Aging lungs present an altered microenvironment, with increased inflammatory response, extracellular matrix remodeling, immune exhaustion, and decreased tight junctions, which contribute to increased tumor growth. This altered lung microenvironment is partially reversed to its youthful state with the overexpression of alpha-1 antitrypsin (AAT).

By integrating multi-omics dataincluding genomic and epigenomic profiles and microenvironmental exposures from both healthy individuals and patients, and performing intra-individual, inter-individual, and cross-species comparative analyses with advanced predictive models, we will uncover deeper insights into cancer evolution and identify potential strategies for individualized prevention.