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Original Article : PNA-Mediated PCR Clamping for the Detection of EGFR
Mutations in Non-Small Cell Lung Cancer
ÀúÀÚ :
À̰迵 ( Kye Young Lee ) , ±èÈñÁ¤ ( Hee Joung Kim ) , ±è¼øÁ¾ ( Sun Jong Kim ) , À¯±¤ÇÏ ( Gwang Ha Yoo ) , ±è¿øµ¿ ( Won Dong Kim ) , ¿À¼¿µ ( Seo Young Oh ) , ±è¿Ï¼· ( Wan Seop Kim )
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´ëÇÑ°áÇÙ ¹× È£Èí±âÇÐȸ , Tuberculosis and Respiratory Diseases | 69±Ç 4È£ 271 ~ 278, ÃÑ 8 pages
¹ßÇ࿬µµ : 2010
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Peptide Nucleic Acids, Receptor, Epidermal Growth Factor, Carcinoma, Non-Small-Cell Lung
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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.
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