Tyrosine kinase inhibitors (TKIs) have dramatically changed the clinical prospects of patients with non-small cell lung cancer harboring epidermal growth factor receptor (EGFR)-activating mutations. Despite prolonged disease control and high tumor response rates, all patients eventually progress on EGFR TKI treatment. Here, we review the mechanisms of acquired EGFR TKI resistance, the methods for monitoring its appearance, as well as current and future efforts to define treatment strategies to overcome resistance. Passaro and colleagues discuss recent advances in treating EGFR-mutant lung cancer, including methods for detecting disease and tracking therapy response, developments in understanding of resistance mechanisms and ongoing clinical trials to circumvent therapeutic resistance to EGFR targeting.

Overcoming therapy resistance in EGFR-mutant lung cancer

Targeted therapies for RET-fusion cancer: Dilemmas and breakthrough.

Background Osimertinib is a novel and irreversible epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) targeting EGFR sensitive mutations and EGFR exon20 p.T790M mutation, which demonstrated superior progression-free survival (PFS) and overall survival (OS). Case presentation We report a patient with lung adenocarcinoma harboring EGFR exon 19 deletion mutant treatment with icotinib. After 6 months, she developed EGFR exon20 p.T790M and then the patient received osimertinib treatment. A novel MYH9 (exon41)-RET (exon12) fusion and EGFR exon20 p.T790M loss were identified using plasma circulation tumor DNA (ctDNA) after osimertinib treatment, which led to rapid progression after osimertinib five months and suggested a potential resistance mechanism. Conclusion Our findings expanded the spectrum of RET arrangement types and provided the basis for this hypothesis: acquired RET rearrangement and EGFR exon20 p.T790M loss potentially serve an additional resistance mechanism to osimertinib in EGFR-mutated non-small-cell lung cancer (NSCLC).

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A Novel MYH9-RET Fusion Occurrence and EGFR T790M Loss as an Acquired Resistance Mechanism to Osimertinib in a Patient with Lung Adenocarcinoma: A Case Report.

e20634Background: EGFR-TKIs is the standard first/second-line treatment for EGFR-mutant advanced non-small-cell lung cancer (NSCLC). The mechanisms of EGFR-TKIs resistance are still under explorati...

RET fusion in first/third-generation EGFR-TKIs resistance in advanced non-small cell lung cancer.

e24267Background: Approximately 4-7% of non-small cell lung cancer (NSCLC) patients have abnormal activation of MET, and MET inhibitors have shown promising results. However, the prevalence of MET ...

MET amplification and activating mutation analysis in solid tumors using comprehensive NGS panel.

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RET fusion in first/third-generation EGFR-TKIs resistance in advanced non-small cell lung cancer.

MET amplification and activating mutation analysis in solid tumors using comprehensive NGS panel.