|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
This finding could possibly be explained by the hypothesis that immune responses to the mutated neo-antigens derived from T790M might prevent the emergence of tumor cell variants with the T790M resistance mutation in NSCLC patients during EGFR-TKI treatment.
|
24223798 |
2013 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
<i>EGFR</i> T790M Detection in Circulating Tumor DNA from Non-small Cell Lung Cancer Patients Using the PNA-LNA Clamp Method.
|
28476851 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In these gefitinib-refractory tumors, T790M developed in 93% (14 of 15) of tumors without MET gene CNGs, in 80% (4 of 5) of tumors with moderate MET gene CNGs (<4-fold), and in only 8% (1 of 13) of tumors with MET amplification (≥4-fold).
|
21062933 |
2010 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
However, the levels of the EGFR exon 19 deletion driver mutation and the T790M resistance mutation in the circulating tumor DNA continued to rise and the patient died from progressive disease 6 weeks after commencement of combination therapy.
|
28843359 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
[<sup>18</sup> F]FEWZ is the first evidence of a radiolabeled third generation anilinopyrimidine-derived tyrosine kinase inhibitor targeting T790M mutation bearing tumours in vivo.
|
31132309 |
2019 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
We hypothesized that treatment with cabozantinib plus erlotinib in <i>EGFR</i> mutation-positive NSCLC following progression on EGFR TKI therapy may allow tumors to overcome this resistance or restore sensitivity to therapy regardless of T790M status.
|
30915273 |
2019 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Our review provides an overview of various commonly used platforms for detecting EGFR T790M mutation in tumor tissue and plasma.
|
29246024 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
T790M was detected in the tumor samples of 23 patients, the blood samples of two patients, and both the tumor and blood samples of five patients.
|
30920616 |
2019 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In this clinical scenario, the tumor may respond transiently to reversible first-generation EGFR inhibitors (gefitinib or erlotinib), but evolving mechanisms of on-target resistance-in clinical specimens and preclinical systems-indicate that EGFR C797S along with EGFR T790M can evolve.
|
31377341 |
2019 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
There is limited information available concerning the prevalence of primary T790M mutations in patients with metastatic NSCLC tumors before treatment with EGFR-TKIs.
|
24789720 |
2014 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Noninvasive monitoring of the predominance of tumors harboring the secondary T790M mutation in the activating mutation in EGFR gene is necessary for precise and effective trea</span>tment of lung adenocarcinoma.
|
26768482 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The T790M mutation was detected more frequently in patients with a larger tumor size (P = 0.019) and those with common EGFR-activating mutations (P = 0.022), as compared with the others.
|
25882755 |
2015 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Especially, compound 6e not only presented strong antiproliferative activities against the tested four tumor cell lines (IC<sub>50</sub> of 1.35, 8.83, 5.53 and 6.08 μM, respectively) which expressed wild type or L858R/T790M double mutant epidermal growth factor receptor (EGFR), but also showed potent inhibitory activity against wild type EGFR (IC<sub>50</sub> = 20.72 nM).
|
28711703 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Temporal changes of EGFR mutations and T790M levels in tumour and plasma DNA following AZD9291 treatment.
|
27393503 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The observed enhancements of tumor growth suppression in xenografts supported the reverse effect of AT-101 in NSCLC with T790M mutation, which has been found in in vitro studies before.
|
27431492 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The response rate to EGFR TKIs, the median progression-free survival (PFS) to TKIs, the percentage of EGFR-T790M TKI resistance and survival had higher trends in EGFR mutant/TP53 wild-type cases when compared to EGFR mutant/TP53 mutant tumors (all p >0.05 without statistical significance); with a significantly longer median PFS in EGFR-exon 19 deletion mutant/TP53 wild-type cancers treated with 1st generation EGFR TKIs (p=0.035).
|
28285689 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Predose tumor biopsy samples were collected from 61 patients with EGFR T790M tumors; 29 patients had no viable postdose biopsy sample because of tumor regression or insufficient tumor sample.
|
28751247 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The cobas plasma test detected the T790M mutation in 61% of tumor tissue T790M mutation-positive patients.
|
28428148 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
As a result of the 30% false-negative rate of plasma genotyping, those with T790M-negative plasma results still need a tumor</span> biopsy to determine presence or absence of T790M.
|
27354477 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Characterization of Factors Affecting the Detection Limit of EGFR p.T790M in Circulating Tumor DNA.
|
30099961 |
2018 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
This could further help avoid unnecessary tumor biopsies for T790M mutation testing.<i></i>.
|
29535126 |
2018 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here, using digital PCR assay as an alternative and noninvasive method, we examined plasma and tumor samples from patients with relapsed NSCLC to establish the inter-relationships existing among T790M mutation, activating EGFR mutations, HER2 amplification, and MET amplification.
|
26334838 |
2015 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In conclusion, addition of BEV to ERL did not enhance antitumor activity in primarily ERL-resistant tumors with T790M mutation; however, BEV+ERL enhanced antitumor activity in T790M mutation- or MET amplification-positive tumors as long as their growth remained significantly suppressed by ERL.
|
26370161 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
These landmark outcomes have been accompanied by new challenges, primarily the additional role of chemotherapy and the management of tumors with the secondary T790M mutation that confers resistance to EGFR TKIs.
|
20973798 |
2010 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Nevertheless, this advance, several unresolved issues of osimertinib should be emphasized including the molecular mechanisms of acquired resistance to osimertinib, the feasibility of testing <i>EGFR</i> T790M mutation from plasma circulating tumor DNA, its efficacy to patients with central nervous system (CNS) metastases or exon 20 mutations, its combination with other therapeutic strategies such as immune checkpoint inhibitors and its role in adjuvant therapy.
|
30174832 |
2018 |