rs121434569
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Drug resistance becomes inevitable due to the emergence of the second-site EGFR T790M mutation within exon 20, MET and HER2 amplification, small cell histologic transformation and rare secondary BRAF mutations.
|
31132355 |
2019 |
rs121434569
|
|
|
0.050 |
GeneticVariation |
BEFREE |
In 23 EGFR mutant cases with acquired resistance to targeted therapy, plasma NGS detected potential resistance mechanisms, including EGFR T790M and C797S mutations and ERBB2 amplification.
|
30891595 |
2019 |
rs121434569
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Several mechanisms have been identified, including EGFR T790M mutation and HER2 amplification.
|
30295016 |
2018 |
rs121434569
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Cancerous cells resist EGFR tyrosine kinase inhibitors (TKIs) through various mechanisms, the most commonly reported ones are the T790M mutation and HER2 amplification.
|
28754471 |
2017 |
rs121434569
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Considering that osimertinib can lead to enhanced HER-2 expression on cell surface and HER-2 overexpression is a mechanism of resistance to osimertinib, this study was addressed to investigate the potential of combining osimertinib with trastuzumab emtansine (T-DM1) in order to improve the efficacy of osimertinib and delay or overcome resistance in NSCLC cell lines with EGFR activating mutation and with T790M mutation or HER-2 amplification.
|
29202823 |
2017 |
rs121913471
|
|
|
0.030 |
GeneticVariation |
BEFREE |
In an independent data set, 2 of 9 (22.2%) ERBB2/HER2-negative BrCa switched to ERBB2/HER2-positive with 1 BrM acquiring ERBB2/HER2 amplification and the other showing metastatic enrichment of the activating V777L ERBB2/HER2 mutation.
|
27926948 |
2017 |
rs121913471
|
|
|
0.030 |
GeneticVariation |
BEFREE |
This is the first report to show that HER2 V777L is coincident with HER2-amplification in breast cancers that have developed trastuzumab resistance.
|
27900589 |
2017 |
rs121913471
|
|
|
0.030 |
GeneticVariation |
BEFREE |
ERBB2/HER2 alterations were identified in 5 pmucBC (23 %): ERBB2 amplification was found in 3 of 3 cases (100 %) that were HER2+ by IHC and/or FISH; 1 pmucBC was negative for HER2 overexpression by IHC, but positive for amplification by CGP; and 2 pmucBC harbored the ERBB2 substitutions D769Y and V777L (one sample also featured ERBB2 amplification).
|
26762307 |
2016 |
rs1057519816
|
|
|
0.020 |
GeneticVariation |
BEFREE |
Clinically, S310F is most frequent among HER2 extracellular domain mutations and patients with the S310F mutation without HER2 amplification responded to trastuzumab with or without the pertuzumab combination.
|
31635022 |
2019 |
rs1057519816
|
|
|
0.020 |
GeneticVariation |
BEFREE |
The NGS revealed HER-2 amplification as well as an activating mutation S310F and PDX models tested several drugs finding that afatinib was the optimal agent with notable efficacy and well tolerance among 6 regimens.
|
30307354 |
2019 |
rs1057519847
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Altogether, NGS detected 12 additional variants, including six KRAS mutations, one BRAF mutation, one RET fusion, one MET amplification concurrent with EGFR L858R, one KRAS amplification together with EGFR 19del, and one ERBB2 amplification.
|
30885850 |
2019 |
rs1057519848
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Altogether, NGS detected 12 additional variants, including six KRAS mutations, one BRAF mutation, one RET fusion, one MET amplification concurrent with EGFR L858R, one KRAS amplification together with EGFR 19del, and one ERBB2 amplification.
|
30885850 |
2019 |
rs1057519861
|
|
|
0.010 |
GeneticVariation |
BEFREE |
In 23 EGFR mutant cases with acquired resistance to targeted therapy, plasma NGS detected potential resistance mechanisms, including EGFR T790M and C797S mutations and ERBB2 amplification.
|
30891595 |
2019 |
rs121434568
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Altogether, NGS detected 12 additional variants, including six KRAS mutations, one BRAF mutation, one RET fusion, one MET amplification concurrent with EGFR L858R, one KRAS amplification together with EGFR 19del, and one ERBB2 amplification.
|
30885850 |
2019 |
rs772092699
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Drug resistance becomes inevitable due to the emergence of the second-site EGFR T790M mutation within exon 20, MET and HER2 amplification, small cell histologic transformation and rare secondary BRAF mutations.
|
31132355 |
2019 |
rs121909644
|
|
|
0.010 |
GeneticVariation |
BEFREE |
ERBB2/HER2 alterations were identified in 5 pmucBC (23 %): ERBB2 amplification was found in 3 of 3 cases (100 %) that were HER2+ by IHC and/or FISH; 1 pmucBC was negative for HER2 overexpression by IHC, but positive for amplification by CGP; and 2 pmucBC harbored the ERBB2 substitutions D769Y and V777L (one sample also featured ERBB2 amplification).
|
26762307 |
2016 |
rs121913468
|
|
|
0.010 |
GeneticVariation |
BEFREE |
ERBB2/HER2 alterations were identified in 5 pmucBC (23 %): ERBB2 amplification was found in 3 of 3 cases (100 %) that were HER2+ by IHC and/or FISH; 1 pmucBC was negative for HER2 overexpression by IHC, but positive for amplification by CGP; and 2 pmucBC harbored the ERBB2 substitutions D769Y and V777L (one sample also featured ERBB2 amplification).
|
26762307 |
2016 |
rs149860212
|
|
|
0.010 |
GeneticVariation |
BEFREE |
ERBB2/HER2 alterations were identified in 5 pmucBC (23 %): ERBB2 amplification was found in 3 of 3 cases (100 %) that were HER2+ by IHC and/or FISH; 1 pmucBC was negative for HER2 overexpression by IHC, but positive for amplification by CGP; and 2 pmucBC harbored the ERBB2 substitutions D769Y and V777L (one sample also featured ERBB2 amplification).
|
26762307 |
2016 |
rs113488022
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Immunohistochemistry is highly specific for p.V600E, and could be used as a first-line method, as is currently performed for HER2 amplification detection.
|
23159108 |
2013 |
rs121913377
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Immunohistochemistry is highly specific for p.V600E, and could be used as a first-line method, as is currently performed for HER2 amplification detection.
|
23159108 |
2013 |
rs780881510
|
|
|
0.010 |
GeneticVariation |
BEFREE |
Breast carcinoma cells with HER-2 gene amplification (21 MT-1 cells) and normal mammary epithelial cells without HER-2 gene amplification from the same patient (H16N-2 cells) were infected with pCMV-dn3 and assessed for HER-2/ HER-3 receptor tyrosine phosphorylation, p85PI 3-kinase and SHC protein activation, growth factor-dependent and -independent proliferation, and transformed growth in culture.
|
10768865 |
2000 |