Evidence map›Paper›PMID 23358475›Full record

ReviewCancer biology & therapy2013

PKC signaling in glioblastoma.

Anália do Carmo, Joana Balça-Silva, Diana Matias, Maria Celeste Lopes

Open access · bronzeAbstract readReview
In one paragraph

Review in Cancer biology & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.0field-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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
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  12. Protein Kinase C as a Therapeutic Target in Non-Small Cell Lung Cancer.International journal of molecular sciences · 2021
    Review
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  15. LPACells · 2021
    Article
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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

4 authors at 3 institutions in 2 countries.

Anália do CarmoCentre for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal. analiacarmo@gmail.com
Joana Balça-Silva
Diana Matias
Maria Celeste Lopes
Centro de Neurociências e Biologia CelularFaculty (United Kingdom) · GBUniversity of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma Multiforme (GBM) is the most aggressive brain tumor characterized by intratumoral heterogeneity at cytopathological, genomic and transcriptional levels. Despite the efforts to develop new therapeutic strategies the median survival of GBM patients is 12-14 months. Results from large-scale gene expression profile studies confirmed that the genetic alterations in GBM affect pathways controlling cell cycle progression, cellular proliferation and survival and invasion ability, which may explain the difficulty to treat GBM patients. One of the signaling pathways that contribute to the aggressive behavior of glioma cells is the protein kinase C (PKC) pathway. PKC is a family of serine/threonine-specific protein kinases organized into three groups according the activating domains. Due to the variability of actions controlled by PKC isoforms, its contribution to the development of GBM is poorly understood. This review intends to highlight the contribution of PKC isoforms to proliferation, survival and invasive ability of glioma cells.

Indexed as

AnimalsBrain NeoplasmsGlioblastomaHumansProtein Kinase CSignal TransductionProtein Kinase Cglioblastoma multiforme (GBM)gliomaprotein kinase C (PKC)signaling pathwaytemozolomide (TMZ)

Identifiers

PMID23358475
PMCPMC3667867
OpenAlexW2022900351

What OpenQuestion holds

Textmetadata
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.