPMC5501302
OpenAlexW2529640771

What OpenQuestion holds

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LicenceTDM
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.