Evidence map›Paper›PMID 25629604›Full record

ArticlePloS one2015

Strategies of eradicating glioma cells: a multi-scale mathematical model with MiR-451-AMPK-mTOR control.

Yangjin Kim, Gibin Powathil, Hyunji Kang, Dumitru Trucu, Hyeongi Kim, Sean Lawler, Mark Chaplain

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

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 53 citations in OpenAlex.

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  13. Collective invasion of glioma cells through OCT1 signalling and interaction with reactive astrocytes after surgery.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Article
  14. Article
  15. Hybrid modeling frameworks of tumor development and treatment.Wiley interdisciplinary reviews. Systems biology and medicine · 2020
    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

7 authors at 3 institutions in 3 countries.

Yangjin KimDepartment of Mathematics, Konkuk University, Seoul, 143-701, Republic of Korea; Department of Mathematics, Ohio State University, Columbus, OH 43210, USA.
Gibin PowathilDivision of Mathematics, University of Dundee, Dundee, UK; Department of Mathematics, Swansea University, Swansea, UK.
Hyunji KangDepartment of Mathematics, Konkuk University, Seoul, 143-701, Republic of Korea.
Dumitru TrucuDivision of Mathematics, University of Dundee, Dundee, UK.
Hyeongi KimDepartment of Physics, Konkuk University, Seoul, 143-701, Republic of Korea.
Sean LawlerDepartment of Neurosurgery, Brigham and Women's Hospital, Harvard Medical School, Boston MA 02115, USA.
Mark ChaplainDivision of Mathematics, University of Dundee, Dundee, UK.
Konkuk University · KRUniversity of Dundee · GBBrigham and Women's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cellular dispersion and therapeutic control of glioblastoma, the most aggressive type of primary brain cancer, depends critically on the migration patterns after surgery and intracellular responses of the individual cancer cells in response to external biochemical and biomechanical cues in the microenvironment. Recent studies have shown that a particular microRNA, miR-451, regulates downstream molecules including AMPK and mTOR to determine the balance between rapid proliferation and invasion in response to metabolic stress in the harsh tumor microenvironment. Surgical removal of main tumor is inevitably followed by recurrence of the tumor due to inaccessibility of dispersed tumor cells in normal brain tissue. In order to address this multi-scale nature of glioblastoma proliferation and invasion and its response to conventional treatment, we propose a hybrid model of glioblastoma that analyses spatio-temporal dynamics at the cellular level, linking individual tumor cells with the macroscopic behaviour of cell organization and the microenvironment, and with the intracellular dynamics of miR-451-AMPK-mTOR signaling within a tumour cell. The model identifies a key mechanism underlying the molecular switches between proliferative phase and migratory phase in response to metabolic stress and biophysical interaction between cells in response to fluctuating glucose levels in the presence of blood vessels (BVs). The model predicts that cell migration, therefore efficacy of the treatment, not only depends on oxygen and glucose availability but also on the relative balance between random motility and strength of chemoattractants. Effective control of growing cells near BV sites in addition to relocalization of invisible migratory cells back to the resection site was suggested as a way of eradicating these migratory cells.

Indexed as

Models, BiologicalAlgorithmsAMP-Activated Protein KinasesBrain NeoplasmsGene Expression Regulation, NeoplasticGliomaHumansMicroRNAsNeoplasm InvasivenessSignal TransductionTOR Serine-Threonine KinasesTreatment OutcomeTumor MicroenvironmentAMP-Activated Protein KinasesMicroRNAsMIRN451 microRNA, humanTOR Serine-Threonine Kinases

Identifiers

PMID25629604
PMCPMC4309536
OpenAlexW1988333927

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.