title: Evaluation of gefitinib efficacy according to body surface area in patients with non-small cell lung cancer harboring an EGFR mutation.
abstract: BACKGROUND
  Exon 19 deletions and L858R point mutation are the most commonly encountered active epidermal growth factor receptor (EGFR) mutations in non-small cell lung cancer (NSCLC), and they predict greater efficacy of gefitinib therapy. The objective of this study was to evaluate whether body surface area (BSA) affects the efficacy of gefitinib in patients with NSCLC harboring an active EGFR mutation.
  
  
  METHODS
  We reviewed the medical records of consecutive patients with advanced NSCLC harboring an active EGFR mutation who received gefitinib monotherapy. The median BSA value was used as the cutoff value to evaluate the impact of BSA on the efficacy of gefitinib.
  
  
  RESULTS
  The median BSA of the 103 NSCLC patients harboring an active EGFR mutation was 1.45 m(2). The overall response rate, progression-free survival (PFS), and median survival time (MST) were 65.0 %, 11.3 months, and 26.2 months, respectively. There were no significant differences in clinical outcomes between the high-BSA group (BSA ≥ 1.45 m(2)) and low-BSA group (BSA < 1.45 m(2)), i.e., the response rates was 60.0 % and 69.8 %, respectively (P = 0.20), and their MST was 24.7 and 26.2 months, respectively (P = 0.78). Although BSA was predictive of PFS between high-BSA group and low-BSA group in the univariate analysis (9.0 and 12.2 months, P = 0.04), the multivariate analysis identified only performance status and smoking status as independent predictors of PFS.
  
  
  CONCLUSIONS
  The efficacy of gefitinib in patients with NSCLC harboring an EGFR mutation does not differ according to their BSA.
authors.affiliation: Department of Respiratory Medicine, Kitasato University School of Medicine, 1-15-1, Kitasato, Minami-ku, Sagamihara-City, Kanagawa, 252-0374, Japan, igawa@kitasato-u.ac.jp.
authors.forename: Satoshi
authors.initials: S
authors.lastname: Igawa
authors.forename: Masashi
authors.initials: M
authors.lastname: Kasajima
authors.forename: Mikiko
authors.initials: M
authors.lastname: Ishihara
authors.forename: Michiko
authors.initials: M
authors.lastname: Kimura
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Hiyoshi
authors.forename: Hideyuki
authors.initials: H
authors.lastname: Niwa
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Kusuhara
authors.forename: Shinya
authors.initials: S
authors.lastname: Harada
authors.forename: Maiko
authors.initials: M
authors.lastname: Asakuma
authors.forename: Sakiko
authors.initials: S
authors.lastname: Otani
authors.forename: Ken
authors.initials: K
authors.lastname: Katono
authors.forename: Jiichiro
authors.initials: J
authors.lastname: Sasaki
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Masuda
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001830:Body Surface Area; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D018572:Disease-Free Survival; D066246:ErbB Receptors / Q000235:genetics*; D005260:Female; D005500:Follow-Up Studies; D000077156:Gefitinib; D006801:Humans; D053208:Kaplan-Meier Estimate; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009154:Mutation; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use; D011799:Quinazolines / Q000627:therapeutic use*; D012189:Retrospective Studies; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D047428:Protein Kinase Inhibitors; D011799:Quinazolines; D066246:ErbB Receptors; D000077156:Gefitinib