UNRAVELLING THE MOLECULAR BASIS OF LUNG CANCER: PATHWAYS TO PROGRESS

Abstract

Lung cancer remains one of the primary causes of cancer-related deaths worldwide. The disease’s intricacy stems from its heterogeneity, which includes numerous genetic, epigenetic, and molecular mechanisms. This review delves into the critical molecular mechanisms driving lung cancer progression, such as genetic mutations, epigenetic changes, signal transduction pathways, and immune evasion strategies. Understanding these pathways sheds light on targeted medicines and personalized medicine methods for lung cancer treatment. Key oncogenic drivers, including KRAS, EGFR, and TP53 mutations, as well as ALK and ROS1 rearrangements, are highlighted for their role in cell cycle dysregulation, apoptosis evasion, and increased metastatic potential. Epigenetic modifications, such as DNA methylation, histone acetylation, and non-coding RNAs, contribute to gene expression changes in lung cancer cells. Dysregulated signaling pathways, including PI3K/AKT/mTOR, RAS/ RAF/MEK/ERK, and Notch, are investigated regarding tumor development, angiogenesis, and therapeutic resistance. Furthermore, the review emphasizes the heterogeneity of lung cancer and the interaction of the tumor microenvironment, immune evasion, and therapy resistance. Recent advances in targeted therapeutics and immunotherapies are briefly discussed, focusing on the implications for personalized medicine. The goal of the review is to offer a thorough grasp of the biology of lung cancer, opening the door for innovative treatment approaches that will enhance patient outcomes.

DOI - https://doi.org/10.65525/SVUP.9788198800473.2025.384-394