EML4-ALK in Non-small Cell Lung Cancer: Molecular Mechanisms and Targeted Therapies.

Abstract

Lung cancer is a malignancy characterized by high global incidence and mortality rates, with approximately 85% of cases classified as non-small cell lung cancer (NSCLC). Advances in molecular biology and targeted therapeutic agents have ushered NSCLC into the era of precision medicine. The echinoderm microtubule-associated protein-like 4 (EML4) and anaplastic lymphoma kinase (ALK) fusion gene represents a pivotal target for personalized treatment in NSCLC. Although ALK inhibitors exhibit significant efficacy against EML4-ALK-positive tumors, addressing drug resistance remains a major challenge. Identifying novel therapeutic targets and implementing combination therapies are essential for optimizing subsequent treatment strategies and improving overall prognosis. In the management of patients with EML4-ALK gene fusion, continuous monitoring of tumor progression and timely adjustment of treatment regimens based on disease status are critical to achieving long-term clinical benefits. This review comprehensively summarizes recent advances in the clinicopathological features, targeted drug development, resistance mechanisms, and potential therapeutic targets associated with the EML4-ALK fusion gene.