This thesis attempts to delineate the association between asthma and lung cancer using epidemiological and molecular studies asthma and lung cancer patients followed by in vitro validation using lung and asthma cell lines. The epidemiological data in this study was able to confirm the real association between asthma and lung cancer by identifying subset of patients who were diagnosed with both diseases. The results showed that asthma severity can be a contributing factor to carcinogenesis and its progression in various tissues specifically lung. Our molecular analysis was able to identify a panel of key genes and pathways distinctly regulated between severe asthmatic patients and lung cancer. Asthma and lung cancer being caused by genetic variations and are influenced by environmental factors, have diverse etiologies, represented in their different pathways. From the in-silico analysis in this study, the lung cancer cohort showed receptor tyrosine kinase signaling, wound healing, and growth factors as significantly enriched active pathways. Similarly, in the severe asthma cell adhesion, extracellular matrix, and epithelial cell proliferation were all found as unique asthma pathways in this investigation. Analysis of the enriched genes derived from the pathway analysis identified seven key genes present in both asthma and lung cancer: BCL3, POSTN, PPARD, STAT1, MYC, CD44, and FOSB. The validation of the genes using archival patient tissue biopsies, cell lines, and liquid biopsy samples revealed significant differential expression between asthma and lung cancer patients, providing possible insights into some of the molecular mechanisms involved in the pathogenesis among asthma and lung cancer. Subsequently, these transcripts may be potentially used as markers for early lung cancer and could be useful in preventing the progression to later stages of lung cancer. RNA-seq validations revealed shared pathways between lung cancer and asthmatic cases which implied more in immune responses, GPCRs pathway and hormonal res