Evidence map›Paper›PMID 33288379›Full record

ReviewSeminars in immunology2020

Targeting novel inhibitory receptors in cancer immunotherapy.

Quan-Quan Ding, Joe-Marc Chauvin, Hassane M Zarour

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunology, 2020. 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
0.7field-weighted citation impact, top 30% 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, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Tim-3 mediates T cell trogocytosis to limit antitumor immunity.The Journal of clinical investigation · 2022
    Article
  10. Review
  11. 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

3 authors at 1 institution in 1 country.

Quan-Quan DingDepartment of Medicine and Division of Hematology/Oncology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA.
Joe-Marc ChauvinDepartment of Medicine and Division of Hematology/Oncology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA.
Hassane M ZarourDepartment of Medicine and Division of Hematology/Oncology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA; Department of Immunology, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15213, USA. Electronic address: zarourhm@upmc.edu.
University of Pittsburgh · US

Funding

Fecal Microbiota Transplant and PD-1 blockade in MelanomaR01CA222203 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZAROUR, HASSANE M · 2018 to 2022
$2.5M
Targeting TIGIT and PD-1 in MelanomaR01CA228181 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ZAROUR, HASSANE M · 2018 to 2022
$1.8M
NCI NIH HHS R01 CA222203NCI NIH HHS R01 CA228181
6 · The paper itself

Abstract

T cells play a critical role in promoting tumor regression in both experimental models and humans. Yet, T cells that are chronically exposed to tumor antigen during cancer progression can become dysfunctional/exhausted and fail to induce tumor destruction. Such tumor-induced T cell dysfunction may occur via multiple mechanisms. In particular, immune checkpoint inhibitory receptors that are upregulated by tumor-infiltrating lymphocytes in many cancers limit T cell survival and function. Overcoming this inhibitory receptor-mediated T cell dysfunction has been a central focus of recent developments in cancer immunotherapy. Immunotherapies targeting inhibitory receptor pathways such as programmed cell death 1 (PD-1)/programmed death ligand 1 and cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), alone or in combination, confer significant clinical benefits in multiple tumor types. However, many patients with cancer do not respond to immune checkpoint blockade, and dual PD-1/CTLA-4 blockade may cause serious adverse events, which limits its indications. Targeting novel non-redundant inhibitory receptor pathways contributing to tumor-induced T cell dysfunction in the tumor microenvironment may prove efficacious and non-toxic. This review presents preclinical and clinical findings supporting the roles of two key pathways-T-cell immunoglobulin and mucin-domain containing-3 (TIM-3) and T cell immunoreceptor with Ig and ITIM domain (TIGIT)/CD226/CD96/CD112R-in cancer immunotherapy.

Indexed as

AnimalsBiomarkers, TumorCostimulatory and Inhibitory T-Cell ReceptorsHumansImmune Checkpoint ProteinsImmunotherapyLymphocyte ActivationLymphocytes, Tumor-InfiltratingMolecular Targeted TherapyNeoplasmsSignal TransductionT-Lymphocyte SubsetsTumor MicroenvironmentBiomarkers, TumorCostimulatory and Inhibitory T-Cell ReceptorsImmune Checkpoint ProteinsCancer immunotherapyCD112RCD96DNAM-1/CD226Inhibitory receptorsTIGITTIM-3

Identifiers

PMID33288379
PMCPMC8045408
OpenAlexW3110797703

What OpenQuestion holds

Textmetadata
LicenceTDM
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.