Abstract
PurposeThe outcome of pretreatment epidermal growth factor receptor (EGFR) T790M mutation in EGFR mutant non-small cell lung cancer (NSCLC) patients treated with EGFR tyrosine kinase inhibitors (TKIs) is controversial, this study aimed to evaluate the prognostic role of pretreatment T790M in advanced NSCLC patients treated with EGFR TKIs.ResultsA total of 7 eligible studies containing 179 cases and 281 controls were included in the meta-analysis. The pooled hazard ratios (HRs) for progression-free survival (PFS) and overall survival (OS) were 2.21 (95% CI 1.49-3.29, P<0.001) and 1.24 (95% CI 0.90-1.71, P=0.186), respectively. We also did subgroup analyses on OS and PFS according to patients from various districts.MethodsIdentified literatures from various databases were reviewed. A meta-analysis was performed to evaluate the prognostic role of pretreatment EGFR T790M in advanced EGFR mutant patients treated with EGFR TKIs.ConclusionsPretreatment T790M may be a poor prognostic factor for PFS in advanced NSCLC patients treated with EGFR TKIs. However, no significant prognostic effect was found between pretreatment T790M mutation and OS. More studies are needed to demonstrate the prognostic role of pretreatment T790M mutation in advanced NSCLC patients.
Highlights
Lung cancer is the leading cause of death worldwide, causing 1.6 million deaths with over 1.8 million new cases reported annually [1]
Pretreatment T790M may be a poor prognostic factor for progression-free survival (PFS) in advanced non-small cell lung cancer (NSCLC) patients treated with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs)
More studies are needed to demonstrate the prognostic role of pretreatment T790M mutation in advanced NSCLC patients
Summary
Lung cancer is the leading cause of death worldwide, causing 1.6 million deaths with over 1.8 million new cases reported annually [1]. Several clinical trials found that advanced NSCLC patients harboring EGFR mutations tended to have an improved progression-free survival (PFS) to TKIs compared with chemotherapy as first-line treatment [6, 7]. One mechanism suggested that de novo T790M exists in a very minor part of pretreatment tumor cells, which remain vial after TKIs treatment and proliferate rapidly until TKIs no longer validate [13, 14]. Methods such as CH (colony hybridization) assay are highly sensitive to detect T790M mutation out of pre-TKIs patients [15]. The prognostic value of pretreatment T790M mutation in advanced NSCLC patients treated with TKIs remains inconclusive
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