ArticleDiscover oncology2025
Shared blood gene signature in lung adenocarcinoma and microbial lung infections: a bioinformatic analysis and in silico validation.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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Who cites it
3 citing papers in PubMed.
- From COPD and asthma to lung cancer: potential candidate genes and their associated biological pathways for the incidence risk of lung cancer.Journal, genetic engineering & biotechnology · 2026Article
- The cell with many faces: lung macrophage plasticity and function in response to environmental and pathogenic insults.Physiological reviews · 2026Review
- Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicrobial lung infections may promote development of lung cancer through overlapping molecular mechanisms. This analysis aimed to identify a co-regulated peripheral blood gene signature in lung adenocarcinoma (LUAD) and microbial lung infections.
methodsA total of 403 peripheral blood transcriptomic profiles from five GEO test datasets-two LUAD (GSE39345, GSE103527) and three infection-related (GSE40012, GSE65682, GSE103119)-were analyzed using the limma package. Differentially expressed genes (DEGs) were defined by|log
resultsNinety-three significant DEGs were shared between LUAD and infection datasets, including 40 upregulated and 53 downregulated genes. Eight hub genes showed consistent differential expression in both LUAD and lung infection: BCL6, CD163, S100A12 (upregulated); and FLT3LG, RPL13, RPL14, RPL22, RPS4X (downregulated), of which BCL6, S100A12, FLT3LG, RPL13, RPL14, RPL22 and RPS4X were significantly co-regulated (R
conclusionThis analysis identified a blood-based 7-gene signature shared between LUAD and microbial lung infections, associated with immunosuppressive microenvironment features, suggesting a potential link between infection-driven inflammation and tumor-promoting immune modulation.
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