Abstract

Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitor (TKI) therapy is associated with improved outcomes in patients with EGFR mutation-positive (EGFRm) non-small cell lung cancer (NSCLC). Despite initial responses, most patients develop resistance. Little is known about treatment following first-line (1L) TKIs. This study aimed to understand real world treatment patterns, T790M testing rates, and disposition of EGFRm patients following availability of newer TKIs. Adult patients with EGFRm stage IV NSCLC treated between Dec 1, 2015 and Aug 31, 2017, were retrospectively identified from the US Oncology Network’s iKnowMedSM (iKM) electronic health record. Patient characteristics, treatment patterns, and T790M testing data were obtained via programmatic database abstraction and supplemented with chart review. 308 patients were identified during the study period. Median age at diagnosis was 69 years, 67% were female, 63% Caucasian, 49% never smokers and 59% with ECOG performance status 0–1. Nearly all patients (n=302; 98%) received treatment with a TKI, 80% (n=246) with a TKI as 1L therapy. The most frequently used TKIs as 1L monotherapy were erlotinib (n=204; 66%), afatinib (n=27; 9%), and gefitinib (n=3; 1%). Combination chemotherapy with or without a TKI was used in 24% of patients. Among all patients treated with a 1L TKI, 19% (n=47) were tested for the T790M mutation after 1L TKI, and 34% (n=16) were positive. The most common 2L therapies in patients who received a 1L TKI (n=44 patients) were pemetrexed-based chemotherapy (n=20; 45%), afatinib (n=7; 16%), and osimertinib (n=7; 16%). Among all patients who received a 1L TKI, 15% (n=41) had died, 18% (n=51) were still alive and on TKI therapy, 12% (n=29) went on to receive subsequent therapy, and 53% (n=149) stopped their TKI and received no subsequent therapy at the end of the follow-up period. The majority of patients with EGFRm advanced NSCLC received 1L TKI therapy, most often with erlotinib. Following 1L TKI, less than 20% of patients were tested for T790M, and most did not receive any subsequent therapy following TKI. As understanding of resistance mechanisms in mutation-driven lung cancer is rapidly evolving, and as ongoing studies evaluate optimal treatments, it is imperative to integrate this information into clinical practice.

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