Shared Transcriptomic Signatures and Network Interactions Between Lung Adenocarcinoma and Asthma.
Seha Akduman1, Elif Düz2, Merve Gündoğdu2,3
1Department of Pulmonary Diseases, School of Medicine, Yeditepe University, Istanbul 34755, Türkiye.
International Journal of Molecular Sciences
|June 26, 2026
Summary
This study reveals shared molecular mechanisms between lung adenocarcinoma (LUAD) and asthma, identifying key genes like DNAJC3, APOBEC3G, and PRDX4. These findings suggest potential for drug repurposing in treating both diseases.
Area of Science:
- Pulmonary Medicine
- Genomics
- Computational Biology
Background:
- Lung adenocarcinoma (LUAD) is a leading cause of cancer mortality.
- Asthma is a widespread chronic respiratory disease.
- Both conditions involve airway inflammation and oxidative stress, suggesting shared risk factors and genetic links.
Purpose of the Study:
- To investigate molecular mechanism similarities between LUAD and asthma.
- To identify shared transcriptomic signatures.
- To explore potential drug repurposing opportunities based on common pathways.
Main Methods:
- Analysis of transcriptomic datasets for asthma and LUAD.
- Identification of shared genes and co-expression interactions.
- Highlighting potential common molecular mediators.
Main Results:
- A set of genes and co-expression interactions common to both asthma and LUAD was identified.
- DNAJC3, APOBEC3G, and PRDX4 were identified as potential common molecular mediators.
- Correlative evidence supports shared pathways and molecular links between the diseases.
Conclusions:
- Shared molecular mechanisms and transcriptomic signatures exist between asthma and LUAD.
- Identified genes may serve as key molecular links in disease pathogenesis.
- Findings provide a computational framework for future therapeutic association and drug-gene relationship studies.
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