Evidence map›Paper›PMID 26549022›Full record

ArticleOncogene2016

Chronophin is a glial tumor modifier involved in the regulation of glioblastoma growth and invasiveness.

M Schulze, O Fedorchenko, T G Zink, C B Knobbe-Thomsen, S Kraus, S Schwinn, A Beilhack, G Reifenberger, C M Monoranu, A-L Sirén and 2 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

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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

12 authors at 3 institutions in 1 country.

M SchulzeInstitute for Pharmacology and Toxicology, University of Würzburg, Würzburg, Germany.
O FedorchenkoInstitute for Biochemistry and Molecular Biology II, Heinrich Heine University Düsseldorf, Düsseldorf, Germany.
T G ZinkInstitute for Pharmacology and Toxicology, University of Würzburg, Würzburg, Germany.
C B Knobbe-ThomsenDepartment of Neuropathology, Heinrich Heine University, Düsseldorf, and German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
S KrausDepartment of Internal Medicine II and Center for Interdisciplinary Clinical Research, University of Würzburg, Würzburg, Germany.
S SchwinnDepartment of Internal Medicine II and Center for Interdisciplinary Clinical Research, University of Würzburg, Würzburg, Germany.
A BeilhackDepartment of Internal Medicine II and Center for Interdisciplinary Clinical Research, University of Würzburg, Würzburg, Germany.
G ReifenbergerDepartment of Neuropathology, Heinrich Heine University, Düsseldorf, and German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), Heidelberg, Germany.
C M MonoranuDepartment of Neuropathology, Institute of Pathology, University of Würzburg, Würzburg, Germany.
A-L SirénDepartment of Neurosurgery, University of Würzburg, Würzburg, Germany.
E JeanclosInstitute for Pharmacology and Toxicology, University of Würzburg, Würzburg, Germany.
A GohlaInstitute for Pharmacology and Toxicology, University of Würzburg, Würzburg, Germany.
University of Würzburg · DEHeinrich Heine University Düsseldorf · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glioblastoma is the most aggressive primary brain tumor in adults. Although the rapid recurrence of glioblastomas after treatment is a major clinical challenge, the relationships between tumor growth and intracerebral spread remain poorly understood. We have identified the cofilin phosphatase chronophin (gene name: pyridoxal phosphatase, PDXP) as a glial tumor modifier. Monoallelic PDXP loss was frequent in four independent human astrocytic tumor cohorts and increased with tumor grade. We found that aberrant PDXP promoter methylation can be a mechanism leading to further chronophin downregulation in glioblastomas, which correlated with shorter glioblastoma patient survival. Moreover, we observed an inverse association between chronophin protein expression and cofilin phosphorylation levels in glioma tissue samples. Chronophin-deficient glioblastoma cells showed elevated cofilin phosphorylation, an increase in polymerized actin, a higher directionality of cell migration, and elevated in vitro invasiveness. Tumor growth of chronophin-depleted glioblastoma cells xenografted into the immunodeficient mouse brain was strongly impaired. Our study suggests a mechanism whereby the genetic and epigenetic alterations of PDXP resulting in altered chronophin expression may regulate the interplay between glioma cell proliferation and invasion.

Indexed as

AnimalsBrain NeoplasmsCell Line, TumorCell ProliferationDNA MethylationFemaleGlioblastomaHeterograftsHumansMiceMice, Inbred NODNeoplasm InvasivenessPhosphoprotein PhosphatasesPromoter Regions, GeneticPDXP protein, humanPhosphoprotein Phosphatases

Identifiers

PMID26549022
OpenAlexW2415322518

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.