Evidence map›Paper›PMID 29259984›Full record

ReviewBioMed research international2017

mTOR-Dependent Cell Proliferation in the Brain.

Larisa Ryskalin, Gloria Lazzeri, Marina Flaibani, Francesca Biagioni, Stefano Gambardella, Alessandro Frati, Francesco Fornai

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.0field-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

52 citing papers in PubMed, 87 citations in OpenAlex.

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  7. Low-Basicity 5-HTInternational journal of molecular sciences · 2024
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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 2 institutions in 1 country.

Larisa RyskalinDepartment of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Roma 55, 56126 Pisa, Italy.ORCID 0000-0003-3150-1863
Gloria LazzeriDepartment of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Roma 55, 56126 Pisa, Italy.
Marina FlaibaniDepartment of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Roma 55, 56126 Pisa, Italy.ORCID 0000-0001-6284-5699
Francesca BiagioniI.R.C.C.S. Neuromed, Via Atinense 18, Pozzilli, 86077 Isernia, Italy.ORCID 0000-0003-3566-4889
Stefano GambardellaI.R.C.C.S. Neuromed, Via Atinense 18, Pozzilli, 86077 Isernia, Italy.ORCID 0000-0002-3727-4502
Alessandro FratiI.R.C.C.S. Neuromed, Via Atinense 18, Pozzilli, 86077 Isernia, Italy.
Francesco FornaiDepartment of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Via Roma 55, 56126 Pisa, Italy.ORCID 0000-0002-3883-5084
University of Pisa · ITIstituto Neurologico Mediterraneo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian Target of Rapamycin (mTOR) is a molecular complex equipped with kinase activity which controls cell viability being key in the PI3K/PTEN/Akt pathway. mTOR acts by integrating a number of environmental stimuli to regulate cell growth, proliferation, autophagy, and protein synthesis. These effects are based on the modulation of different metabolic pathways. Upregulation of mTOR associates with various pathological conditions, such as obesity, neurodegeneration, and brain tumors. This is the case of high-grade gliomas with a high propensity to proliferation and tissue invasion. Glioblastoma Multiforme (GBM) is a WHO grade IV malignant, aggressive, and lethal glioma. To date, a few treatments are available although the outcome of GBM patients remains poor. Experimental and pathological findings suggest that mTOR upregulation plays a major role in determining an aggressive phenotype, thus determining relapse and chemoresistance. Among several activities, mTOR-induced autophagy suppression is key in GBM malignancy. In this article, we discuss recent evidence about mTOR signaling and its role in normal brain development and pathological conditions, with a special emphasis on its role in GBM.

Indexed as

AutophagyBrainBrain NeoplasmsCell ProliferationGlioblastomaHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTOR Serine-Threonine KinasesMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanTOR Serine-Threonine Kinases

Identifiers

PMID29259984
PMCPMC5702949
OpenAlexW2769881657

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.