Evidence map›Paper›PMID 36194675›Full record

ArticleEMBO reports2022

Concomitant deletion of Ptpn6 and Ptpn11 in T cells fails to improve anticancer responses.

Pedro M O Ventura, Milica Gakovic, Berenice A Fischer, Laura Spinelli, Giorgia Rota, Shalini Pathak, Hanif J Khameneh, Alessandro Zenobi, Sarah Thomson, Walter Birchmeier and 2 more

Open access · hybridAbstract read
In one paragraph

Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Article
  3. T lymphocyte-specific deletion of SHP1 and SHP2 promotes activation-induced cell death of CD4Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Effects ofCurrent issues in molecular biology · 2024
    Article
  7. Article
  8. Review
  9. Consideration of SHP-1 as a Molecular Target for Tumor Therapy.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
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 4 institutions in 3 countries.

Pedro M O Ventura *Institute for Research in Biomedicine, Università della Svizzera Italiana, Bellinzona, Switzerland.
Milica Gakovic *Cell Signalling and Immunology Division, School of Life Sciences, University of Dundee, Dundee, UK.
Berenice A FischerInstitute for Research in Biomedicine, Università della Svizzera Italiana, Bellinzona, Switzerland.
Laura SpinelliCell Signalling and Immunology Division, School of Life Sciences, University of Dundee, Dundee, UK.ORCID 0000-0002-5801-6297
Giorgia RotaDepartment of Biochemistry, University of Lausanne, Epalinges, Switzerland.
Shalini PathakCell Signalling and Immunology Division, School of Life Sciences, University of Dundee, Dundee, UK.ORCID 0000-0001-9871-2214
Hanif J KhamenehInstitute for Research in Biomedicine, Università della Svizzera Italiana, Bellinzona, Switzerland.ORCID 0000-0002-1737-0388
Alessandro ZenobiInstitute for Research in Biomedicine, Università della Svizzera Italiana, Bellinzona, Switzerland.ORCID 0000-0003-2837-7638
Sarah ThomsonBiological Services, University of Dundee, Dundee, UK.
Walter BirchmeierMax-Delbrueck-Center for Molecular Medicine (MDC) in the Helmholtz Society, Berlin, Germany.
Doreen A Cantrell *Cell Signalling and Immunology Division, School of Life Sciences, University of Dundee, Dundee, UK.
Greta Guarda *Institute for Research in Biomedicine, Università della Svizzera Italiana, Bellinzona, Switzerland.ORCID 0000-0001-9243-6116
Università della Svizzera italiana · CHUniversity of Dundee · GBMax Delbrück Center · DEUniversity of Lausanne · CH

Funding

Wellcome TrustWellcome Trust 205023/Z/16/Z
6 · The paper itself

Abstract

Anticancer T cells acquire a dysfunctional state characterized by poor effector function and expression of inhibitory receptors, such as PD-1. Blockade of PD-1 leads to T cell reinvigoration and is increasingly applied as an effective anticancer treatment. Recent work challenged the commonly held view that the phosphatase PTPN11 (known as SHP-2) is essential for PD-1 signaling in T cells, suggesting functional redundancy with the homologous phosphatase PTPN6 (SHP-1). Therefore, we investigated the effect of concomitant Ptpn6 and Ptpn11 deletion in T cells on their ability to mount antitumour responses. In vivo data show that neither sustained nor acute Ptpn6/11 deletion improves T cell-mediated tumor control. Sustained loss of Ptpn6/11 also impairs the therapeutic effects of anti-PD1 treatment. In vitro results show that Ptpn6/11-deleted CD8

Indexed as

CD8-Positive T-LymphocytesProgrammed Cell Death 1 ReceptorProtein Tyrosine Phosphatase, Non-Receptor Type 6Signal TransductionProgrammed Cell Death 1 ReceptorProtein Tyrosine Phosphatase, Non-Receptor Type 6PTPN6 protein, humanPD-1 checkpoint blockadePtpn11Ptpn6T cell exhaustion

Identifiers

PMID36194675
PMCPMC9638855
OpenAlexW4301183343

What OpenQuestion holds

Textmetadata
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.