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Updated: Jun 20, 2026

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
09:38

Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure

Published on: August 11, 2017

Epidermal growth factor receptor and K-RAS mutations in 411 lung adenocarcinoma: a population-based prospective study

Laura Boldrini1, Greta Alì, Silvia Gisfredi

  • 1Department of Surgery, University of Pisa, Pisa, Italy.

Oncology Reports
|September 3, 2009
PubMed

Insights

Epidermal growth factor receptor (EGFR) mutations are common in female, non-smoking lung adenocarcinoma patients. These mutations, along with a non-smoking history, predict positive responses to targeted therapies like gefitinib or erlotinib.

Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • Targeting the epidermal growth factor receptor (EGFR) is crucial in advanced non-small cell lung cancer (NSCLC).
  • Understanding genetic mutations in EGFR and K-RAS is key for personalized treatment strategies.
  • Previous research has highlighted the importance of EGFR in NSCLC, but further investigation into specific patient populations and treatment responses is needed.

Purpose of the Study:

  • To investigate the frequency and clinical significance of epidermal growth factor receptor (EGFR) and K-RAS gene mutations in lung adenocarcinoma.
  • To evaluate the association of these mutations with patient demographics, smoking status, and histological features.
  • To assess the efficacy of tyrosine kinase inhibitors (TKIs) in a cohort of female patients with advanced lung adenocarcinoma.

Main Methods:

  • Collected 411 lung adenocarcinoma samples from clinical centers.
  • Assessed EGFR mutations (exons 18-21) and K-RAS mutations (codons 12 and 13) using sequencing and RFLP analysis.
  • Analyzed treatment response in 21 female patients receiving gefitinib or erlotinib as second/third-line therapy.

Main Results:

  • EGFR mutations (12.6%) were more frequent in females, non-smokers, and patients with bronchioloalveolar features.
  • K-RAS mutations (17.9%) were more common in males and associated with smoking.
  • EGFR and K-RAS mutations were mutually exclusive.
  • Partial response to gefitinib/erlotinib in female patients was linked to classic EGFR mutations and non-smoking history.
  • No K-RAS alterations were observed in female patients with partial response or stable disease.

Conclusions:

  • EGFR and K-RAS mutations are distinct molecular events in lung adenocarcinoma.
  • EGFR mutations are predictive biomarkers for TKI efficacy, particularly in non-smoking females.
  • These findings support the use of targeted therapies for specific subgroups of lung cancer patients.

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