Evidence map›Paper›PMID 25431955›Full record

ArticleOncotarget2014

An NCR1-based chimeric receptor endows T-cells with multiple anti-tumor specificities.

Yair Tal, Shlomo Yaakobi, Miryam Horovitz-Fried, Einav Safyon, Benyamin Rosental, Angel Porgador, Cyrille J Cohen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Adoptive T-cell Immunotherapy: Perfecting Self-Defenses.Experientia supplementum (2012) · 2022
    Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  20. CAR T-cell therapy for pancreatic cancer.Journal of surgical oncology · 2017
    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

7 authors at 2 institutions in 1 country.

Yair TalLaboratory of Tumor Immunology and Immunotherapy, The Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 52900 Israel.
Shlomo YaakobiLaboratory of Tumor Immunology and Immunotherapy, The Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 52900, Israel.
Miryam Horovitz-FriedLaboratory of Tumor Immunology and Immunotherapy, The Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 52900, Israel.
Einav SafyonLaboratory of Tumor Immunology and Immunotherapy, The Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 52900, Israel.
Benyamin RosentalThe Shraga Segal Department of Microbiology, Immunology and Genetics, and the National Institute for Biotechnology in the Negev, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.
Angel PorgadorThe Shraga Segal Department of Microbiology, Immunology and Genetics, and the National Institute for Biotechnology in the Negev, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.
Cyrille J CohenLaboratory of Tumor Immunology and Immunotherapy, The Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 52900, Israel.
Bar-Ilan University · ILBen-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Ral (Ras-like) GTP-binding proteins (RalA and RalB), as effectors of the proto-oncogene Natural killer (NK) cells are an important component of the anti-tumor response. Tumor recognition by NK cells was found to be partly triggered by molecules termed natural cytotoxic receptors (NCRs). Adoptive transfer of genetically-engineered tumor-reactive T-lymphocytes can mediate remarkable tumor regressions mostly in melanoma and leukemia patients. Yet, the application of such treatments to other cancers is needed and dependent on the isolation of receptors that could facilitate efficient recognition of these malignancies. Herein, we aimed at combining NK tumor recognition capability with the genetic modification of T-cells to provide the latter with a means to recognize several tumors in a non-MHC restricted way. Consequently, we generated and evaluated several chimeric receptors based on the extracellular domain of NCR1 (NKp46) fused to multiple signaling moieties and assess their antitumor activity when retrovirally expressed in T-cells. Following co-culture with different tumors, primary human T-lymphocytes expressing a chimeric NCR1 molecule recognized target cells derived from lung, cervical carcinoma, leukemia and pancreatic cancer. In addition, this receptor mediated an upregulation of surface activation markers and significant antitumor cytotoxicity both in vitro and in vivo. These results have meaningful implications for the immunotherapeutic treatment of cancer using gene-modified T-cells.

Indexed as

Cell ProliferationAnimalsApoptosisBlotting, WesternCells, CulturedFemaleFlow CytometryHumansKiller Cells, NaturalMiceMice, NudeNatural Cytotoxicity Triggering Receptor 1NeoplasmsNerve Tissue ProteinsProto-Oncogene MasReceptors, Nerve Growth FactorMAS1 protein, humanNatural Cytotoxicity Triggering Receptor 1NCR1 protein, humanNerve Tissue ProteinsNGFR protein, humanProto-Oncogene MasReceptors, Nerve Growth Factor

Identifiers

PMID25431955
PMCPMC4279421
OpenAlexW2171121813

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.