Patients with exon 19 deletion were associated with longer progression-free survival compared to those with L858R mutation after first-line EGFR-TKIs for advanced non-small cell lung cancer: a meta-analysis

PLoS One. 2014 Sep 15;9(9):e107161. doi: 10.1371/journal.pone.0107161. eCollection 2014.

Abstract

Backgrounds: It has been extensively proved that the efficacy of epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) is superior to that of cytotoxic chemotherapy in advanced non-small cell lung cancer (NSCLC) patients harboring sensitive EGFR mutations. However, the question of whether the efficacy of EGFR-TKIs differs between exon 19 deletion and exon 21 L858R mutation has not been yet statistically answered.

Methods: Subgroup data on hazard ratio (HR) for progression-free survival (PFS) of correlative studies were extracted and synthesized based on random-effect model. Comparison of outcomes between specific mutations was estimated through indirect and direct methods, respectively.

Results: A total of 13 studies of advanced NSCLC patients with either 19 or 21 exon alteration receiving first-line EGFR-TKIs were included. Based on the data from six clinical trials for indirect meta-analysis, the pooled HRTKI/chemotherapy for PFS were 0.28 (95% CI 0.20-0.38, P<0.001) in patients with 19 exon deletion and 0.47 (95% CI 0.35-0.64, P<0.001) in those with exon 21 L858R mutation. Indirect comparison revealed that the patients with exon 19 deletion had longer PFS than those with exon 21 L858R mutation (HR19 exon deletion/exon 21 L858R mutation = 0.59, 95% CI 0.38-0.92; P = 0.019). Additionally, direct meta-analysis showed similar result (HR19 exon deletion/exon 21 L858R mutation = 0.75, 95% CI 0.65 to 0.85; P<0.001) by incorporating another seven studies.

Conclusions: For advanced NSCLC patients, exon 19 deletion might be associated with longer PFS compared to L858 mutation at exon 21 after first-line EGFR-TKIs.

Publication types

  • Meta-Analysis
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Afatinib
  • Antineoplastic Agents / therapeutic use*
  • Carcinoma, Non-Small-Cell Lung / drug therapy*
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Disease-Free Survival
  • ErbB Receptors / genetics*
  • Erlotinib Hydrochloride
  • Gefitinib
  • Humans
  • Mutation*
  • Proportional Hazards Models
  • Quinazolines / therapeutic use

Substances

  • Antineoplastic Agents
  • Quinazolines
  • Afatinib
  • Erlotinib Hydrochloride
  • EGFR protein, human
  • ErbB Receptors
  • Gefitinib

Grants and funding

This work was supported by the National High Technology Research and Development Program of China, Grant No. 2012AA02A502; Innovative drug R&D center based on real-time high-throughput cell-based screening platform and large capacity compound library, Grant No. 2013ZX09401003-002; National Natural Science Funds of China, Grant No. 81372502; Wu Jieping Medical Foundation Project, Grant No. 320.6750.131. All the funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.