Evidence map›Paper›PMID 28878363›Full record

ArticleScientific reports2017

A TCR-based Chimeric Antigen Receptor.

Even Walseng, Hakan Köksal, Ibrahim M Sektioglu, Anne Fåne, Gjertrud Skorstad, Gunnar Kvalheim, Gustav Gaudernack, Else Marit Inderberg, Sébastien Wälchli

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
5.4field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 89 citations in OpenAlex.

  1. Advances inMolecular therapy. Nucleic acids · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Significant Advancements and Evolutions in Chimeric Antigen Receptor Design.International journal of molecular sciences · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. 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

9 authors at 2 institutions in 2 countries.

Even WalsengExperimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Hakan KöksalDepartment for Cellular Therapy, Department for Cancer Therapy, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Ibrahim M SektiogluDepartment for Cellular Therapy, Department for Cancer Therapy, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Anne FåneDepartment for Cellular Therapy, Department for Cancer Therapy, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Gjertrud SkorstadDepartment for Cellular Therapy, Department for Cancer Therapy, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Gunnar KvalheimDepartment for Cellular Therapy, Department for Cancer Therapy, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Gustav GaudernackDepartment for Cancer Immunology, Institute for Cancer Research, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Else Marit InderbergDepartment for Cellular Therapy, Department for Cancer Therapy, Oslo University Hospital Radiumhospitalet, Oslo, Norway.
Sébastien WälchliDepartment for Cellular Therapy, Department for Cancer Therapy, Oslo University Hospital Radiumhospitalet, Oslo, Norway. sebastw@rr-research.no.ORCID 0000-0001-5869-1746
Oslo University Hospital · NONational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Effector T cells equipped with engineered antigen receptors specific for cancer targets have proven to be very efficient. Two methods have emerged: the Chimeric Antigen Receptors (CARs) and T-cell Receptor (TCR) redirection. Although very potent, CAR recognition is limited to membrane antigens which represent around 1% of the total proteins expressed, whereas TCRs have the advantage of targeting any peptide resulting from cellular protein degradation. However, TCRs depend on heavy signalling machinery only present in T cells which restricts the type of eligible therapeutic cells. Hence, an introduced therapeutic TCR will compete with the endogenous TCR for the signalling proteins and carries the potential risk of mixed dimer formation giving rise to a new TCR with unpredictable specificity. We have fused a soluble TCR construct to a CAR-signalling tail and named the final product TCR-CAR. We here show that, if expressed, the TCR-CAR conserved the specificity and the functionality of the original TCR. In addition, we demonstrate that TCR-CAR redirection was not restricted to T cells. Indeed, after transduction, the NK cell line NK-92 became TCR positive and reacted against pMHC target. This opens therapeutic avenues combing the killing efficiency of NK cells with the diversified target recognition of TCRs.

Indexed as

Cell Line, TumorCytokinesCytotoxicity, ImmunologicFlow CytometryGene ExpressionGene OrderGenetic VectorsHistocompatibility Antigens Class IHumansImmunotherapy, AdoptiveKiller Cells, NaturalProtein Interaction Domains and MotifsReceptors, Antigen, T-CellReceptors, Chimeric AntigenRecombinant Fusion ProteinsT-LymphocytesCytokinesHistocompatibility Antigens Class IReceptors, Antigen, T-CellReceptors, Chimeric AntigenRecombinant Fusion Proteins

Identifiers

PMID28878363
PMCPMC5587706
OpenAlexW2753012794

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.