title: Is the importance of achieving stable disease different between epidermal growth factor receptor tyrosine kinase inhibitors and cytotoxic agents in the second-line setting for advanced non-small cell lung cancer?
abstract: BACKGROUND
  It is controversial whether achieving stable disease leads to a survival benefit and whether the importance of achieving stable disease differs between cytotoxic agents and molecular targeted agents. To examine these questions, the authors retrospectively reviewed phase II and III studies in the second-line setting for advanced non-small cell lung cancer using epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) and cytotoxic agents separately.
  
  
  METHODS
  The authors chose 45 trials for the chemotherapy group and nine for the EGFR TKI group by searching the PubMed database. All nine trials in the EGFR TKI group concern gefitinib and erlotinib.
  
  
  RESULTS
  The median survival time increased 0.0375 month with each 1% increase in stable disease rate (p = 0.039), and each 1% increase in response rate resulted in 0.0744 (p < 0.001) month of median survival time in the analysis combined with both cytotoxic agents and EGFR TKIs. Main and interaction terms for EGFR TKI treatment were not statistically significant. With respect to time to progression, only response rate showed a statistically significant relationship with survival.
  
  
  CONCLUSIONS
  To obtain response seems to be more important than to achieve stable disease for both cytotoxic agents and EGFR TKIs, although achieving stable disease is still valuable. The relationship between survival and response or stable disease appears similar for cytotoxic agents and EGFR TKIs.
authors.affiliation: Department of Medical Oncology, Kinki University School of Medicine, Osaka, Japan. kurata@hp.pref.hyogo.jp
authors.forename: Takayasu
authors.initials: T
authors.lastname: Kurata
authors.forename: Keitaro
authors.initials: K
authors.lastname: Matsuo
authors.forename: Minoru
authors.initials: M
authors.lastname: Takada
authors.forename: Masaaki
authors.initials: M
authors.lastname: Kawahara
authors.forename: Masahiro
authors.initials: M
authors.lastname: Tsuji
authors.forename: Yuka
authors.initials: Y
authors.lastname: Matsubara
authors.forename: Nagahiro
authors.initials: N
authors.lastname: Otani
authors.forename: Shigeki
authors.initials: S
authors.lastname: Matsuyama
authors.forename: Kenya
authors.initials: K
authors.lastname: Muraishi
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Fujita
authors.forename: Masato
authors.initials: M
authors.lastname: Ishikawa
authors.forename: Keita
authors.initials: K
authors.lastname: Koyano
authors.forename: Isamu
authors.initials: I
authors.lastname: Okamoto
authors.forename: Taroh
authors.initials: T
authors.lastname: Satoh
authors.forename: Kenji
authors.initials: K
authors.lastname: Tamura
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Nakagawa
authors.forename: Masahiro
authors.initials: M
authors.lastname: Fukuoka
mesh_terms: D000970:Antineoplastic Agents / Q000627:therapeutic use*; D002289:Carcinoma, Non-Small-Cell Lung / Q000188:drug therapy* / Q000401:mortality; D066246:ErbB Receptors / Q000037:antagonists & inhibitors*; D006801:Humans; D008175:Lung Neoplasms / Q000188:drug therapy* / Q000401:mortality; D015996:Survival Rate
chemical_list: D000970:Antineoplastic Agents; D066246:ErbB Receptors