Evidence map›Paper›PMID 40402452›Full record

ArticleMethods in molecular biology (Clifton, N.J.)2025

Kinetic Assessment of HMGB1 Exodus by Automated Live Cell Imaging.

Marion Leduc, Sabrina Forveille, Guido Kroemer, Allan Sauvat, Oliver Kepp

Abstract read
PubMed Publisher
In one paragraph

Article in Methods in molecular biology (Clifton, N.J.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

5 authors.

Marion LeducMetabolomics and Cell Biology Platforms, Gustave Roussy Cancer Center, Université Paris Saclay, Villejuif, France.
Sabrina ForveilleMetabolomics and Cell Biology Platforms, Gustave Roussy Cancer Center, Université Paris Saclay, Villejuif, France.
Guido KroemerMetabolomics and Cell Biology Platforms, Gustave Roussy Cancer Center, Université Paris Saclay, Villejuif, France.
Allan SauvatMetabolomics and Cell Biology Platforms, Gustave Roussy Cancer Center, Université Paris Saclay, Villejuif, France.
Oliver KeppMetabolomics and Cell Biology Platforms, Gustave Roussy Cancer Center, Université Paris Saclay, Villejuif, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The successful implementation of immune checkpoint inhibitors (ICIs) immunotherapy into clinical routine has underlined the importance of immunotherapy for the treatment of cancer. Nevertheless, benefits from ICI monotherapy remain limited to a subset of patients. The induction of immunogenic cell death (ICD) can prime tumors for subsequent ICI via the onset of adaptive immune responses leading to an infiltration of cytotoxic T lymphocytes. The nuclear and cellular nuclear release of high mobility group box 1 (HMGB1) is one of the hallmarks of ICD. Binding of HMGB1 to Toll-like receptor 4 (TLR4) expressed on dendritic cells plays a pivotal role in stimulating their maturation and antigen presentation, facilitating the onset of adaptive immunity. Here we describe microscopic assessments of HMGB1 release that can be applied to the screening of chemical compound libraries for novel ICD inducing agents. Thus, quantitative measurement of HMGB1 release kinetics can be useful for the discovery of new immuno-oncology drugs.

Indexed as

HMGB1 ProteinCell Line, TumorDendritic CellsHumansImmunogenic Cell DeathKineticsNeoplasmsToll-Like Receptor 4HMGB1 ProteinHMGB1 protein, humanToll-Like Receptor 4Anticancer immunityCancerImmune checkpoint blockadeImmunotherapy

Identifiers

What OpenQuestion holds

Textmetadata
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.