title: Phase II study of erlotinib in advanced non-small-cell lung cancer after failure of gefitinib.
abstract: OBJECTIVE
  This study was designed to evaluate the efficacy and toxicity of erlotinib in patients with advanced non-small-cell lung cancer (NSCLC) who experienced disease progression after treatment with gefitinib.
  
  
  METHODS
  The study included stage IIIB/IV recurrent or metastatic NSCLC patients who received two or three prior chemotherapy regimens and showed progressive disease within 4 months of gefitinib therapy discontinuation. Patients received erlotinib 150 mg/d until disease progression or unacceptable toxicity. Epidermal growth factor receptor (EGFR) mutations and other genetic abnormalities were analyzed from available tumor samples.
  
  
  RESULTS
  Patient and disease characteristics (N = 21) included median age 56 years; number of prior chemotherapy regimens (three; n = 11); female sex (n = 11); adenocarcinoma (n = 15); and never-smoker status (n = 11). Among the 17 patients with tumor samples available, EGFR mutations were detected in five. The disease control rate (DCR) and response rate (RR) for all patients were 28.6% and 9.5%, respectively. The median duration of disease control was 125 days. The median time to progression and overall survival were 60 days and 158 days, respectively. Patients who had stable disease (SD) while receiving gefitinib showed significantly higher DCR (75% v 17.6% in non-SD patients; P = .050) and RR (50.0% v 0% in non-SD patients; P = .029). Among 17 patients with biomarker results available, those lacking EGFR mutations who had SD while receiving gefitinib showed significantly higher DCR and RR.
  
  
  CONCLUSIONS
  Erlotinib seems to be a potential therapeutic option for the treatment of advanced NSCLC patients with wild-type EGFR who had SD while receiving gefitinib.
authors.affiliation: Yonsei Cancer Center, Seoul, Korea.
authors.forename: Byoung Chul
authors.initials: BC
authors.lastname: Cho
authors.forename: Chong-Kun
authors.initials: CK
authors.lastname: Im
authors.forename: Moo-Suk
authors.initials: MS
authors.lastname: Park
authors.forename: Se Kyu
authors.initials: SK
authors.lastname: Kim
authors.forename: Joon
authors.initials: J
authors.lastname: Chang
authors.forename: Jong Pil
authors.initials: JP
authors.lastname: Park
authors.forename: Hye Jin
authors.initials: HJ
authors.lastname: Choi
authors.forename: Yu Jin
authors.initials: YJ
authors.lastname: Kim
authors.forename: Sang-Joon
authors.initials: SJ
authors.lastname: Shin
authors.forename: Joo Hyuk
authors.initials: JH
authors.lastname: Sohn
authors.forename: Hoguen
authors.initials: H
authors.lastname: Kim
authors.forename: Joo Hang
authors.initials: JH
authors.lastname: Kim
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D014408:Biomarkers, Tumor / Q000032:analysis; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy* / Q000473:pathology; D018450:Disease Progression; D019008:Drug Resistance, Neoplasm; D000069347:Erlotinib Hydrochloride; D005260:Female; D000077156:Gefitinib; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use*; D011799:Quinazolines / Q000627:therapeutic use*; D015996:Survival Rate; D016896:Treatment Outcome
chemical_list: D000970:Antineoplastic Agents; D014408:Biomarkers, Tumor; D047428:Protein Kinase Inhibitors; D011799:Quinazolines; D000069347:Erlotinib Hydrochloride; D000077156:Gefitinib