De Novo Resistance to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors
|ClinicalTrials.gov Identifier: NCT01697163|
Recruitment Status : Unknown
Verified September 2012 by Joo Hang Kim, Severance Hospital.
Recruitment status was: Not yet recruiting
First Posted : October 2, 2012
Last Update Posted : October 2, 2012
This study is based on the following hypothesis "De novo resistance to EGFR-TKI in EGFR mutation positive patients is related with mutations in EGFR downstream genes".
Investigators will prospectively collect genomic DNA and clinical data regarding treatment outcomes to EGFR-TKI in NSCLC patients with activating EGFR mutations. Investigators will sequence candidate mutations of EGFR downstream genes and analyze c-met gene amplification and protein expression in PTEN, HGF, and IGFR. To identify genetic mutations, amplification, and protein over expression as predictive markers of treatment outcomes, investigators analyzed the association of treatment outcomes with the presence of genetic alteration or protein over expression. Investigators will attempt to identify biomarkers that are able to predict de novo resistance to EGFR-TKI in EGFR mutated NSCLC.
|Condition or disease|
|Study Type :||Observational|
|Estimated Enrollment :||155 participants|
|Official Title:||Pilot Study to Identify the Mechanism of De Novo Resistance to Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors (EGFR-TKIs) in NSCLC With EGFR Mutation.|
|Study Start Date :||October 2012|
|Estimated Primary Completion Date :||September 2014|
|Estimated Study Completion Date :||September 2014|
Lung cancer patients with EGFR mutation
- hazard rates of PFS [ Time Frame: 1year ]The primary objective is to compare hazard rates of PFS in patients treated with Iressa between with and without any molecular aberrancy in EGFR-downstream genes/proteins.
- OS [ Time Frame: 2years ]Overall survival (OS) of EGFR-TKI according to each biomarker (i.e. PIK3CA, AKT, PTEN, and STK11 mutation and HGF, c-met, and IGFR amplification) Disease control rate (DCR) of EGFR-TKI according to each biomarker (i.e. PIK3CA, AKT, PTEN, and STK11 mutation and HGF, c-met, and IGFR amplification) Progression-free survival (PFS) of EGFR-TKI according to each biomarker (i.e. PIK3CA, AKT, PTEN, and STK11 mutation and HGF, c-met, and IGFR amplification)
Biospecimen Retention: Samples With DNA
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT01697163
|Contact: Joo Hang Kim, MD, PhDemail@example.com|
|Principal Investigator:||Joo Hang Kim, MD, PhD||Severance Hospital|