ArticleCancers2021
Nicotinic Acetylcholine Receptor Subunit α7 Mediates Cigarette Smoke-Induced PD-L1 Expression in Human Bronchial Epithelial Cells.
Article in Cancers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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.
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.
Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Activation of lung megakaryocyte α7 nAChR exacerbates allergic airway inflammation via IL-33/p38 MAPK signaling.JCI insight · 2026Article
- ADHD-anchored partitioning of non-small cell lung cancer genetic covariance identifiesFrontiers in immunology · 2026Article
- Uncovering a novel role of nAChRs in oxidative stress-mediated vascular dysfunction in COPD.Redox biology · 2025Article
- The role of acetylcholine and its receptors in tumor immune regulation: mechanisms and potential therapeutic targets.Molecular cancer · 2025Review
- Tobacco smoke exposure is a driver of altered oxidative stress response and immunity in head and neck cancer.Journal of translational medicine · 2025Article
- PD-L1 expression in patients with non-small-cell lung cancer is associated with sex and genetic alterations: A retrospective study within the Caucasian population.Thoracic cancer · 2024Article
- Article
- An integral perspective of canonical cigarette and e-cigarette-related cardiovascular toxicity based on the adverse outcome pathway framework.Journal of advanced research · 2023Review
- The Role of the Acetylcholine System in Common Respiratory Diseases and COVID-19.Molecules (Basel, Switzerland) · 2023Review
- Investigating the crosstalk between chronic stress and immune cells: implications for enhanced cancer therapy.Frontiers in neuroscience · 2023Review
- Neurotransmitters: promising immune modulators in the tumor microenvironment.Frontiers in immunology · 2023Review
- Expression, correlation, and prognostic significance of different nicotinic acetylcholine receptors, programed death ligand 1, and dopamine receptor D2 in lung adenocarcinoma.Frontiers in oncology · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Tobacco smoking is the top risk factor for lung cancer development. Nicotine in cigarettes can induce addiction, and its derivatives become potent carcinogens after metabolic activation and activate oncogenic signaling in lung epithelial cells through their expressed nicotinic acetylcholine receptors (nAChRs). However, the effects of smoking on the tumor immune microenvironment are under investigation. In the current study, we investigated whether nicotine activation of nicotinic acetylcholine receptor subunit α7 (nAChRα7,
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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.