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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Detection of low-level EGFR T790M mutation in lung cancer tissues.
|
21635547 |
2011 |
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 |
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 |
rs397517132
|
|
|
0.050 |
GeneticVariation |
BEFREE |
The incidence of BRAF mutations other than V600E is significantly higher in lung cancer than in melanoma.
|
21483012 |
2011 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |
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 |