Evidence map›Paper›PMID 26741508›Full record

ArticleOncotarget2016

Tumor sialylation impedes T cell mediated anti-tumor responses while promoting tumor associated-regulatory T cells.

Maurizio Perdicchio, Lenneke A M Cornelissen, Ingeborg Streng-Ouwehand, Steef Engels, Marleen I Verstege, Louis Boon, Dirk Geerts, Yvette van Kooyk, Wendy W J Unger

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 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

69 citing papers in PubMed, 107 citations in OpenAlex.

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  17. Article
  18. Glycosylation Targeting: A Paradigm Shift in Cancer Immunotherapy.International journal of biological sciences · 2024
    Review
  19. Article
  20. The new progress in cancer immunotherapy.Clinical and experimental medicine · 2023
    Review

9 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 2 countries.

Maurizio PerdicchioDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
Lenneke A M CornelissenDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
Ingeborg Streng-OuwehandDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
Steef EngelsDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
Marleen I VerstegeDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
Louis BoonEPIRUS Biopharmaceuticals, Leiden, The Netherlands.
Dirk GeertsDepartment of Pediatric Oncology/Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands.
Yvette van KooykDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
Wendy W J UngerDepartment of Molecular Cell Biology and Immunology, VU University Medical Center, Amsterdam, The Netherlands.
Amsterdam UMC Location VUmc · NLErasmus MC · NLFred Hutch Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increased presence of sialylated glycans on the tumor surface has been linked to poor prognosis, yet the effects on tumor-specific T cell immunity are hardly studied. We here show that hypersialylation of B16 melanoma substantially influences tumor growth by preventing the formation of effector T cells and facilitating the presence of high regulatory T cell (Treg) frequencies. Knock-down of the sialic acid transporter created "sialic acid low" tumors, that grew slower in-vivo than hypersialylated tumors, altered the Treg/Teffector balance, favoring immunological tumor control. The enhanced effector T cell response in developing "sialic acid low" tumors was preceded by and dependent on an increased influx and activity of Natural Killer (NK) cells. Thus, tumor hypersialylation orchestrates immune escape at the level of NK and Teff/Treg balance within the tumor microenvironment, herewith dampening tumor-specific T cell control. Reducing sialylation provides a therapeutic option to render tumors permissive to immune attack.

Indexed as

AnimalsApoptosisBlotting, WesternCell AdhesionCell CycleCell MovementCell ProliferationFlow CytometryImmunoenzyme TechniquesKiller Cells, NaturalMelanoma, ExperimentalMiceMice, Inbred C57BLN-Acetylneuraminic AcidPolysaccharidesReal-Time Polymerase Chain ReactionN-Acetylneuraminic AcidPolysaccharidesRNA, Messengerimmune regulationnatural killer cellsregulatory T cellssialic acidtumor

Identifiers

PMID26741508
PMCPMC4891003
OpenAlexW2274336449

What OpenQuestion holds

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LicenceCC BY
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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.