Evidence map›Paper›PMID 35661198›Full record

ArticleCancer research2022

The "Inside" Story on Tumor-Expressed PD-L1.

Brent A Hanks

Open access · bronzeAbstract readEditorialComment
In one paragraph

Article in Cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Brent A HanksDivision of Medical Oncology, Department of Medicine, Duke Cancer Institute, Duke University, Durham, North Carolina.ORCID 0000-0002-2803-3272
Duke University · US

Funding

Investigating the PD-L1:NLRP3 signaling axis as a tumor intrinsic mechanism of adaptive resistance to anti-PD-1 antibody immunotherapyR37CA249085 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HANKS, BRENT ALLEN · 2020 to 2025
$2.5M
NCI NIH HHS R37 CA249085
6 · The paper itself

Abstract

While the extracellular domain of PD-L1 is well-recognized for playing a critical role in immune evasion by suppressing CD8+ T-cell activity through direct PD-1 interactions, a series of studies has evolved highlighting important functional roles for the PD-L1 cytoplasmic domain in supporting various aspects of tumorigenesis. Kornepati and colleagues contribute to our overall understanding of PD-L1 in tumor biology by describing a link between tumor PD-L1 expression and DNA repair. These studies demonstrate that PD-L1 promotes breast cancer type 1 (BRCA1)-mediated homologous recombination while inhibiting cytosolic DNA sensing, thus suppressing tumor immunogenicity. Notably, these effects could not be reversed with anti-PD-L1 antibodies utilized in the clinic, suggesting that pharmacologic agents promoting PD-L1 degradation may be a more effective treatment strategy for select tumors. Studies that are improving our understanding of the pathways driven by PD-L1 cytoplasmic signaling are providing increased insight into the design of next generation combinatorial immunotherapy strategies. See related article by Kornepati et al., p. 2156.

Indexed as

Antineoplastic AgentsNeoplasmsB7-H1 AntigenDNA RepairHumansPoly(ADP-ribose) Polymerase InhibitorsSynthetic Lethal MutationsAntineoplastic AgentsB7-H1 AntigenPoly(ADP-ribose) Polymerase Inhibitors

Identifiers

PMID35661198
PMCPMC9885868
OpenAlexW4281640965

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.