Evidence map›Paper›PMID 32602900›Full record

ArticleCarcinogenesis2020

Modulation of the PD-1/PD-L1 immune checkpoint axis during inflammation-associated lung tumorigenesis.

Sreekanth Chanickal Narayanapillai, Yong Hwan Han, Jung Min Song, Manaye Ebabu Kebede, Pramod Upadhyaya, Fekadu Kassie

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Carcinogenesis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Sreekanth Chanickal NarayanapillaiMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Yong Hwan HanMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Jung Min SongMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Manaye Ebabu KebedeMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Pramod UpadhyayaMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
Fekadu KassieMasonic Cancer Center, University of Minnesota, Minneapolis, MN, USA.
University of Minnesota Medical Center · USUniversity of Minnesota · US

Funding

Chemoprevention of inflammation-driven lung cancerR01CA166615 · NCI · UNIVERSITY OF MINNESOTA · PI KASSIE, FEKADU · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA166615
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a significant risk factor for lung cancer. One potential mechanism through which COPD contributes to lung cancer development could be through generation of an immunosuppressive microenvironment that allows tumor formation and progression. In this study, we compared the status of immune cells and immune checkpoint proteins in lung tumors induced by the tobacco smoke carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) or NNK + lipopolysaccharide (LPS), a model for COPD-associated lung tumors. Compared with NNK-induced lung tumors, NNK+LPS-induced lung tumors exhibited an immunosuppressive microenvironment characterized by higher relative abundances of PD-1+ tumor-associated macrophages, PD-L1+ tumor cells, PD-1+ CD4 and CD8 T lymphocytes and FOXP3+ CD4 and CD8 T lymphocytes. Also, these markers were more abundant in the tumor tissue than in the surrounding 'normal' lung tissue of NNK+LPS-induced lung tumors. PD-L1 expression in lung tumors was associated with IFNγ/STAT1/STAT3 signaling axis. In cell line models, PD-L1 expression was found to be significantly enhanced in phorbol-12-myristate 13-acetate activated THP-1 human monocytes (macrophages) treated with LPS or incubated in conditioned media (CM) generated by non-small cell lung cancer (NSCLC) cells. Similarly, when NSCLC cells were incubated in CM generated by activated THP-1 cells, PD-L1 expression was upregulated in EGFR- and ERK-dependent manner. Overall, our observations indicate that COPD-like chronic inflammation creates a favorable immunosuppressive microenvironment for tumor development and COPD-associated lung tumors might show a better response to immune checkpoint therapies.

Indexed as

AnimalsB7-H1 AntigenCarcinogenesisCarcinoma, Non-Small-Cell LungFemaleHumansInflammationLipopolysaccharidesLung NeoplasmsMiceMice, Inbred AProgrammed Cell Death 1 ReceptorPulmonary Disease, Chronic ObstructiveTumor MicroenvironmentB7-H1 AntigenLipopolysaccharidesProgrammed Cell Death 1 Receptor

Identifiers

PMID32602900
PMCPMC8241221
OpenAlexW3038938609

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.