Differential clinicopathological features, treatments and outcomes in patients with Exon 19 deletion and Exon 21 L858R EGFR mutation-positive adenocarcinoma non-small-cell lung cancer

Abstract

The most common oncogenic driver in non-small-cell lung cancer (NSCLC) is the epidermal growth factor receptor (EGFR) gene mutations that occur more frequently among Asians (30%–50%) as opposed to Caucasians (10%–15%). Lung cancer is one of the most prevalent cancers in India, with a reported adenocarcinoma positivity ranging between 26.1% and 86.9% in NSCLC patients. The prevalence ofEGFRmutations in adenocarcinoma patients (36.9%) in India is higher than that of Caucasian patients and lower than that of East Asian patients. The exon 19 deletion (Ex19del) is more common than exon 21 L858R mutations in Indian patients with NSCLC. Studies have shown that the clinical behaviour of patients with advanced NSCLC differs betweenEGFREx19del and exon 21 L858R mutation status. In this study, we investigated the differences in clinicopathological features and survival outcomes after first line and second-line treatment withEGFRtyrosine kinase inhibitors (EGFRTKIs) in NSCLC patients with Ex19del and exon 21 L858REGFRmutation status. This study also focuses on the role and potential benefits of dacomitinib, a second-generation irreversibleEGFRTKI, in patients with Ex19del and exon 21 L858REGFRmutation-positive advanced NSCLC in Indian settings.

The Importance of Screening for EGFR Mutation in Lung Cancer

“…Point mutations, insertions, and in-frame deletions in the kinase domain of the EGFR gene are examples of EGFR mutations [9]. L858R point mutation and exon 19 deletions are two frequent EGFR mutations in non-small cell lung cancer (NSCLC) [10].…”

A study of high dose furmonertinib in EGFR exon 20 insertion mutation-positive advanced non-small cell lung cancer

“…The EGFR gene is cmposed of 28 exons, and most of the mutations occur in exons 18-21. Common mutations include exon 19 inframe deletion (ex19del) and exon 21 L858R alterations (ex21L858R), which accounts for 80%-85% of all EGFR mutations ( 2 ). These two classical EGFR mutations have good sensitivity to first-generation EGFR-TKIs (erlotinib, gefitinib), second-generation EGFR-TKIs (afatinib, dacotinib) and third-generation EGFR-TKIs (osimertinib) drugs.…”