|
rs1057519847
|
|
|
0.800 |
GeneticVariation |
BEFREE |
These findings further characterize a mechanism by which gefitinib treatment of NSCLC harboring EGFR(L858R) leads to a dramatic response to gefitinib.
|
15492241 |
2004 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
These findings further characterize a mechanism by which gefitinib treatment of NSCLC harboring EGFR(L858R) leads to a dramatic response to gefitinib.
|
15492241 |
2004 |
|
rs121434568
|
|
|
0.800 |
GeneticVariation |
BEFREE |
These findings further characterize a mechanism by which gefitinib treatment of NSCLC harboring EGFR(L858R) leads to a dramatic response to gefitinib.
|
15492241 |
2004 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
These inhibitors also show effective inhibition of signaling by T790M-mutant EGFR and killing of NSCLC cells with the T790M mutation.
|
15897464 |
2005 |
|
rs1057519847
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Here, we show that L858R and deletion mutant EGFR proteins found in NSCLC interact with the chaperone and are sensitive to degradation following Hsp90 inhibition.
|
16024644 |
2005 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Here, we show that L858R and deletion mutant EGFR proteins found in NSCLC interact with the chaperone and are sensitive to degradation following Hsp90 inhibition.
|
16024644 |
2005 |
|
rs121434568
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Here, we show that L858R and deletion mutant EGFR proteins found in NSCLC interact with the chaperone and are sensitive to degradation following Hsp90 inhibition.
|
16024644 |
2005 |
|
rs1057519847
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Patients with NSCLC and EGFR exon 19 deletions have a longer survival following treatment with gefitinib or erlotinib compared with those with the L858R mutation.
|
16818686 |
2006 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Patients with NSCLC and EGFR exon 19 deletions have a longer survival following treatment with gefitinib or erlotinib compared with those with the L858R mutation.
|
16818686 |
2006 |
|
rs121434568
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Patients with NSCLC and EGFR exon 19 deletions have a longer survival following treatment with gefitinib or erlotinib compared with those with the L858R mutation.
|
16818686 |
2006 |
|
rs1057519847
|
|
|
0.800 |
GeneticVariation |
BEFREE |
The mutations consisted of the recurrent missense L858R and in-frame deletion delE746-A750, previously characterized as activating EGFR mutations in non-small cell lung cancer.
|
16857803 |
2006 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
The mutations consisted of the recurrent missense L858R and in-frame deletion delE746-A750, previously characterized as activating EGFR mutations in non-small cell lung cancer.
|
16857803 |
2006 |
|
rs121434568
|
|
|
0.800 |
GeneticVariation |
BEFREE |
The mutations consisted of the recurrent missense L858R and in-frame deletion delE746-A750, previously characterized as activating EGFR mutations in non-small cell lung cancer.
|
16857803 |
2006 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Our results indicate that the T790M mutation is sometimes present in a minor population of tumor cells during the development of NSCLC and suggest that the detection of small fractions of T790M mutant alleles may be useful for predicting gefitinib resistance of NSCLCs with sensitive EGFR mutations.
|
16912157 |
2006 |
|
rs1057519847
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Mutations of the epidermal growth factor receptor (EGFR), particularly deletional mutations (DEL) in exon 19 and L858R in exon 21, are reportedly correlated with clinical outcome in patients with non-small cell lung cancer (NSCLC) receiving the EGFR tyrosine kinase inhibitors gefitinib and erlotinib, suggesting that detection of EGFR mutations would have an important role in clinical decision making.
|
16938658 |
2006 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Mutations of the epidermal growth factor receptor (EGFR), particularly deletional mutations (DEL) in exon 19 and L858R in exon 21, are reportedly correlated with clinical outcome in patients with non-small cell lung cancer (NSCLC) receiving the EGFR tyrosine kinase inhibitors gefitinib and erlotinib, suggesting that detection of EGFR mutations would have an important role in clinical decision making.
|
16938658 |
2006 |
|
rs121434568
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Mutations of the epidermal growth factor receptor (EGFR), particularly deletional mutations (DEL) in exon 19 and L858R in exon 21, are reportedly correlated with clinical outcome in patients with non-small cell lung cancer (NSCLC) receiving the EGFR tyrosine kinase inhibitors gefitinib and erlotinib, suggesting that detection of EGFR mutations would have an important role in clinical decision making.
|
16938658 |
2006 |
|
rs1057519847
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exogenous expression of either the L858R point mutant or the DeltaE746-E750 deletion mutant form of EGFR in immortalized human bronchial epithelial cells, p53 WT NSCLC (A549), or p53-null NSCLC (NCI-H1299) resulted in dramatically increased sensitivity to IR.
|
17018617 |
2006 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exogenous expression of either the L858R point mutant or the DeltaE746-E750 deletion mutant form of EGFR in immortalized human bronchial epithelial cells, p53 WT NSCLC (A549), or p53-null NSCLC (NCI-H1299) resulted in dramatically increased sensitivity to IR.
|
17018617 |
2006 |
|
rs121434568
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exogenous expression of either the L858R point mutant or the DeltaE746-E750 deletion mutant form of EGFR in immortalized human bronchial epithelial cells, p53 WT NSCLC (A549), or p53-null NSCLC (NCI-H1299) resulted in dramatically increased sensitivity to IR.
|
17018617 |
2006 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The gefitinib-resistant, T790M-mutant H1975 NSCLC cell line undergoes prominent growth arrest and apoptosis when treated with the irreversible EGFR inhibitor, CL-387,785.
|
17145885 |
2006 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The detection of a small fraction of T790M-positive alleles may be useful to predict the clinical course of the gefitinib-treated non-small-cell lung cancer patients.
|
17335935 |
2007 |
|
rs2227983
|
|
|
0.050 |
GeneticVariation |
BEFREE |
We determined the genotypes for R497K and intron1 (CA) n repeat genetic polymorphisms of 70 Chinese patients with advanced non-small cell lung cancer.
|
17597605 |
2007 |
|
rs1057519847
|
|
|
0.800 |
GeneticVariation |
BEFREE |
HRMA is a precise method for detecting DEL and L858R mutations and is useful for predicting clinical outcomes in patients with advanced NSCLC treated with gefitinib.
|
17875767 |
2007 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
HRMA is a precise method for detecting DEL and L858R mutations and is useful for predicting clinical outcomes in patients with advanced NSCLC treated with gefitinib.
|
17875767 |
2007 |