title: EGFR-TKI is effective regardless of treatment timing in pulmonary adenocarcinoma with EGFR mutation.
abstract: OBJECTIVE
  Although epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have become key therapeutic agents for non-small cell lung cancer (NSCLC) patients with EGFR mutation, little is known about the efficacy of EGFR-TKIs according to different treatment timings.
  
  
  METHODS
  A total of 1,250 patients with NSCLC were screened for EGFR mutations at a single institution between March 2006 and May 2010. The efficacy of EGFR-TKIs in terms of response rate (RR), progression-free survival (PFS), and overall survival (OS) were compared according to the treatment timing.
  
  
  RESULTS
  Among the 437 patients (36.1 %) with EGFR mutation, we analyzed 222 patients who received EGFR-TKI treatment. With a median follow-up duration of 27.5 months (range 8.3-69.2), EGFR-TKI was given to 97 (43.7 %), 109 (49.1 %), and 16 (7.2 %) patients as first-line, second-line, and third-line therapy, respectively. All three groups showed similar RR (71.1, 72.5, and 75.0 %, respectively) to EGFR-TKI (p = 0.802). No significant difference was observed according to treatment timing of EGFR-TKI in terms of PFS (median 10.6, 13.0, and 10.4 months; p = 0.670) and OS (median 20.5, 26.2, and 17.1 months; p = 0.142). The treatment timing of EGFR-TKI still showed no association with PFS or OS after adjusting significant prognostic factors including performance, disease status, and EGFR mutation types.
  
  
  CONCLUSIONS
  EGFR-TKIs showed similar efficacy in patients with EGFR mutation-positive adenocarcinoma in terms of RR, PFS, and OS irrespective of treatment timing. Although EGFR-TKIs are currently the treatment of choice of first-line treatment in patients with EGFR-positive tumors, the sequential treatment with EGFR-TKI could be a reasonable option when EGFR mutation status cannot be obtained in a short time.
authors.affiliation: Department of Oncology, Asan Medical Center, University of Ulsan College of Medicine, 86, Asanbyeongwon-gil, Songpa-gu, Seoul, 138-736, Korea.
authors.forename: Dong-Hoe
authors.initials: DH
authors.lastname: Koo
authors.forename: Kyu-pyo
authors.initials: KP
authors.lastname: Kim
authors.forename: Chang-Min
authors.initials: CM
authors.lastname: Choi
authors.forename: Dae-Ho
authors.initials: DH
authors.lastname: Lee
authors.forename: Jae Cheol
authors.initials: JC
authors.lastname: Lee
authors.forename: Jung-Shin
authors.initials: JS
authors.lastname: Lee
authors.forename: Se Jin
authors.initials: SJ
authors.lastname: Jang
authors.forename: Sang-We
authors.initials: SW
authors.lastname: Kim
mesh_terms: D000230:Adenocarcinoma / Q000175:diagnosis / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000970:Antineoplastic Agents / Q000627:therapeutic use*; D002289:Carcinoma, Non-Small-Cell Lung / Q000175:diagnosis / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism; D003937:Diagnosis, Differential; D066246:ErbB Receptors / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D005260:Female; D005500:Follow-Up Studies; D056726:Genetic Association Studies; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009154:Mutation; D009363:Neoplasm Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000378:metabolism; D011379:Prognosis; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D056910:Republic of Korea; D012189:Retrospective Studies; D016019:Survival Analysis
chemical_list: D000970:Antineoplastic Agents; D009363:Neoplasm Proteins; D047428:Protein Kinase Inhibitors; C512478:EGFR protein, human; D066246:ErbB Receptors