PNA-Mediated PCR Clamping for the Detection of EGFR Mutations in Non-Small Cell Lung Cancer.
10.4046/trd.2010.69.4.271
- Author:
Kye Young LEE
1
;
Hee Joung KIM
;
Sun Jong KIM
;
Gwang Ha YOO
;
Won Dong KIM
;
Seo Young OH
;
Wan Seop KIM
Author Information
1. Department of Internal Medicine, Konkuk University School of Medicine, Seoul, Korea. kyleemd@kuh.ac.kr
- Publication Type:Original Article
- Keywords:
Peptide Nucleic Acids;
Receptor, Epidermal Growth Factor;
Carcinoma, Non-Small-Cell Lung
- MeSH:
Adenocarcinoma;
Carcinoma, Non-Small-Cell Lung;
Constriction;
Female;
Genotype;
Humans;
Male;
Mutation Rate;
Peptide Nucleic Acids;
Phosphotransferases;
Polymerase Chain Reaction;
Quinazolines;
Receptor, Epidermal Growth Factor
- From:Tuberculosis and Respiratory Diseases
2010;69(4):271-278
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Recent studies have demonstrated that the epidermal growth factor receptor (EGFR) genotype is the most important predictive marker to EGFR-tyrosine kinase inhibitors (TKIs) and first-line gefitinib treatment will be approved in the near future for use in non-small cell lung cancer (NSCLC) patients with the EGFR mutation. Direct sequencing is known to be the standard for detecting EGFR mutations; however, it has limited sensitivity. Peptide nucleic acids (PNA)-mediated PCR clamping method is a newly introduced method for analyzing EGFR mutations with increased sensitivity and stability. METHODS: A total of 71 NSCLC patients were analyzed for EGFR mutations using the PNA-mediated PCR clamping technique. Sixty-nine patients were analyzed for clinicopathologic correlation with EGFR genotype; 2 patients with indeterminate results were excluded. In order to determine EGFR-TKI drug response, 57 patients (42 gefitinib, 15 erlotinib) were included in the analysis. RESULTS: The EGFR mutation rate was 47.8%. Being female, a non-smoker, and having adenocarcinoma were favorable clinicopathologic factors, as expected. However, more than a few smokers (33.3%), male (28.1%), and patients with non-adenocarcinoma (28.6%) had the EGFR mutation. Having a combination of favorable clinicopathologic factors did not increase the EGFR mutation rate significantly. Drug response to EGFR-TKIs showed significant differences depending on the EGFR genotype; ORR was 14.3% for wild type vs 69.0% for mutant type; DCR is 28.6% for wild type vs 96.6% for mutant type. The median EGFR-TKI treatment duration is 7.6 months for mutant type group and 1.4 months for wild type group. CONCLUSION: EGFR genotype determined using the PNA-mediated PCR clamping method is significantly correlated with the clinical EGFR-TKI responses and PNA-mediated PCR.
