rs121434569
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0.100 |
GeneticVariation |
BEFREE |
Clinical resistance to gefitinib, an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI), in patients with lung cancer has been linked to acquisition of the T790M resistance mutation in activated EGFR or amplification of MET.
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23592446 |
2013 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In preclinical studies, afatinib not only inhibited the growth of models with common activating EGFR mutations, but was also active in lung cancer models harboring wild-type EGFR or the EGFR L858R/T790M double mutant.
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23664448 |
2013 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In EGFR mutant lung cancer, modeling of acquired resistance (AR) with drug-sensitive cell lines has identified clinically relevant EGFR tyrosine kinase inhibitor (TKI) resistance mechanisms such as the second-site mutation, EGFR T790M, amplification of the gene encoding an alternative kinase, MET, and epithelial-mesenchymal transition (EMT).
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23733853 |
2013 |
rs121434569
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|
|
0.100 |
GeneticVariation |
BEFREE |
EGFR-mutated lung cancer with T790M-acquired resistance in the brain and histologic transformation in the lung.
|
24029120 |
2013 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In conclusion, a low gefitinib dose caused tumors to become drug-resistant prior to acquisition of the T790M mutation or MET amplification in EGFR-mutated models of lung cancer.
|
24033722 |
2013 |
rs121434569
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|
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0.100 |
GeneticVariation |
BEFREE |
Serial plasma genotyping of EGFR-mutant lung cancer on erlotinib demonstrated pretreatment detection of EGFR mutations, complete plasma response in most cases, and increasing levels of EGFR T790M emerging before objective progression.
|
24429876 |
2014 |
rs121434569
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|
|
0.100 |
GeneticVariation |
BEFREE |
A patient with metastatic lung adenocarcinoma harboring concurrent EGFR L858R, EGFR germline T790M, and PIK3CA mutations: the challenge of interpreting results of comprehensive mutational testing in lung cancer.
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24453288 |
2014 |
rs121434569
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|
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0.100 |
GeneticVariation |
BEFREE |
Two percent of all pre-treatment EGFR-mutant lung cancers harbored an EGFR T790M mutation.
|
24478319 |
2014 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Germline T790M mutations result in a unique hereditary lung cancer syndrome that targets never smokers, with a preliminary estimate of 31% risk for lung cancer in never smoker carriers, and this risk may be lower for heavy smokers.
|
24736066 |
2014 |
rs121434569
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|
0.100 |
GeneticVariation |
BEFREE |
A preexisting EGFR T790M mutation was noted in 25% of patients with EGFR-mutant lung cancer.
|
24737599 |
2014 |
rs121434569
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|
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0.100 |
GeneticVariation |
BEFREE |
AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer.
|
24893891 |
2014 |
rs121434569
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0.100 |
GeneticVariation |
BEFREE |
We identify mammalian target of rapamycin (mTOR) as potentially valuable target for EGFR mutant lung cancer. mTOR is activated in human lung cancers with EGFR mutations, and this increases with acquisition of T790M mutation.
|
24931608 |
2014 |
rs121434569
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0.100 |
GeneticVariation |
BEFREE |
Dual inhibition of EGFR with afatinib and cetuximab in kinase inhibitor-resistant EGFR-mutant lung cancer with and without T790M mutations.
|
25074459 |
2014 |
rs121434569
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0.100 |
GeneticVariation |
BEFREE |
In conclusion, the combination of new generation EGFR TKIs and SAHA may be a new strategy to overcome the acquired resistance to EGFR TKIs in T790M mutant lung cancer.
|
25382705 |
2015 |
rs121434569
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|
|
0.100 |
GeneticVariation |
BEFREE |
The clinical features of EGFR T790M-mutant lung cancer were similar to those of sensitive EGFR-mutant lung cancer, except for the overrepresentation of never-smokers and brain metastasis.
|
25450875 |
2015 |
rs121434569
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0.100 |
GeneticVariation |
BEFREE |
We investigated the effect of CK2 inhibition in lung cancer cells with T790M-mediated resistance to the EGFR-TK inhibitor.
|
25486409 |
2014 |
rs121434569
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0.100 |
GeneticVariation |
BEFREE |
AZD9291 was highly active in patients with lung cancer with the EGFR T790M mutation who had had disease progression during prior therapy with EGFR tyrosine kinase inhibitors.
|
25923549 |
2015 |
rs121434569
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|
0.100 |
GeneticVariation |
BEFREE |
This report documents that half of T790M-positive EGFR-mutant lung cancers treated with rociletinib are T790-wild-type upon progression, suggesting that T790-wild-type clones can emerge as the dominant source of resistance.
|
25934077 |
2015 |
rs121434569
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|
|
0.100 |
GeneticVariation |
BEFREE |
Although this class of mutant-selective EGFR inhibitors is effective clinically in lung cancer patients harboring EGFR(T790M), prior preclinical studies demonstrate that acquired resistance can occur through genomic alterations that activate ERK1/2 signaling.
|
26036643 |
2015 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The T790M mutation in EGFR accounts for approximately half of all lung cancer cases with acquired resistance to the current clinical EGFR tyrosine kinase inhibitors.
|
26058074 |
2015 |
rs121434569
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|
|
0.100 |
GeneticVariation |
BEFREE |
Shades of T790M: Intratumor Heterogeneity in EGFR-Mutant Lung Cancer.
|
26152920 |
2015 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Our findings contrast with the observations made in lung cancer patients where the EGFR-T790M-mutation is classified as a typical "second mutation"causing resistance to TKI-therapy during ongoing anticancer therapy.
|
26267891 |
2015 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
We analyzed gene expression profiles of gefitinib-resistant PC9M2 cells that were derived from gefitinib-sensitive lung cancer PC9 cells and do not have known resistance mechanisms including EGFR mutation T790M.
|
26268703 |
2015 |
rs121434569
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|
|
0.100 |
GeneticVariation |
BEFREE |
Small cell lung cancer transformation and T790M mutation: complimentary roles in acquired resistance to kinase inhibitors in lung cancer.
|
26400668 |
2015 |
rs121434569
|
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|
0.100 |
GeneticVariation |
BEFREE |
Some of the most important lung cancer drivers are mutations in the EGFR gene, for example, the exon 19 deletions and the L858R variant that confer sensitivity to the front line drugs erlotinib and gefitinib; the acquired T790M variants confer drug resistance and a poor prognosis.
|
26522274 |
2015 |