|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Since the shortcomings of tumor tissue detection are well known, the liquid biopsy is more appropriate to track T790M status.
|
31805270 |
2020 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Discrepancies between tissue and plasma <i>EGFR</i> mutational profiles were mainly attributable to spatial and temporal tumor heterogeneity, mutation inhibition due to therapy response and drug resistance (T790M).
|
28529628 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Osimertinib has favorable efficacy in patients with NSCLC harboring T790M, detected from ctDNA with unknown tumor mutation status, in whom disease had progressed during prior EGFR-TKI therapy.
|
30189719 |
2019 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Plasma-based cfDNA analysis identified 93% of the initial EGFR activating and 85% of the EGFR T790M resistance mutations in pretreatment samples with detectable tumor DNA.
|
30279111 |
2018 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Furthermore, preclinical data suggest dacomitinib can achieve responses in tumors harboring the T790M, gatekeeper mutation, present in up to 50% of tumors that have acquired resistant to first-generation inhibitors.
|
23294134 |
2013 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
However, both resistance through a secondary T790M mutation at the gatekeeper residue and dose-limiting toxicities from wild-type (WT) EGFR inhibition ultimately limit the full potential of these therapies to control mutant EGFR-driven tumors and new therapies are urgently needed.
|
27433829 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
After progression while receiving their latest line of therapy, patients with EGFR mutation-positive advanced NSCLC provided tumor samples for mandatory central T790M testing for the study selection criteria.
|
28527899 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
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
|
|
Neoplasms
|
|
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
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
However, detection of T790M at repeat biopsy might be associated with smaller target tumour size and selection of metastatic lesions as biopsy targets.
|
28786010 |
2018 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The induction of EMT was a feature of tumors treated with gefitinib when given before pemetrexed, whereas T790M was recorded only in tumors treated with gefitinib alone.
|
27006151 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
The T790M ratio to EGFR activating mutation in tumor may correlate with the response to osimertinib, and patients with a higher T790M ratio have a longer treatment history.
|
29496249 |
2018 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
T790M mutations were detected in the pleural effusions after the tumors had acquired EGFR-TKI resistance.
|
30145590 |
2018 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
In the plasma DNA of each patient, the activating mutation found in the corresponding primary tumor and the T790M resistance mutation were quantified by BEAMing.
|
21976538 |
2011 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Insights into the role of EGFR-sensitizing mutations and acquired and de novo T790M resistance mutations followed, and differences in progression-free survival for patients with EGFR Del19- and L858R-mutated tumors treated with reversible first-generation EGF receptor tyrosine kinase inhibitors were reported.
|
25629371 |
2015 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Real-time PCR analysis showed that the right-sided tumor had an epidermal growth factor receptor (EGFR) mutation presenting as point mutation T790M in exon 20, while the left-sided tumor had a point mutation L858R in exon 21 of EGFR.
|
31426797 |
2019 |
|
rs121434569
|
|
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 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Standard treatment for cases of non-small cell lung cancer (NSCLC) exhibiting acquired drug resistance includes tumor rebiopsy, epidermal growth factor receptor (<i>EGFR</i>) mutation testing (e.g., for T790M mutations), and the subsequent administration of third-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs).
|
31124335 |
2019 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
During the EGFR-tyrosine kinase inhibitors treatment, next-generation sequencing revealed phosphatidylinositol 3-kinase/Akt/mammalian target of rapamycin pathway amplifications in tumor specimen and subsequent T790M mutation via plasma circulating tumor DNA.
|
28979143 |
2017 |
|
rs121434569
|
|
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 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
We showed a dramatic tumor response with cetuximab in an exon 19 deletion/T790M EGFR mutant lung adenocarcinoma PDX model, which suggests a role for the autocrine feedback loop in the mutant EGFR signaling pathway.
|
26926157 |
2016 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
Compared to T790M-positive tumors, T790M-negative tumors</span> showed relatively</span> high tumor mutation burden and shorter survival, suggesting T790M-negative patients as a potential candidate for immune checkpoint inhibitors.
|
29110836 |
2017 |
|
rs121434569
|
|
Neoplasms
|
|
0.100 |
GeneticVariation
|
BEFREE |
A diagnostic tool for unambiguous identification of T790M-mutated minor tumor clones is now available enabling optimized therapy.
|
24517913 |
2014 |
|
rs121434569
|
|
Neoplasms
|
|
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 |
|
rs121434569
|
|
Neoplasms
|
|
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 |