Introduction: Lung cancer is the most important cause of cancer related deaths across the world. The aim of the study is to find key genes and enriched pathways associated with lung cancer using bioinformatics and statistical techniques, hence providing potential targets for the identification and treatment of the cancer. Methods: Differentially expressed genes (DEGs) data of 54674 genes based on stage, tumor and status of the lung cancer was taken from 66 patients of African American (AAs) origin. 2392 DEGs were found based on stage, 13502 DEGs were found based on tumor, 2927 DEGs were found based on status having p value (p<0.05). Results: Total 33 common DEGs were found from stage, tumor and status of lung cancer patients. Gene ontology (GO) and KEGG pathway enrichment analysis is performed and 49 significant pathways were obtained, out of which 10 pathways were found that were exclusively involved in lung cancer development. Protein-protein interaction (PPI) network analysis found 69 nodes and 324 edges and identified 10 hub genes based on their highest degrees. Additionally, module analysis of PPI found that ‘Viral carcinogenesis’, ‘pathways in cancer’, ‘notch signaling pathway’, ‘AMPK signaling pathways’ had close association with lung cancer. Conclusion: it is seen that these identified DEGs do not directly participate in growth of lung cancer but regulate other genes which play important role in growth of lung cancer. The key genes and enriched pathways identified can thus help in better identification and prediction of lung cancer.
Ever since the war on cancer was declared in 1971, there has been an explosion in our understanding of this diverse group of diseases. The application of molecular genetics and molecular biology technologies have enabled a deep understanding of the genetic, epigenetic, signaling cascades, survival pathways, and invasive mechanisms that underlie the cancer phenotype. Concomitantly this has translated in the development of ever more effective and safe medications that work through different mechanisms of action and target fundamental aspects of the biology of the tumor. The paradigm has been chronic myeloid leukemia where the discovery of the Philadelphia chromosome, ultimately led to the identification of the BCR-ABL oncogene and the development of tyrosine kinase inhibitors such as imatinib, nilotinib, dasatinib and others and lead to rapid, deep and long-lasting remissions in this disease. Another success story has been acute promyelocytic leukemia with the vast majority of patients now being cured of the disease without the need for any classical chemotherapy.