1336 - Clinical modes of EGFR tyrosine kinase inhibitor failure and subsequent management in advanced non-small cell lung cancer

Date 28 September 2012
Event ESMO Congress 2012
Session Publication Only
Topics Anti-Cancer Agents & Biologic Therapy
Non-Small-Cell Lung Cancer, Metastatic
Presenter Huajun Chen
Authors H. Chen1, J. Yang2, H. Yan2, X. Zhang2, Z. Wu2, Y. Wu2
  • 1Guangdong General Hospital (GGH) & Guangdong Academy of Medical Sciences, 510080 - Guangzhou/CN
  • 2Guangdong Lung Cancer Institute, Guangdong General Hospital (GGH) & Guangdong Academy of Medical Sciences, 510080 - Guangzhou/CN



The diversity of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) failure in advanced non-small cell lung cancer (NSCLC) has been reported sporadically, but there is no published overview of EGFR-TKI failure modes, which could hinder the appropriate management for patients with distinct failure modes.


This study mainly aimed to classify the diversity of TKI failure, and to investigate the usefulness of clinical modes in subsequent management and prognosis.

Patients and methods

The retrospective study accrued 227 Chinese advanced NSCLC patients with EGFR-TKI failure. One-hundred and twenty consecutive clinical trial patients were enrolled as the training set to establish a clinical model based on clinical factors. Another 107 routine patients were enrolled as the validating set according to a Bayes discriminant analysis. EGFR mutations and c-MET amplification were analyzed. Kaplan–Meier survival analysis was used to test the differences of prognosis and subsequent management in clinical modes.


The duration of disease control, symptom improvement, and evolution of tumor burden were verified as feasible grouping variables. A correct grouping rate achieved 84.1%. The cohort was classified into three groups, as follows: 130 patients with dramatic progression, 42 with gradual progression, and 55 with local progression. Progression-free survivals (PFSs) for the dramatic progression, gradual progression, and local progression groups were 9.3, 12.9, and 9.2 months, respectively (P =0.007). Overall survivals for the groups (OSs) were 17.1, 39.4, and 23.1 months, respectively (P <0.001). TKI continuation was superior to switching chemotherapy in a subsequent setting for gradual progression (39.4 vs. 17.8 months, P =0.02). The difference of EGFR mutations or c-MET amplification among the three groups was not significant.


Clinical modes of EGFR-TKI failure could favor strategies for subsequent treatment and predicting a survival benefit in advanced NSCLC.


All authors have declared no conflicts of interest.