Evidence map›Paper›PMID 33063451›Full record

ArticleEMBO reports2020

MLLT6 maintains PD-L1 expression and mediates tumor immune resistance.

Sandeep Sreevalsan, Marietta Döring, Maciej Paszkowski-Rogacz, Melanie Brux, Carolina Blanck, Marten Meyer, Frank Momburg, Frank Buchholz, Mirko Theis

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 24% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

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  8. Nucleolar protein TAAP1/Life science alliance · 2024
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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

9 authors at 2 institutions in 1 country.

Sandeep SreevalsanNational Center for Tumor Diseases (NCT/UCC) Dresden, German Cancer Research Center (DKFZ), University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz-Zentrum Dresden-Rossendorf (HZDR), Dresden, Germany.
Marietta DöringNational Center for Tumor Diseases (NCT/UCC) Dresden, German Cancer Research Center (DKFZ), University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz-Zentrum Dresden-Rossendorf (HZDR), Dresden, Germany.
Maciej Paszkowski-RogaczMedical Systems Biology, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.ORCID 0000-0002-8245-6006
Melanie BruxNational Center for Tumor Diseases (NCT/UCC) Dresden, German Cancer Research Center (DKFZ), University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz-Zentrum Dresden-Rossendorf (HZDR), Dresden, Germany.
Carolina BlanckMedical Systems Biology, Medical Faculty Carl Gustav Carus, Technische Universität Dresden, Dresden, Germany.
Marten MeyerAntigen Presentation & T/NK Cell Activation Group, Clinical Cooperation Unit 'Applied Tumor Immunity', German Cancer Research Center (DKFZ), Heidelberg, Germany.
Frank MomburgAntigen Presentation & T/NK Cell Activation Group, Clinical Cooperation Unit 'Applied Tumor Immunity', German Cancer Research Center (DKFZ), Heidelberg, Germany.
Frank BuchholzNational Center for Tumor Diseases (NCT/UCC) Dresden, German Cancer Research Center (DKFZ), University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz-Zentrum Dresden-Rossendorf (HZDR), Dresden, Germany.ORCID 0000-0002-4577-3344
Mirko TheisNational Center for Tumor Diseases (NCT/UCC) Dresden, German Cancer Research Center (DKFZ), University Hospital Carl Gustav Carus, Technische Universität Dresden, Helmholtz-Zentrum Dresden-Rossendorf (HZDR), Dresden, Germany.ORCID 0000-0003-3840-6156
German Cancer Research Center · DEUniversity Hospital Carl Gustav Carus · DE

Funding

German Cancer Research Center (DKFZ)National Center for Tumor DiseasesTechnische Universität Dresden (TUD)
6 · The paper itself

Abstract

Tumor cells subvert immune surveillance by harnessing signals from immune checkpoints to acquire immune resistance. The protein PD-L1 is an important component in this process, and inhibition of PD-L1 elicits durable anti-tumor responses in a broad spectrum of cancers. However, immune checkpoint inhibition that target known pathways is not universally effective. A better understanding of the genetic repertoire underlying these processes is necessary to expand our knowledge in tumor immunity and to facilitate identification of alternative targets. Here, we present a CRISPR/Cas9 screen in human cancer cells to identify genes that confer tumors with the ability to evade the cytotoxic effects of the immune system. We show that the transcriptional regulator MLLT6 (AF17) is required for efficient PD-L1 protein expression and cell surface presentation in cancer cells. MLLT6 depletion alleviates suppression of CD8

Indexed as

B7-H1 AntigenNeoplasmsDNA-Binding ProteinsHumansInterferon-gammaNeoplasm ProteinsSignal TransductionB7-H1 AntigenCD274 protein, humanDNA-Binding ProteinsInterferon-gammaMLLT6 protein, humanNeoplasm ProteinscancerCRISPR screenimmune resistanceMLLT6PD-L1

Identifiers

PMID33063451
PMCPMC7726806
OpenAlexW3093027885

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.