Targeted Therapies for Lung Cancer: Molecular Drivers, Resistance Mechanisms, and Clinical Integration (2015–2025)

University of Nottingham, University Park, Nottingham, United Kingdom, NG7 2RD

^* Corresponding author: This email address is being protected from spambots. You need JavaScript enabled to view it.

Abstract

Lung cancer is a particularly serious form of cancer that garners significant attention worldwide. While there have been advancements in surgery, radiation, and chemotherapy, survival rates remain low, especially in advanced stages. Key genes, such as mutations in EGFR and gene fusions involving ALK, have transformed treatment through the development of targeted therapies. Mutations in EGFR activate signalling pathways that promote tumour growth, support the formation of new blood vessels, and help the tumour evade the immune system. Similarly, ALK fusions keep the kinase active, leading to rapid cell proliferation. However, resistance to treatment continues to pose a significant challenge. For example, the tumours will trigger secondary mutations, or there are some alternative signalling pathways activated. The target of the drug might be lost at this stage. A deeper understanding of how tumours grow and develop resistance at the molecular level is essential for creating more effective drugs and devising innovative combination therapy strategies.