Therapeutic insights into epidermal growth factor receptor/reactive oxygen species proto-oncogene 1-receptor co-mutated non-small cell lung cancer: Crizotinib as a promising option.

Abstract

This letter provides a review of the report by Peng et al on a unique case of non-small cell lung cancer (NSCLC), specifically lung adenocarcinoma, featuring reactive oxygen species proto-oncogene 1-receptor (ROS1) co-mutation. The case involves a 64-year-old patient who exhibited both epidermal growth factor receptor (EGFR) L858R mutation and ROS1 rearrangement, achieving significant disease stabilization following treatment with crizotinib. This rare EGFR/ROS1 co-mutation poses distinct challenges for clinical management and highlights the necessity of personalized treatment strategies. While third-generation EGFR tyrosine kinase inhibitors (TKIs), such as osimertinib, are commonly regarded as first-line therapies, recent studies indicate that crizotinib may offer superior disease control in certain EGFR-mutant patients, particularly those who exhibit poor responses to EGFR TKIs. The case also examines the influence of tumor cell genetic heterogeneity on treatment response, underscoring the importance of evaluating tumor characteristics. In patients with EGFR/ROS1 co-mutation, gefitinib is generally effective as a first-line treatment; however, its efficacy can be limited, whereas crizotinib has demonstrated improved disease control. Future research should focus on identifying optimal treatment strategies for patients with EGFR/ROS1 co-mutation to enhance patient outcomes. In conclusion, this case report not only illustrates the effectiveness of crizotinib in managing patients with EGFR/ROS1 co-mutation but also underscores the importance of personalized treatment approaches, offering valuable insights for improving clinical outcomes in NSCLC patients with complex genetic profiles.