|
Adenocarcinoma of lung (disorder)
|
|
0.100 |
GeneticVariation
|
BEFREE |
Herein, we report the first case of a patient with EGFR-mutant lung adenocarcinoma with a long-lasting response to first-line erlotinib treatment who acquired resistance to treatment because of acquisition of both EGFR-T790M mutation and "high-grade" large cell neuroendocrine transformation.
|
28778263 |
2017 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Here, we sought to determine the feasibility of tumor rebiopsy and to more accurately assess the prevalence of the T790M using a highly sensitive locked nucleic acid (LNA) PCR/sequencing assay.MET amplification was also analyzed.
|
21248300 |
2011 |
|
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 |
|
Malignant neoplasm of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
BIM Deletion Polymorphism Confers Resistance to Osimertinib in EGFR T790M Lung Cancer: a Case Report and Literature Review.
|
29907952 |
2018 |
|
Non-Small Cell Lung Carcinoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
Intermittent pulsatile dacomitinib is safe and relatively well tolerated but is not effective in patients that harbor EGFR T790M or in unselected patients with non-small cell lung cancer.
|
29191595 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
|
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 |
|
Primary malignant neoplasm of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
Different resistance mechanisms, especially, T790M secondary acquired point mutation and in some cases amplification of cMET, have been a major setback for the lung cancer therapies.
|
28362115 |
2017 |
|
Primary malignant neoplasm of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
Monitoring T790M with plasma DNA using MBP-QP reflects the clinical course of lung cancer patients treated with EGFR-TKI.
|
26577492 |
2016 |
|
Non-Small Cell Lung Carcinoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
We hypothesized that plasma-based EGFR mutation analysis for NSCLC may be feasible for monitoring treatment response to EGFR TKIs and also predict drug resistance.Clinically relevant mutations including exon 19 deletion (ex19del), L858R and T790M were analyzed using droplet digital PCR (ddPCR) in longitudinally collected plasma samples (n = 367) from 81 NSCLC patients treated with EGFR TKI.
|
26755650 |
2016 |
|
Primary malignant neoplasm of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
AZD9291, an irreversible EGFR TKI, overcomes T790M-mediated resistance to EGFR inhibitors in lung cancer.
|
24893891 |
2014 |
|
Malignant neoplasm of lung
|
|
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).
|
23733853 |
2013 |
|
Non-Small Cell Lung Carcinoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
A twenty patient trial (NSCLC cohort) (cetuximab-based regimen) included two participants with EGFR TKI-resistant mutations ((i) exon 20 D770>GY; and (ii) exon 19 LREA plus exon 20 T790M mutations).
|
25760241 |
2015 |
|
Small cell carcinoma of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
Our case report uncovered the underling relationship between SCLC transformation and the T790M mutation, and the fluid biopsy approach may help overcome the problem of heterogeneity in acquired resistance to EGFR-tyrosine kinase inhibitors.
|
28723866 |
2017 |
|
Carcinoma of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
Different resistance mechanisms, especially, T790M secondary acquired point mutation and in some cases amplification of cMET, have been a major setback for the lung cancer therapies.
|
28362115 |
2017 |
|
Malignant neoplasm of lung
|
|
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 |
|
Adenocarcinoma of lung (disorder)
|
|
0.100 |
GeneticVariation
|
BEFREE |
This study aimed to assess the total cost of care of a urine-testing strategy (UTS) versus a tissue-testing strategy (TTS) for T790M detection, in patients with EGFR-mutation positive lung adenocarcinoma and progression on prior TKI therapy.
|
28676213 |
2017 |
|
Non-Small Cell Lung Carcinoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
Osimertinib showed greater treatment benefit for patients with NSCLC with EGFR mutation than EGFR-TKIs/chemotherapy, especially for T790M mutation-positive patients.
|
31651902 |
2019 |
|
Malignant neoplasm of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
Osimertinib or Platinum-Pemetrexed in EGFR T790M-Positive Lung Cancer.
|
27959700 |
2017 |
|
Primary malignant neoplasm of lung
|
|
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 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Finally, in a 'double resistant' EGFR T790M-positive, high c-Met model (cell line HCC827-GR-T790M), the EGFR TKIs erlotinib, afatinib, and rociletinib, as well as tepotinib as a single agent or in combination with erlotinib or afatinib, slowed tumor growth, but only tepotinib in combination with rociletinib induced complete tumor regression.
|
28469968 |
2017 |
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The presence of the EGFR (epidermal growth factor receptor) T790M mutation in tumor tissue or body fluids from patients treated with EGFR tyrosine kinase inhibitors may indicate the onset of resistance to treatment.
|
21325655 |
2011 |
|
Small cell carcinoma of lung
|
|
0.100 |
GeneticVariation
|
BEFREE |
Two T790-wild-type cancers underwent small cell lung cancer transformation; three T790M-positive cancers acquired EGFR amplification.
|
25934077 |
2015 |
|
Non-Small Cell Lung Carcinoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
T790M germline mutations occurred in approximately 1% of non-small-cell lung cancer cases and in less than one in 7500 subjects without lung cancer.
|
24736066 |
2014 |
|
Non-Small Cell Lung Carcinoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
The third-generation EGFR tyrosine kinase inhibitor osimertinib has been approved in many countries to treat advanced NSCLC in patients with the EGFR T790M mutation.
|
29857056 |
2018 |
|
Adenocarcinoma
|
|
0.100 |
GeneticVariation
|
BEFREE |
Using histological and gene sequencing analysis, we observed that the primary adenocarcinoma acquired T790M mutation in EGFR exon 20, and a secondary sarcomatoid carcinoma developed in the vicinity.
|
28786540 |
2017 |