Lung Adenocarcinoma Harboring Concomitant EGFR Mutation and EML4-ALK Fusion That Benefits From Three Kinds of Tyrosine Kinase Inhibitors: A Case Report and Literature Review

During the past decade, the emerging effect of targeted therapies has led to a therapeutic paradigm shift in lung cancer. A driver gene alteration has been detected in 64% of lung adenocarcinoma cases. The epidermal growth factor receptor (EGFR) and echinoderm microtubule-associated protein-like 4 anaplastic lymphoma kinase (EML4-ALK) are important driver genes that have been found in 17% and 8% of patients, respectively.1 Previous studies have shown that an EGFR mutation and EML4-ALK fusion are mutually exclusive and that the coexistence of these 2 genes is associated with resistance to both EGFR tyrosine kinase inhibitors (TKIs) and ALK inhibitors.