Evidence map›Paper›PMID 23625198›Full record

ReviewJournal of leukocyte biology2013

At the bench: preclinical rationale for CTLA-4 and PD-1 blockade as cancer immunotherapy.

Andrew M Intlekofer, Craig B Thompson

2 registry-linked trialsOpen access · bronzeAbstract readReview
In one paragraph

Review in Journal of leukocyte biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 192 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 2 pooled it
13.5field-weighted citation impact, top 1% 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.

NCT03844763 phase1 / phase2unknown statusnot on this mapstarted 2019, after this paper: background citation

The CONFRONT Phase I - II Trial: ACtivatiON oF Immune RespONse in paTients With R-M Head and Neck Cancer. Multimodality Immunotherapy With Avelumab, Short Course Radiotherapy and Cyclophosphamide in Head and Neck Cancer.

TypeinterventionalSponsorGruppo Oncologico del Nord-OvestRan2019 to 2024Enrolled71ConditionsHead and Neck CancerArmsAvelumab, CTX, RT
NCT04276025 completednot on this mapstarted 2016, after this paper: background citation

Relationship Between Histopathological Features, Mutation Status, 18F-FDG PET/CT Radiomic Imaging Parameters as Well as Clinical Outcome in Patients With Treatment-naïve Non-small Cell Lung Cancer

TypeobservationalSponsorKlinikum Bayreuth GmbHRan2016 to 2020Enrolled2,000ConditionsNSCLCArmsClinical routine F18-FDG-PET/CT, molecular pathology and clinical outcome
3 · Its place in the literature

Who cites it

192 citing papers in PubMed, 2 syntheses or guidelines pooled it, 376 citations in OpenAlex.

  1. Clinical Application of Oncolytic Viruses: A Systematic Review.International journal of molecular sciences · 2020
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  20. Janus kinase inhibitor overcomes resistance to immune checkpoint inhibitor treatment in peritoneal dissemination of gastric cancer in C57BL/6 J mice.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2024
    Article

132 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

2 authors at 1 institution in 1 country.

Andrew M IntlekoferDepartment of Medicine, Cancer Biology and Genetics Program, and Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, New York, USA.
Craig B Thompson
Memorial Sloan Kettering Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumors can avoid immune surveillance by stimulating immune inhibitory receptors that function to turn off established immune responses. By blocking the ability of tumors to stimulate inhibitory receptors on T cells, sustained, anti-tumor immune responses can be generated in animals. Thus, therapeutic blockade of immune inhibitory checkpoints provides a potential method to boost anti-tumor immunity. The CTLA-4 and PD-1Rs represent two T cell-inhibitory receptors with independent mechanisms of action. Preclinical investigations revealed that CTLA-4 enforces an activation threshold and attenuates proliferation of tumor-specific T lymphocytes. In contrast, PD-1 functions primarily as a stop signal that limits T cell effector function within a tumor. The unique mechanisms and sites of action of CTLA-4 and PD-1 suggest that although blockade of either has the potential to promote anti-tumor immune responses, combined blockade of both might offer even more potent anti-tumor activity. See related review At the Bedside: CTLA-4 and PD-1 blocking antibodies in cancer immunotherapy.

Indexed as

ImmunotherapyAnimalsAntibodies, BlockingCTLA-4 AntigenDrug Evaluation, PreclinicalHumansNeoplasmsProgrammed Cell Death 1 ReceptorAntibodies, BlockingCTLA-4 AntigenPDCD1 protein, humanProgrammed Cell Death 1 ReceptorcoinhibitorycostimulationcostimulatoryinhibitoryipilimumabPD-L1receptortumor

Identifiers

PMID23625198
PMCPMC3685017
OpenAlexW2140521865

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.