Evidence map›Paper›PMID 34112738›Full record

ArticleJournal for immunotherapy of cancer2021

Δ133p53α enhances metabolic and cellular fitness of TCR-engineered T cells and promotes superior antitumor immunity.

Kevin Jan Legscha, Edite Antunes Ferreira, Antonios Chamoun, Alexander Lang, Mohamed Hemaid Sayed Awwad, Gigi Nu Hoang Quy Ton, Danuta Galetzka, Borhane Guezguez, Michael Hundemer, Jean-Christophe Bourdon and 3 more

Abstract read
In one paragraph

Article in Journal for immunotherapy of cancer, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
–field-weighted citation impact
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

10 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Enhancing chimeric antigen receptor T cell therapy by modulating the p53 signaling network with Δ133p53α.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Review
  6. MDSCs-derived GPR84 induces CD8Journal for immunotherapy of cancer · 2023
    Article
  7. Adenosine A2A receptor activation reduces chondrocyte senescence.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  8. Tcf-1 protects anti-tumor TCR-engineered CD8Cancer immunology, immunotherapy : CII · 2022
    Article
  9. Article
  10. Review
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

13 authors.

Kevin Jan LegschaDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Edite Antunes FerreiraDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Antonios ChamounDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Alexander LangDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Mohamed Hemaid Sayed AwwadDepartment of Internal Medicine V, University of Heidelberg, Heidelberg, Germany.
Gigi Nu Hoang Quy TonDepartment of Internal Medicine V, University of Heidelberg, Heidelberg, Germany.
Danuta GaletzkaDepartment of Radiation Oncology and Radiotherapy, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Borhane GuezguezDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Michael HundemerDepartment of Internal Medicine V, University of Heidelberg, Heidelberg, Germany.
Jean-Christophe BourdonSchool of Medicine, University of Dundee, Dundee, UK.
Markus MunderDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Matthias TheobaldDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany.
Hakim EchchannaouiDepartment of Hematology, Oncology and Pneumology, University Medical Centre of the Johannes Gutenberg University Mainz, Mainz, Germany echchann@uni-mainz.de.ORCID 0000-0001-9980-9974

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundTumor microenvironment-associated T cell senescence is a key limiting factor for durable effective cancer immunotherapy. A few studies have demonstrated the critical role of the tumor suppressor TP53-derived p53 isoforms in cellular senescence process of non-immune cells. However, their role in lymphocytes, in particular tumor-antigen (TA) specific T cells remain largely unexplored.

methodsHuman T cells from peripheral blood were retrovirally engineered to coexpress a TA-specific T cell receptor and the Δ133p53α-isoform, and characterized for their cellular phenotype, metabolic profile and effector functions.

resultsPhenotypic analysis of Δ133p53α-modified T cells revealed a marked reduction of the T-cell inhibitory molecules (ie, CD160 and TIGIT), a lower frequency of senescent-like CD57

conclusionThis study uncovered a broad effect of Δ133p53α isoform in regulating T lymphocyte function. Enhancing fitness and effector functions of senescent T cells by modulation of p53 isoforms could be exploited for future translational research to improve cancer immunotherapy and immunosenescence-related diseases.

Indexed as

AnimalsCell Line, TumorHumansImmunotherapyMaleMiceNeoplasmsReceptors, Antigen, T-CellT-LymphocytesTumor MicroenvironmentReceptors, Antigen, T-Celladoptiveantigencell engineeringcostimulatory and inhibitory T-cell receptorsimmunotherapyreceptorsT-lymphocytes

Identifiers

PMID34112738
PMCPMC8194333

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Registered trials

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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.