Response to: Successful afatinib rechallenge in a patient with non‐small cell lung cancer harboring EGFR G719C and S768I mutations

Abstract

The genetic landscape of nonsquamous non-small cell lung cancer (NSCLC) includes specific mutations involving primarily epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK) and the proto-oncogene ROS1. With regard to EGFR, exon 19 deletion and exon 21 (L858R) mutations are most frequently detected and correlate with a prolonged and significant response in patients to first-line osimertinib. “Uncommon” EGFR mutations have been previously reported to represent 18% of all EGFR mutations and large retrospective and perspective studies have confirmed their major sensitivity to first-line treatment with afatinib. They include single or complex punctiform mutations of the exons 18, 19, 20 and 21 and amino acidic insertions of exon 20. We read with interest the paper by Masuda and colleagues reporting the case of a substantial response to afatinib rechallenge in a patient affected by metastatic lung adenocarcinoma harboring EGFR complex uncommon mutations. We report the case of an 81-year-old patient who was referred to our center after a diagnosis of lung adenocarcinoma with brain metastases. Disease stage was clinical T4N2M1 according to the eighth edition of the International Association for the Study of Lung Cancer (IASLC). EGFR mutational analysis revealed concomitant G719S exon 18 and S768I exon 20 mutations. The patient who was a previous smoker of 40 pack/years started first-line afatinib at a full dose of 40 mg in July 2020.