Evidence map›Paper›PMID 27034234›Full record

ReviewCancer immunology, immunotherapy : CII2016

4-1BB agonism: adding the accelerator to cancer immunotherapy.

Cariad Chester, Siddhant Ambulkar, Holbrook E Kohrt

Open access · hybridAbstract readReview
In one paragraph

Review in Cancer immunology, immunotherapy : CII, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

72 citing papers in PubMed, 131 citations in OpenAlex.

  1. Immunodeficiency and EBV-induced lymphoproliferation caused by 4-1BB deficiency.The Journal of allergy and clinical immunology · 2019
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12 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Cariad ChesterDepartment of Medicine, Division of Oncology, Stanford University Medical Center, Stanford University, 269 Campus Drive, CCSR 1140, Stanford, CA, 94305-5151, USA. cchester@stanford.edu.
Siddhant AmbulkarDepartment of Medicine, Division of Oncology, Stanford University Medical Center, Stanford University, 269 Campus Drive, CCSR 1140, Stanford, CA, 94305-5151, USA.
Holbrook E KohrtDepartment of Medicine, Division of Oncology, Stanford University Medical Center, Stanford University, 269 Campus Drive, CCSR 1140, Stanford, CA, 94305-5151, USA.
Stanford University · USStanford Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The success of checkpoint inhibitors has validated immunomodulatory agents as a valuable class of anticancer therapeutics. A promising co-stimulatory immunologic target is 4-1BB, or CD137, a member of the tumor necrosis factor receptor superfamily. Ligation of 4-1BB induces an activating signal in CD8(+) T cells and natural killer cells, resulting in increased pro-inflammatory cytokine secretion, cytolytic function, and antibody-dependent cell-mediated cytotoxicity. Targeting 4-1BB with agonistic monoclonal antibody (mAb) therapy demonstrated potent antitumor effects in murine tumor models. While anti-4-1BB mAbs have entered clinical trials, optimal efficacy of 4-1BB-targeted agents will inevitably come from combination therapeutic strategies. Checkpoint blockade is a compelling combination partner for 4-1BB agonism. This novel immunotherapeutic approach has the potential to active antitumor immune effectors by a complementary mechanism: simultaneously "removing the brakes" via blocking inhibitory signaling and "stepping on the accelerator" via co-stimulation. While important considerations should be given to 4-1BB-mediated toxicities, the current understanding of 4-1BB biology suggests it may play a key role in advancing the capabilities of cancer combination therapy.

Indexed as

AnimalsAntibodies, MonoclonalAntibody-Dependent Cell CytotoxicityAntineoplastic Combined Chemotherapy ProtocolsClinical Trials as TopicCytotoxicity, ImmunologicHumansImmunotherapyKiller Cells, NaturalNeoplasmsT-Lymphocytes, CytotoxicTumor Necrosis Factor Receptor Superfamily, Member 9Antibodies, MonoclonalTNFRSF9 protein, humanTumor Necrosis Factor Receptor Superfamily, Member 94-1BBAntibody-dependent cell-mediated cytotoxicityCheckpoint inhibitorsCIMT 2015Combination therapyImmunotherapy

Identifiers

PMID27034234
PMCPMC5035667
OpenAlexW2321746654

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.