|
rs751295137
|
|
|
0.010 |
GeneticVariation |
BEFREE |
A point mutation in the TP53 tumor suppressor gene (c.524G>A; R175H) and no epidermal growth factor receptor gene amplification were revealed on molecular genetic analysis.
|
11302659 |
2001 |
|
rs760101437
|
|
|
0.010 |
GeneticVariation |
BEFREE |
A point mutation in the TP53 tumor suppressor gene (c.524G>A; R175H) and no epidermal growth factor receptor gene amplification were revealed on molecular genetic analysis.
|
11302659 |
2001 |
|
rs765091640
|
|
|
0.010 |
GeneticVariation |
BEFREE |
A point mutation in the TP53 tumor suppressor gene (c.524G>A; R175H) and no epidermal growth factor receptor gene amplification were revealed on molecular genetic analysis.
|
11302659 |
2001 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Tumor cells from a sixth patient with a drug-sensitive EGFR mutation whose tumor progressed on adjuvant gefitinib after complete resection also contained the T790M mutation.
|
15737014 |
2005 |
|
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 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
A secondary T790M mutation of EGFR accounted for half the tumors with acquired resistance to gefitinib in Japanese patients.
|
17020982 |
2006 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
These EGFR-dependent tumors eventually become TKI resistant, and the common secondary T790M mutation accounts for half the tumors with acquired resistance to gefitinib.
|
17973572 |
2007 |
|
rs28929495
|
|
|
0.020 |
GeneticVariation |
BEFREE |
Moreover, known variants, such as epidermal growth factor receptor G719S, that were shown to mediate anticancer drug sensitivity could be detected in other than the previously reported tumor types.
|
18056464 |
2007 |
|
rs377444977
|
|
|
0.010 |
GeneticVariation |
BEFREE |
A murine in vivo xenograft model of A127T paxillin showed an increase in tumor growth, cell proliferation, and invasion.
|
18172305 |
2008 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The next challenge is to identify accurately the subgroup of patients with NSCLC whose tumours harbour EGFR T790M.
|
18513582 |
2008 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In addition, T790M was detected in a small fraction of treated lesions of 3 cases, and MET amplification was revealed in 3 treated tumors of Case 2.
|
18785203 |
2008 |
|
rs1057519847
|
|
|
0.100 |
GeneticVariation |
BEFREE |
We aim to develop a digital PCR-based method for the quantitative detection of the two common epidermal growth factor receptor (EGFR) mutations (in-frame deletion at exon 19 and L858R at exon 21) in the plasma and tumor tissues of patients suffering from non-small cell lung cancers.
|
19276259 |
2009 |
|
rs1057519848
|
|
|
0.100 |
GeneticVariation |
BEFREE |
We aim to develop a digital PCR-based method for the quantitative detection of the two common epidermal growth factor receptor (EGFR) mutations (in-frame deletion at exon 19 and L858R at exon 21) in the plasma and tumor tissues of patients suffering from non-small cell lung cancers.
|
19276259 |
2009 |
|
rs121434568
|
|
|
0.100 |
GeneticVariation |
BEFREE |
We aim to develop a digital PCR-based method for the quantitative detection of the two common epidermal growth factor receptor (EGFR) mutations (in-frame deletion at exon 19 and L858R at exon 21) in the plasma and tumor tissues of patients suffering from non-small cell lung cancers.
|
19276259 |
2009 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Both EGFR-activating and EGFR T790M were identified in 70% of patients with known tumor EGFR-activating (21 of 30) or T790M (5 of 7) mutations.
|
19351754 |
2009 |
|
rs866211550
|
|
|
0.010 |
GeneticVariation |
BEFREE |
We found PXN polymorphisms including nonsynonymous ones but no PXN amplification and only 1/159 (<1%) somatic tumor mutation F416L.
|
19353596 |
2009 |
|
rs1057519847
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In 10 patients, 5 patients had a deletion in exon 19 and another 5 did L858R mutation in exon 21 of EGFR in gefitinib pre-treatment tumors.
|
19589612 |
2010 |
|
rs1057519848
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In 10 patients, 5 patients had a deletion in exon 19 and another 5 did L858R mutation in exon 21 of EGFR in gefitinib pre-treatment tumors.
|
19589612 |
2010 |
|
rs121434568
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In 10 patients, 5 patients had a deletion in exon 19 and another 5 did L858R mutation in exon 21 of EGFR in gefitinib pre-treatment tumors.
|
19589612 |
2010 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Neither MET gene amplification nor HGF were observed in their gefitinib-resistant tumors without T790M mutation.
|
19589612 |
2010 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Importantly, we observed that the combination of PI3K-mTOR and MEK inhibitors effectively shrunk tumors in a transgenic and xenograft model of EGFR T790M-L858R cancers.
|
19850869 |
2009 |
|
rs1169803481
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Tumor status was found significantly associated with HER2 I655V as well as with two previously studied markers in the thyroid hormone receptor A and estrogen receptor 1 (ESR1) genes (D17S2189 and D6S440, respectively).
|
19860576 |
2009 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Combined treatment of T790M-mutant tumor cells with BIBW-2992 and the phosphoinositide-3-kinase/mammalian target of rapamycin inhibitor PI-103 led to synergistic induction of apoptosis.
|
20103621 |
2010 |
|
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Irreversible EGFR inhibitors, including PF00299804, are effective in vitro and in vivo against EGFR mutant tumors that contain EGFR T790M and are currently under clinical development.
|
20118985 |
2010 |
|
rs1057519847
|
|
|
0.100 |
GeneticVariation |
BEFREE |
As the L858R mutation within exon 21 of the EGFR gene was identified in the middle-lobe tumor and the subcarinal node but not in the upper-lobe tumor, we diagnosed as double primary cancers.
|
20307913 |
2010 |