Evidence map›Paper›PMID 31331834›Full record

ArticleEBioMedicine2019

Quantitative proteomics reveals reduction of endocytic machinery components in gliomas.

Dominik P Buser, Marie-Françoise Ritz, Suzette Moes, Cristobal Tostado, Stephan Frank, Martin Spiess, Luigi Mariani, Paul Jenö, Jean-Louis Boulay, Gregor Hutter

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

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  10. Analysis of human brain tissue derived from DBS surgery.Translational neurodegeneration · 2022
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  12. Landscape of surfaceome and endocytome in human glioma is divergent and depends on cellular spatial organization.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

10 authors at 2 institutions in 1 country.

Dominik P BuserBiozentrum, University of Basel, CH-4056 Basel, Switzerland. Electronic address: dominik-pascal.buser@unibas.ch.
Marie-Françoise RitzBrain Tumor Biology and Immunotherapy group, Department of Biomedicine, University Hospital Basel, University of Basel, CH-4031 Basel, Switzerland.
Suzette MoesProteomics Core Facility, Biozentrum, University of Basel, CH-4056 Basel, Switzerland.
Cristobal TostadoBrain Tumor Biology and Immunotherapy group, Department of Biomedicine, University Hospital Basel, University of Basel, CH-4031 Basel, Switzerland.
Stephan FrankInstitute of Pathology, University Hospital Basel, CH-4031 Basel, Switzerland.
Martin SpiessBiozentrum, University of Basel, CH-4056 Basel, Switzerland.
Luigi MarianiBrain Tumor Biology and Immunotherapy group, Department of Biomedicine, University Hospital Basel, University of Basel, CH-4031 Basel, Switzerland; Department of Neurosurgery, University Hospital Basel, CH-4031 Basel, Switzerland.
Paul JenöProteomics Core Facility, Biozentrum, University of Basel, CH-4056 Basel, Switzerland. Electronic address: paul.jenoe@unibas.ch.
Jean-Louis BoulayBrain Tumor Biology and Immunotherapy group, Department of Biomedicine, University Hospital Basel, University of Basel, CH-4031 Basel, Switzerland. Electronic address: jean-louis.boulay@unibas.ch.
Gregor HutterBrain Tumor Biology and Immunotherapy group, Department of Biomedicine, University Hospital Basel, University of Basel, CH-4031 Basel, Switzerland; Department of Neurosurgery, University Hospital Basel, CH-4031 Basel, Switzerland. Electronic address: gregor.hutter@usb.ch.
University of Basel · CHUniversity Hospital of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGliomas are the most frequent and aggressive malignancies of the central nervous system. Decades of molecular analyses have demonstrated that gliomas accumulate genetic alterations that culminate in enhanced activity of receptor tyrosine kinases and downstream mediators. While the genetic alterations, like gene amplification or loss, have been well characterized, little information exists about changes in the proteome of gliomas of different grades.

methodsWe performed unbiased quantitative proteomics of human glioma biopsies by mass spectrometry followed by bioinformatic analysis.

findingsVarious pathways were found to be up- or downregulated. In particular, endocytosis as pathway was affected by a vast and concomitant reduction of multiple machinery components involved in initiation, formation, and scission of endocytic carriers. Both clathrin-dependent and -independent endocytosis were changed, since not only clathrin, AP-2 adaptins, and endophilins were downregulated, but also dynamin that is shared by both pathways. The reduction of endocytic machinery components caused increased receptor cell surface levels, a prominent phenotype of defective endocytosis. Analysis of additional biopsies revealed that depletion of endocytic machinery components was a common trait of various glioma grades and subclasses.

interpretationWe propose that impaired endocytosis creates a selective advantage in glioma tumor progression due to prolonged receptor tyrosine kinase signaling from the cell surface. FUND: This work was supported by Grants 316030-164105 (to P. Jenö), 31003A-162643 (to M. Spiess) and PP00P3-176974 (to G. Hutter) from the Swiss National Science Foundation. Further funding was received by the Department of Surgery from the University Hospital Basel.

Indexed as

EndocytosisProteomeProteomicsBiopsyComputational BiologyGliomaHumansMass SpectrometryNeoplasm GradingNeoplasm StagingNeoplastic Cells, CirculatingProteomeAP-2ClathrinDynaminEndocytosisGliomaRTK

Identifiers

PMID31331834
PMCPMC6711119
OpenAlexW2945002941

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.