Clinical and Translational Oncology

, Volume 13, Issue 11, pp 812–818

Epidermal growth factor receptor (EGFR) mutations in a series of non-small-cell lung cancer (NSCLC) patients and response rate to EGFR-specific tyrosine kinase inhibitors (TKIs)

Authors

    • Molecular Genetics Laboratory Plataforma de OncologíaUSP Hospital San Jaime
  • Joseba Rebollo
    • Medical Oncology Plataforma de OncologíaUSP Hospital San Jaime
  • Ramón González-Manzano
    • Molecular Genetics Laboratory Plataforma de OncologíaUSP Hospital San Jaime
  • Manuel Sureda
    • Medical Oncology Plataforma de OncologíaUSP Hospital San Jaime
  • Elena Evgenyeva
    • Pathology Plataforma de OncologíaUSP Hospital San Jaime
  • Belén Valenzuela
    • Pharmacotherapy Plataforma de OncologíaUSP Hospital San Jaime
  • Francisco José Fernández
    • Pathology Plataforma de OncologíaUSP Hospital San Jaime
  • Jerónimo Forteza
    • PathologyComplejo Hospitalario Universitario de Santiago (CHUS)
  • Antonio Brugarolas
    • Medical Oncology Plataforma de OncologíaUSP Hospital San Jaime
Research Articles

DOI: 10.1007/s12094-011-0739-1

Cite this article as:
Martínez-Navarro, E.M., Rebollo, J., González-Manzano, R. et al. Clin Transl Oncol (2011) 13: 812. doi:10.1007/s12094-011-0739-1

Abstract

Introduction

Epidermal growth factor receptor (EGFR) mutation related to tyrosine kinase inhibitors’ (TKIs) responsiveness in non-small cell lung cancer (NSCLC) has become an important issue for therapeutic decision-making in NSCLC patients.

Material and methods

Sixty-nine Caucasian NSCLC patients were screened for mutations in the tyrosine kinase (TK) domain of EGFR by direct sequencing from December 2005 to September 2010.

Results

Activating mutations in the EGFR TK domain were found in 8 of 69 (11.6%) (7 deletions in exon 19 and one L858R mutation in exon 21). Seven of those mutations were found in adenocarcinoma and one mutation in bronchiolo-alveolar carcinoma; five of them in females (one smoker) and three of them in males (one smoker). All patients carrying activating mutations in the TK domain of EGFR were treated with TKIs. Ten patients not carrying an activating mutation in EGFR, who progressed after chemotherapy, were also treated with compassionate use of EGFR-specific TKIs (gefitinib or erlotinib). An objective response (partial response) was observed in all patients carrying an activating mutation in EGFR that received TKIs. Median overall survival for these patients has not been reached, however mean survival has been estimated at 39.5 months (95% CI, 22–57).

Conclusions

As previously reported, EGFR TK mutational analysis was a predictive test for response to targeted therapy with EGFR TKIs. The early identification of these patients consistently attains disease response and clearly improves outcomes.

Keywords

EGFRNSCLCMutationLung cancerTKIs

Copyright information

© Feseo 2011