Shared Transcriptomic Signatures and Network Interactions Between Lung Adenocarcinoma and Asthma

Lung adenocarcinoma (LUAD) remains the leading cause of mortality worldwide, while asthma is the most prevalent chronic disease affecting individuals of all ages. The shared airway involvement in these global health concerns results in exposure to common risk factors, suggesting a potential overlap in their genetic background. Given the roles oxidative stress and chronic inflammation play in both LUAD and asthma, we aimed to investigate similarities in their molecular mechanisms and to explore whether these shared transcriptomic signatures may prove useful for potential drug repurposing hypotheses by analyzing relevant transcriptomic datasets. This analysis identified a set of genes and co-expression interactions shared between asthma and LUAD, suggesting potential common molecular mechanisms underlying both diseases. Specifically, DNAJC3, APOBEC3G, and PRDX4 were highlighted as potential common molecular mediators underlying both diseases, offering correlative evidence for shared pathways. These genes may represent key molecular links connecting the pathogenic processes of asthma and LUAD. The transcriptomic profiles of asthma and lung cancer datasets reveal common molecular interactions, suggesting potential shared biological mechanisms between the two diseases. These findings provide a computational framework that may guide future studies investigating therapeutic associations and possible drug–gene relationships in lung adenocarcinoma and asthma.