ArticleBMC pulmonary medicine2025
Checkpoint inhibitor-associated pneumonitis in non-small cell lung cancer: a cohort study with transcriptomic analysis of inflammatory mechanisms.
Article in BMC pulmonary medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune checkpoint inhibitors (ICIs) have significantly improved outcomes in non-small cell lung cancer (NSCLC), yet their use is associated with a notable risk of immune-related adverse events, including checkpoint inhibitor–associated pneumonitis (CIP). The real-world incidence, risk magnitude, and underlying immunopathogenesis of CIP in NSCLC remain inadequately defined.
methodsWe conducted a retrospective cohort study using electronic health records from 21,671 NSCLC patients, categorized into ICI (n = 8,744) and non-ICI (n = 12,927) groups. Incidence of pneumonitis was evaluated using propensity score–matched analysis, Kaplan-Meier curves, and Cox regression models. Subgroup analyses were performed across demographic and clinical variables. Differentially expressed genes (DEGs) from transcriptomic datasets were analyzed to explore inflammatory mechanisms, including GO/KEGG pathway enrichment, protein–protein interaction (PPI) network construction, and single-sample gene set enrichment analysis (ssGSEA).
resultsThe incidence of pneumonitis was significantly higher in the ICI group (28.9%) compared to the non-ICI group (10.0%) (hazard ratio [HR] = 2.86; 95% confidence interval [CI], 2.43–3.29; P < 0.001). This elevated risk persisted across age, sex, BMI, comorbidities, and autoimmune status. Transcriptomic analysis revealed distinct upregulation of immune-related genes (e.g., TCF7L1, ATP1B4, RPL18A), with enrichment of pathways including IFN-γ signaling, Th17 differentiation, TNF and JAK-STAT signaling. ssGSEA confirmed increased immune activation scores in CIP samples. PPI network and hub gene analysis identified GHRH, ZBTB21, and PLAU as central regulators.
conclusionsICI use in NSCLC is associated with a markedly increased risk of pneumonitis. Transcriptomic profiling suggests that overactivation of pro-inflammatory immune pathways underlies CIP pathogenesis.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.