Evidence map›Paper›PMID 32929051›Full record

ReviewJournal for immunotherapy of cancer2020

LAG-3: from molecular functions to clinical applications.

Takumi Maruhashi, Daisuke Sugiura, Il-Mi Okazaki, Taku Okazaki

Open access · goldAbstract readReview
In one paragraph

Review in Journal for immunotherapy of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 278 papers.

0numbers the graph read from it
0cells of the map it votes in
278citing papers in PubMed
21.3field-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.

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

278 citing papers in PubMed, 452 citations in OpenAlex.

  1. LRP1b Loss Predicts Sensitivity to Immunotherapy in Patients with NSCLC: An Analysis of the Phase III CheckMate-026 Randomized Trial.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025
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  12. Current and future immunotherapies for NSCLC.Journal of hematology & oncology · 2026
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218 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

4 authors at 1 institution in 2 countries.

Takumi MaruhashiLaboratory of Molecular Immunology, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0003-2944-1611
Daisuke SugiuraLaboratory of Molecular Immunology, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0002-3865-3889
Il-Mi OkazakiLaboratory of Molecular Immunology, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan.ORCID 0000-0001-8644-0100
Taku OkazakiLaboratory of Molecular Immunology, Institute for Quantitative Biosciences, The University of Tokyo, Tokyo, Japan tokazaki@iqb.u-tokyo.ac.jp.ORCID 0000-0003-4790-1925
Quantitative BioSciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To prevent the destruction of tissues owing to excessive and/or inappropriate immune responses, immune cells are under strict check by various regulatory mechanisms at multiple points. Inhibitory coreceptors, including programmed cell death 1 (PD-1) and cytotoxic T lymphocyte antigen 4 (CTLA-4), serve as critical checkpoints in restricting immune responses against self-tissues and tumor cells. Immune checkpoint inhibitors that block PD-1 and CTLA-4 pathways significantly improved the outcomes of patients with diverse cancer types and have revolutionized cancer treatment. However, response rates to such therapies are rather limited, and immune-related adverse events are also observed in a substantial patient population, leading to the urgent need for novel therapeutics with higher efficacy and lower toxicity. In addition to PD-1 and CTLA-4, a variety of stimulatory and inhibitory coreceptors are involved in the regulation of T cell activation. Such coreceptors are listed as potential drug targets, and the competition to develop novel immunotherapies targeting these coreceptors has been very fierce. Among such coreceptors, lymphocyte activation gene-3 (LAG-3) is expected as the foremost target next to PD-1 in the development of cancer therapy, and multiple clinical trials testing the efficacy of LAG-3-targeted therapy are underway. LAG-3 is a type I transmembrane protein with structural similarities to CD4. Accumulating evidence indicates that LAG-3 is an inhibitory coreceptor and plays pivotal roles in autoimmunity, tumor immunity, and anti-infection immunity. In this review, we summarize the current understanding of LAG-3, ranging from its discovery to clinical application.

Indexed as

Adaptive ImmunityAmino AcidsCaenorhabditis elegans ProteinsHumansImmunotherapyTranscription FactorsAmino AcidsCaenorhabditis elegans ProteinsSEL-8 protein, C elegansTranscription Factorsadaptive immunityimmune tolerance

Identifiers

PMID32929051
PMCPMC7488795
OpenAlexW3085860981

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.