title: Comparison of clinical outcome of patients with non-small-cell lung cancer harbouring epidermal growth factor receptor exon 19 or exon 21 mutations.
abstract: OBJECTIVE
  Deletion of exon 19 of the epidermal growth factor receptor (EGFR) and mutation of exon 21 are the most common EGFR mutations and predict higher response to EGFR tyrosine kinase inhibitors (TKI). Accumulating data show clinical differences in both response and survival between these two EGFR mutations. This study investigated the clinical impact of EGFR exon 19 deletion and L858R mutation by retrospectively analysing the clinical outcome of patients with advanced non-small-cell lung cancer (NSCLC) treated with EGFR TKI.
  
  
  METHODS
  Patients harbouring EGFR exon 19 deletion or L858R mutations and who had received gefitinib or erlotinib treatment were identified. The response rate (RR), progression-free survival (PFS) and overall survival (OS) were determined for the two groups. EGFR mutation was determined by PCR-based direct sequencing.
  
  
  RESULTS
  The study indentified 87 patients harbouring EGFR exon 19 deletion (n=61) or L858R mutation (n=26) who were treated with either gefitinib (n=83) or erlotinib (n=4). Patients with exon 19 deletion had significantly longer PFS, compared with patients with L858R mutation (9.3 vs 6.9 months, p=0.02). In a multivariate Cox regression model, EGFR exon 19 deletion was independently predictive of longer PFS (p=0.02). However, no significant differences in RR (64% vs 62%, p=0.83) and OS (17.7 vs 20.5 months, p=0.65) were observed between these two mutations.
  
  
  CONCLUSIONS
  While no significant difference in OS was observed between EGFR exon 19 deletion and L858R mutation, EGFR exon 19 deletion was predictive of longer PFS following EGFR TKI treatment in patients with advanced NSCLC.
authors: Center for Clinical Trials, National Cancer Center Hospital, National Cancer Center, Goyang-si, Republic of Korea.
authors: Young-Woong
authors: YW
authors: Won
authors: Ji-Youn
authors: JY
authors: Han
authors: Geon Kook
authors: GK
authors: Lee
authors: Seog-Yun
authors: SY
authors: Park
authors: Kun Young
authors: KY
authors: Lim
authors: Kyong-Ah
authors: KA
authors: Yoon
authors: Tak
authors: T
authors: Yun
authors: Heung Tae
authors: HT
authors: Kim
authors: Jin Soo
authors: JS
authors: Lee
mesh_terms: D000328:Adult; D000368:Aged; D000970:Antineoplastic Agents / Q000627:therapeutic use; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy / Q000235:genetics* / Q000401:mortality; D018572:Disease-Free Survival; D066246:ErbB Receptors / Q000235:genetics*; D000069347:Erlotinib Hydrochloride; D005091:Exons / Q000235:genetics*; D005260:Female; D000077156:Gefitinib; D005838:Genotype; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000401:mortality; D008297:Male; D008875:Middle Aged; D009154:Mutation / Q000235:genetics*; D011799:Quinazolines / Q000627:therapeutic use; D012189:Retrospective Studies; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D011799:Quinazolines; D000069347:Erlotinib Hydrochloride; D066246:ErbB Receptors; D000077156:Gefitinib