Evidence map›Paper›PMID 26956048›Full record

ArticleOncotarget2016

Diagnostic and clinical relevance of the autophago-lysosomal network in human gliomas.

Lukas Jennewein, Michael W Ronellenfitsch, Patrick Antonietti, Elena I Ilina, Jennifer Jung, Daniela Stadel, Lisa-Marie Flohr, Jenny Zinke, Janusz von Renesse, Ulrich Drott and 14 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

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  12. Autophagy as a Potential Therapy for Malignant Glioma.Pharmaceuticals (Basel, Switzerland) · 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

24 authors at 4 institutions in 2 countries.

Lukas JenneweinNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Michael W RonellenfitschSenckenberg Institute of Neurooncology, Goethe University, Frankfurt am Main, Germany.
Patrick AntoniettiExperimental Neurosurgery, Department of Neurosurgery, Goethe University, Frankfurt am Main, Germany.
Elena I IlinaNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Jennifer JungInstitute of Biochemistry II, Goethe University, Frankfurt am Main, Germany.
Daniela StadelInstitute of Biochemistry II, Goethe University, Frankfurt am Main, Germany.
Lisa-Marie FlohrNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Jenny ZinkeNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Janusz von RenesseNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Ulrich DrottNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Peter BaumgartenNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Anne K BraczynskiNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Cornelia PenskiNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Michael C BurgerSenckenberg Institute of Neurooncology, Goethe University, Frankfurt am Main, Germany.
Jean-Philippe TheurillatInstitute of Cell Biology, ETH Zürich, Switzerland.
Joachim P SteinbachSenckenberg Institute of Neurooncology, Goethe University, Frankfurt am Main, Germany.
Karl-Heinz PlateNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Ivan DikicGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Simone FuldaGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Christian BrandtsGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Donat KögelGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Christian BehrendsGerman Cancer Consortium (DKTK) and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Patrick N HarterNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Michel MittelbronnNeurological Institute (Edinger Institute), Goethe University, Frankfurt am Main, Germany.
Goethe University Frankfurt · DEGerman Cancer Research Center · DEHeidelberg University · DEETH Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recently, the conserved intracellular digestion mechanism 'autophagy' has been considered to be involved in early tumorigenesis and its blockade proposed as an alternative treatment approach. However, there is an ongoing debate about whether blocking autophagy has positive or negative effects in tumor cells. Since there is only poor data about the clinico-pathological relevance of autophagy in gliomas in vivo, we first established a cell culture based platform for the in vivo detection of the autophago-lysosomal components. We then investigated key autophagosomal (LC3B, p62, BAG3, Beclin1) and lysosomal (CTSB, LAMP2) molecules in 350 gliomas using immunohistochemistry, immunofluorescence, immunoblotting and qPCR. Autophagy was induced pharmacologically or by altering oxygen and nutrient levels. Our results show that autophagy is enhanced in astrocytomas as compared to normal CNS tissue, but largely independent from the WHO grade and patient survival. A strong upregulation of LC3B, p62, LAMP2 and CTSB was detected in perinecrotic areas in glioblastomas suggesting micro-environmental changes as a driver of autophagy induction in gliomas. Furthermore, glucose restriction induced autophagy in a concentration-dependent manner while hypoxia or amino acid starvation had considerably lesser effects. Apoptosis and autophagy were separately induced in glioma cells both in vitro and in vivo. In conclusion, our findings indicate that autophagy in gliomas is rather driven by micro-environmental changes than by primary glioma-intrinsic features thus challenging the concept of exploitation of the autophago-lysosomal network (ALN) as a treatment approach in gliomas.

Indexed as

AutophagyAdaptor Proteins, Signal TransducingAdolescentAdultAgedAged, 80 and overApoptosis Regulatory ProteinsBeclin-1Biomarkers, TumorBrain NeoplasmsCathepsin BChildChild, PreschoolFemaleFollow-Up StudiesGliomaAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsBAG3 protein, humanBeclin-1Biomarkers, TumorCathepsin BCTSB protein, humanLAMP2 protein, humanLysosomal-Associated Membrane Protein 2MAP1LC3B protein, humanMicrotubule-Associated ProteinsP62 protein, humanRNA-Binding ProteinsapoptosisastrocytomaautophagyglioblastomaLC3B

Identifiers

PMID26956048
PMCPMC4991435
OpenAlexW2294269630

What OpenQuestion holds

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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.