Variant Gene Risk Allele Score vda Association Type Original DB Sentence supporting the association PMID PMID Year
dbSNP: rs776375114
rs776375114
0.010 GeneticVariation BEFREE Four novel mutations (E709K, V765G, Ins770G, and G1022S) and one mutation well-known in lung cancer (L858R) were identified in six HNSCC samples (7%), but we could not find any mutations in the extracellular domain of EGFR, such as EGFRvIII, in this study. 19726454

2009

dbSNP: rs1057519847
rs1057519847
0.100 GeneticVariation BEFREE Denaturing capillary electrophoresis for automated detection of L858R mutation in exon 21 of the epidermal growth factor receptor gene in prediction of the outcome of lung cancer therapy. 20574956

2010

dbSNP: rs1057519848
rs1057519848
0.100 GeneticVariation BEFREE Denaturing capillary electrophoresis for automated detection of L858R mutation in exon 21 of the epidermal growth factor receptor gene in prediction of the outcome of lung cancer therapy. 20574956

2010

dbSNP: rs121434568
rs121434568
0.100 GeneticVariation BEFREE Denaturing capillary electrophoresis for automated detection of L858R mutation in exon 21 of the epidermal growth factor receptor gene in prediction of the outcome of lung cancer therapy. 20574956

2010

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Reciprocal and complementary role of MET amplification and EGFR T790M mutation in acquired resistance to kinase inhibitors in lung cancer. 21062933

2010

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE It will be clinically valuable to investigate the involvement of HGF-MET-mediated signaling in de novo and acquired resistance to irreversible EGFR-TKIs in lung cancer harboring T790M mutation in EGFR. 20008840

2010

dbSNP: rs104886026
rs104886026
0.010 GeneticVariation BEFREE Recently, to identify genetic factors that modify lung cancer risk, CHRNA5 non-synonymous variant amino acid position 398 (D398N) was identified. 19577767

2010

dbSNP: rs1057519847
rs1057519847
0.100 GeneticVariation BEFREE The loop-hybrid mobility shift assay (LH-MSA) was previously developed for the rapid detection of the EGFR mutation L858R for predicting clinical responses to gefitinib in lung cancer. 21741959

2011

dbSNP: rs1057519848
rs1057519848
0.100 GeneticVariation BEFREE The loop-hybrid mobility shift assay (LH-MSA) was previously developed for the rapid detection of the EGFR mutation L858R for predicting clinical responses to gefitinib in lung cancer. 21741959

2011

dbSNP: rs121434568
rs121434568
0.100 GeneticVariation BEFREE The loop-hybrid mobility shift assay (LH-MSA) was previously developed for the rapid detection of the EGFR mutation L858R for predicting clinical responses to gefitinib in lung cancer. 21741959

2011

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Rebiopsy of lung cancer patients with acquired resistance to EGFR inhibitors and enhanced detection of the T790M mutation using a locked nucleic acid-based assay. 21248300

2011

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Acquired resistance to EGFR tyrosine kinase inhibitors in EGFR-mutant lung cancer: distinct natural history of patients with tumors harboring the T790M mutation. 21135146

2011

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Detection of low-level EGFR T790M mutation in lung cancer tissues. 21635547

2011

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE High-level HGF expression was detected more frequently than EGFR T790M secondary mutation or MET amplification in tumors with intrinsic and acquired EGFR-TKI resistance in EGFR mutant lung cancer in Japanese patients. 22052230

2011

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE We found that EMT developed in a lung cancer patient who had an acquired resistance to erlotinib while there were no known resistant mechanisms such as T790M and MET amplification. 21168239

2011

dbSNP: rs397517132
rs397517132
0.050 GeneticVariation BEFREE The incidence of BRAF mutations other than V600E is significantly higher in lung cancer than in melanoma. 21483012

2011

dbSNP: rs770443325
rs770443325
0.010 GeneticVariation BEFREE However, the frequency of the HIF1A C1772T variant allele was significantly higher in lung cancer patients with TP53 LOH (P = 0.015). 21435097

2011

dbSNP: rs1057519847
rs1057519847
0.100 GeneticVariation BEFREE Approximately 50% of lung cancer patients with epidermal growth factor receptor (EGFR)-mutations (deletion in exon 19 or L858R) who develop acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) reportedly carry a secondary EGFR T790M mutation. 22899358

2012

dbSNP: rs1057519847
rs1057519847
0.100 GeneticVariation BEFREE A total of 50 lung cancer patients' tumor tissues were analyzed, and two frequent mutations associated with therapeutic efficiency of lung cancer were identified, including deletion of exon 19 (8/50) and L858R point mutation in exon 21 (12/50). 22901298

2012

dbSNP: rs1057519848
rs1057519848
0.100 GeneticVariation BEFREE A total of 50 lung cancer patients' tumor tissues were analyzed, and two frequent mutations associated with therapeutic efficiency of lung cancer were identified, including deletion of exon 19 (8/50) and L858R point mutation in exon 21 (12/50). 22901298

2012

dbSNP: rs1057519848
rs1057519848
0.100 GeneticVariation BEFREE Approximately 50% of lung cancer patients with epidermal growth factor receptor (EGFR)-mutations (deletion in exon 19 or L858R) who develop acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) reportedly carry a secondary EGFR T790M mutation. 22899358

2012

dbSNP: rs121434568
rs121434568
0.100 GeneticVariation BEFREE A total of 50 lung cancer patients' tumor tissues were analyzed, and two frequent mutations associated with therapeutic efficiency of lung cancer were identified, including deletion of exon 19 (8/50) and L858R point mutation in exon 21 (12/50). 22901298

2012

dbSNP: rs121434568
rs121434568
0.100 GeneticVariation BEFREE Approximately 50% of lung cancer patients with epidermal growth factor receptor (EGFR)-mutations (deletion in exon 19 or L858R) who develop acquired resistance to EGFR tyrosine kinase inhibitors (TKIs) reportedly carry a secondary EGFR T790M mutation. 22899358

2012

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE Here, we report increased activation of AXL and evidence for epithelial-to-mesenchymal transition (EMT) in multiple in vitro and in vivo EGFR-mutant lung cancer models with acquired resistance to erlotinib in the absence of the EGFR p.Thr790Met alteration or MET activation. 22751098

2012

dbSNP: rs121434569
rs121434569
0.100 GeneticVariation BEFREE The three major clinically relevant mechanisms of acquired resistance to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) in EGFR mutant lung cancer are a second mutation in the EGFR gene (T790M), Met amplification, and increased expression of hepatocyte growth factor (HGF). 22592212

2012