Evidence map›Paper›PMID 33604565›Full record

ReviewCytokine: X2021

Using CRISPR to enhance T cell effector function for therapeutic applications.

Julian J Freen-van Heeren

Open access · hybridAbstract readReview
In one paragraph

Review in Cytokine: X, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Employing CRISPR-Cas9 to Enhance T Cell Effector Function.Methods in molecular biology (Clifton, N.J.) · 2024
    Article
  6. Review
  7. Review
  8. Molecular and therapeutic effect of CRISPR in treating cancer.Medical oncology (Northwood, London, England) · 2023
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. 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

1 author.

Julian J Freen-van HeerenIndependent Scientist, the Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

T cells are critical to fight pathogenic microbes and combat malignantly transformed cells in the fight against cancer. To exert their effector function, T cells produce effector molecules, such as the pro-inflammatory cytokines IFN-γ, TNF-α and IL-2. Tumors possess many inhibitory mechanisms that dampen T cell effector function, limiting the secretion of cytotoxic molecules. As a result, the control and elimination of tumors is impaired. Through recent advances in genomic editing, T cells can now be successfully modified via CRISPR/Cas9 technology. For instance, engaging (post-)transcriptional mechanisms to enhance T cell cytokine production, the retargeting of T cell antigen specificity or rendering T cells refractive to inhibitory receptor signaling can augment T cell effector function. Therefore, CRISPR/Cas9-mediated genome editing might provide novel strategies for cancer immunotherapy. Recently, the first-in-patient clinical trial was successfully performed with CRISPR/Cas9-modified human T cell therapy. In this review, a brief overview of currently available techniques is provided, and recent advances in T cell genomic engineering for the enhancement of T cell effector function for therapeutic purposes are discussed.

Indexed as

AP-1, activator protein 1ARE, AU-rich elementARE-Del, deletion of the 3′UTR AREs from the Ifng/IFNG geneCAR, Chimeric Antigen ReceptorCAR T cellsCas9Cas, CRISPR-associatedCRISPRCRISPR, Clustered Regularly Interspaced Short Palindromic RepeatCRS, cytokine release syndromeCTLA-4, cytotoxic T-lymphocyte-associated protein 4CytokinesDGK, Diacylglycerol kinaseDHX37, DEAH-box helicase 37EBV, Epstein Barr virusFOXP3, Forkhead box P3GATA, GATA binding proteinGenome editingIFN, interferonIL, interleukinLAG-3, Lymphocyte Activating 3NF-κB, nuclear factor of activated B cellsPD-1, Programmed cell Death 1Pdia3, Protein Disulfide Isomerase Family A Member 3PD-L1, Programmed Death Ligand 1PTPN2, Protein Tyrosine Phosphatase Non-Receptor 2RBP, RNA-binding proteinRNP, ribonuclear proteinT cell effector functionT cellsTCR, T cell receptorTGF, transforming growth factorTIL, Tumor Infiltrating LymphocyteTLRs, Toll-like receptorsTNF, tumor necrosis factorTRAC, TCR-α chainTRBC, TCR-β chaintTCR, transgenic TCRUTR, untranslated region

Identifiers

PMID33604565
PMCPMC7885876
OpenAlexW3117127679

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.