Detection EGFR exon 19 status of lung cancer patients by DNA electrochemical biosensor

2016 ◽  
Vol 80 ◽  
pp. 411-417 ◽  
Author(s):  
Xiong-Wei Xu ◽  
Xiu-Hua Weng ◽  
Chang-Lian Wang ◽  
Wei-Wei Lin ◽  
Ai-Lin Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Electrochemical Biosensor ◽  
Dna Electrochemical Biosensor ◽  
Lung Cancer Patients ◽  
Exon 19

Epidemiology of PD-L1 and ALK expression and EGFR mutational status in Argentinian patients with lung cancer.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e20565-e20565 ◽  
Author(s):  
Ruben Salanova ◽  
Julio C Calderazzo Pereyra ◽  
Laura Leguina ◽  
Asuncion Bena ◽  
Mariana Barberis ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Egfr Mutation ◽  
Egfr Mutations ◽  
Alk Rearrangement ◽  
Lung Cancer Patients ◽  
Mutational Status ◽  
Alk Positive ◽  
Egfr Mutant ◽  
Exon 19

e20565 Background: Until now, the results of the correlation between PD-L1, ALK expression and EGFR mutations remain controversial. We prospectively evaluated patterns among EGFR mutant, ALK positive and PD-L1 positive lung cancer patients. Methods: PD-L1 and ALK expression was evaluated in 342 adenocarcinomas (AD) of the lung using inmunohistochemestry (anti-PD-L1 22C3, anti-ALK D5F3), and EGFR mutations using real time PCR (therascreen EGFR RGQ PCR Kit version 2). PD-L1 was also evaluated in 36 squamous (SQ) cell carcinomas. Results: 181 of 342 patients with AD were positive for PD-L1. 108 were positive with a TPS value between 1 and 49, and 73 were positive with a TPS value higher than 50 (p = 0.002). 25 of 36 patients with SQ were positive for PD-L1. 17 were positive with a TPS value between 1 and 49, and 8 were positive with a TPS value higher than 50. 133 samples with AD PD-L1 positive and 97 PD-L1 negative were tested for EGFR and ALK, 33 and 14 respectively were positive for EGFR mutations (p = 0.15), with 45% for exon 19 deletions (p = 0.003), 5 and 0 respectively were positive for ALK translocations (p = 0.053). 210 of 342 patients were men and 132 were women, 117 and 64 were positive for PD-L1 expression respectively (p > 0.1). Conclusions: NSCLC with EGFR mutation showed a trend for higher frequency of positive PD-L1 expression and NSCLC harboring ALK rearrangement was significantly associated with PD-L1 expression. These findings might contribute to the understanding of the regulation of PD-L1 expression in lung cancer and its relation to ALK expression and EGFR mutation.

Genotyping of common EGFR mutations in lung cancer patients by electrochemical biosensor

2018 ◽  
Vol 150 ◽  
pp. 176-182 ◽  
Author(s):  
Xiu-Hua Weng ◽  
Xiong-Wei Xu ◽  
Chang-Lian Wang ◽  
Wei-Wei Lin ◽  
Ai-Lin Liu ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Electrochemical Biosensor ◽  
Egfr Mutations ◽  
Lung Cancer Patients

scholarly journals Diagnostic Accuracy of Noninvasive Genotyping of EGFR in Lung Cancer Patients by Deep Sequencing of Plasma Cell-Free DNA

2015 ◽  
Vol 61 (9) ◽  
pp. 1191-1196 ◽  
Author(s):  
Junji Uchida ◽  
Kikuya Kato ◽  
Yoji Kukita ◽  
Toru Kumagai ◽  
Kazumi Nishino ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Deep Sequencing ◽  
Limit Of Detection ◽  
Detection System ◽  
Egfr Mutations ◽  
Plasma Dna ◽  
Lung Cancer Patients ◽  
Therapeutic Decisions ◽  
Exon 19

Abstract BACKGROUND Genotyping of EGFR (epidermal growth factor receptor) mutations is indispensable for making therapeutic decisions regarding whether to use EGFR tyrosine kinase inhibitors (TKIs) for lung cancer. Because some cases might pose challenges for biopsy, noninvasive genotyping of EGFR in circulating tumor DNA (ctDNA) would be beneficial for lung cancer treatment. METHODS We developed a detection system for EGFR mutations in ctDNA by use of deep sequencing of plasma DNA. Mutations were searched in >100 000 reads obtained from each exon region. Parameters corresponding to the limit of detection and limit of quantification were used as the thresholds for mutation detection. We conducted a multi-institute prospective study to evaluate the detection system, enrolling 288 non–small cell lung cancer (NSCLC) patients. RESULTS In evaluating the performance of the detection system, we used the genotyping results from biopsy samples as a comparator: diagnostic sensitivity for exon 19 deletions, 50.9% (95% CI 37.9%–63.9%); diagnostic specificity for exon 19 deletions, 98.0% (88.5%–100%); sensitivity for the L858R mutation, 51.9% (38.7%–64.9%); and specificity for L858R, 94.1% (83.5%–98.6%). The overall sensitivities were as follows: all cases, 54.4% (44.8%–63.7%); stages IA–IIIA, 22.2% (11.5%–38.3%); and stages IIIB–IV, 72.7% (60.9%–82.1%). CONCLUSIONS Deep sequencing of plasma DNA can be used for genotyping of EGFR in lung cancer patients. In particular, the high specificity of the system may enable a direct recommendation for EGFR-TKI on the basis of positive results with plasma DNA. Because sensitivity was low in early-stage NSCLC, the detection system is preferred for stage IIIB–IV NSCLC.

scholarly journals P3.02b-026 Association of EGFR Exon 19 Deletion and EGFR-TKI treatment duration with Frequency of T790M Mutation in EGFR-Mutant Lung Cancer Patients

2017 ◽  
Vol 12 (1) ◽  
pp. S1201-S1202
Author(s):  
Norikazu Matsuo ◽  
Koichi Azuma ◽  
Kazuko Sakai ◽  
Akihiko Kawahara ◽  
Hidenobu Ishii ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Treatment Duration ◽  
T790m Mutation ◽  
Lung Cancer Patients ◽  
Exon 19 Deletion ◽  
Tki Treatment ◽  
Egfr Mutant ◽  
Egfr Tki ◽  
Exon 19

MUC16 germline mutations may predispose inherited cancer family members to lung adenocarcinomas.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e13039-e13039
Author(s):  
Tao Wang ◽  
Hong Liu ◽  
Shanshan Xiao ◽  
Ruifang Mao ◽  
Rui Lin
Keyword(s):  
Lung Cancer ◽  
Cancer Patients ◽  
Family Members ◽  
Germline Mutations ◽  
Cancer Family ◽  
Inherited Cancer ◽  
Lung Cancer Patients ◽  
Exon 19 Deletion ◽  
Lung Adenocarcinomas ◽  
Exon 19

e13039 Background: Familial lung cancer is rare. Previous studies have identified random EGFR mutations associated with the inherited lung cancer. Reports also show that TP53 and CDKN2A mutations may predispose individuals to lung cancer, and MUC16 plays important roles in tumorigenesis and metastasis of lung cancer cells through regulating TP53. However, the molecular findings of familial lung cancer are still few. Methods: We have identified an extremely rare family, four siblings diagnosed with lung adenocarcinomas and one with bladder cancer; all lung cancer patients had multiple synchronous nodules. Their father was also lung cancer patient and deceased. We extracted tumor tissue DNA, genomic DNA (gDNA) and circulating cell-free DNA (ctDNA) from the 5 patients and analyzed the DNA samples using a 500-gene next generation sequencing (NGS) panel. Results: TP53 P72R and other 3 CDKN2B-AS1 germline mutations were identified in all the 5 patients. Although the 3 CDKN2B-AS1 mutations are commonly occurred in population according to dbSNP, these observations are consistent with a hypothesis that TP53 P72R and the CDKN2B-AS1 germline mutants may synergize in predisposing the family members to cancer. Interestingly, 3 MUC16 mutations ((rs754254000, rs754856910, and rs746152510) were all identified in the four lung cancer patients, but none were identified in the bladder cancer patient. All of the 3 MUC16 mutants had very low population allele frequency (all below 0.1%,) suggesting that the MUC16 germline mutations may play roles in the familial lung cancer, which is consistent with previous reports demonstrating the involvement of MUC16 in lung cancer cell growth. Moreover, all the four lung cancer patients had somatic mutations of EGFR L858R/exon 19 deletion prior to treatment with EGFR tyrosine kinase inhibitor (TKI), including one patient with L858R and exon 19 deletion in different tumor nodules, which is consistent with molecular characteristics in synchronous primary lung cancer. Conclusions: We have demonstrated in this study that germline MUC16 mutations may predispose the inherited cancer family members to lung adenocarcinomas. This study provides a clue of the cause of familial lung cancer and also warrants further mechanistic study of MUC16 gene in lung cancer.

EGFR Exon 19 Deletion is Associated With Favorable Overall Survival After First-line Gefitinib Therapy in Advanced Non–Small Cell Lung Cancer Patients

2016 ◽  
pp. 1 ◽  
Author(s):  
Yong Won Choi ◽  
So Yeon Jeon ◽  
Geum Sook Jeong ◽  
Hyun Woo Lee ◽  
Seong Hyun Jeong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Overall Survival ◽  
Small Cell Lung Cancer ◽  
Cancer Patients ◽  
Small Cell ◽  
Small Cell Lung ◽  
First Line ◽  
Lung Cancer Patients ◽  
Exon 19 Deletion ◽  
Exon 19

Better survival with EGFR exon 19 than exon 21 mutations in gefitinib-treated non-small cell lung cancer patients is due to differential inhibition of downstream signals

2008 ◽  
Vol 265 (2) ◽  
pp. 307-317 ◽  
Author(s):  
Jian-quan Zhu ◽  
Wen-zhao Zhong ◽  
Guo-chun Zhang ◽  
Rong Li ◽  
Xu-chao Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cancer Patients ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Differential Inhibition ◽  
Small Cell Lung ◽  
Lung Cancer Patients ◽  
Exon 19

scholarly journals P1.03-005 High Resolution Metabolomics in Discovering Plasma Biomarkers of Lung Cancer Patients with EGFR Common Mutations (Exon 19 or 21)

2017 ◽  
Vol 12 (1) ◽  
pp. S544-S545
Author(s):  
Sung Yong Lee ◽  
Kyung Ho Kang ◽  
Aryo D. Pamungkas ◽  
Youngja Park
Keyword(s):  
Lung Cancer ◽  
High Resolution ◽  
Cancer Patients ◽  
Plasma Biomarkers ◽  
Lung Cancer Patients ◽  
High Resolution Metabolomics ◽  
Exon 19
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