Abstract
BackgroundApproximately 3–5% of patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) harbor exon 18 mutations. The appropriate treatment for such patients has not been clarified. The aim of this study was to investigate the response of patients with NSCLC harboring EGFR exon 18 mutations to different therapeutic options.MethodsBetween May 2014 and September 2020, the clinical outcomes of 82 patients harboring EGFR exon 18 mutations who received first-generation (1G) EGFR-tyrosine kinase inhibitor (TKI), second-generation (2G) EGFR-TKI afatinib, chemotherapy, and 1G TKI in combination with chemotherapy as the initial therapy were retrospectively analyzed.ResultsA total of 82 NSCLC patients harboring EGFR 18 mutations with whose treatment and survival outcomes were available were analyzed. The median age was 59 years, and 47 (57.3%) were female. The most common kind of EGFR exon 18 mutation was G719X (75.6%), followed by E709X (15.9%), E709_T710delinsD (3.6%), and other subtypes (4.9%). There was a significant difference in median progression-free survival (mPFS) by therapeutic strategy (P = 0.017). The mPFS of 1G TKI, 2G TKI afatinib, chemotherapy, and 1G TKI in combination with chemotherapy were 7.7 (95% CI, 4.2–11.2), 11.3 (95% CI, 5.6–17.0), 5.0 (95% CI, 2.3–17.7), and 11.1 (95% CI, 5.9–16.4) months, respectively. No significant difference in PFS was observed between afatinib and 1G TKI in combination with chemotherapy (P = 0.709).ConclusionsLike afatinib, 1G TKI in combination with chemotherapy might be an effective treatment option for patients harboring EGFR exon 18 mutations.
Highlights
Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein with cytoplasmic kinase activity that can transduce essential growth factor signals from extracellular cues to cellular responses, thereby regulating cellular proliferation, differentiation, angiogenesis, and metastasis
There was a significant difference in median progression-free survival by therapeutic strategy (P = 0.017)
The median progression-free survival (mPFS) of 1G tyrosine kinase inhibitor (TKI), 2G TKI afatinib, chemotherapy, and 1G TKI in combination with chemotherapy were 7.7, 11.3, 5.0, and 11.1 months, respectively
Summary
Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein with cytoplasmic kinase activity that can transduce essential growth factor signals from extracellular cues to cellular responses, thereby regulating cellular proliferation, differentiation, angiogenesis, and metastasis. 10–20% of patients with non-small cell lung cancer (NSCLC) harbor uncommon or rare EGFR mutation [3,4,5,6]. Exon 18 mutations involve missense mutations G719X and E709X, insertion-deletion (indel) mutation E709_T710delinsX, and other molecular subtypes, comprising approximately 3–5% of all the EGFR alterations [8, 9]. Compared to patients with tyrosine kinase inhibitor (TKI)-sensitizing EGFR mutations, NSCLC patients with EGFR exon 18 mutations generally respond slightly worse to first-generation (1G) EGFR-TKI [7, 10, 11]. 3–5% of patients with epidermal growth factor receptor (EGFR) mutation-positive non-small cell lung cancer (NSCLC) harbor exon 18 mutations. The aim of this study was to investigate the response of patients with NSCLC harboring EGFR exon 18 mutations to different therapeutic options
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