rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
In conclusion, the real-world clinical adoption of the combination approach with both tissue rebiopsy and liquid biopsy for T790M genotyping may provide significant benefits to patients who have developed PD after first-generation TKI treatments.
|
30927306 |
2019 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The presence of an EGFRm (excluding T790M) was associated with untreated or progressive disease, p = 0.04.
|
31027703 |
2019 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
The incidence of <i>EGFR</i> T790M tended to be higher among patients with CNS PD than in those without CNS PD, although the difference was not statistically significant (66.7% <i>vs.</i> 40.4%; P=0.23).
|
31179076 |
2019 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Total duration of EGFR-TKI treatment before rebiopsy, TKI-free interval, EGFR-TKI treatment history immediately before rebiopsy, continuation of initial EGFR-TKI beyond progressive disease, progression-free survival after initial TKI treatment, and rebiopsy site (other than fluid samples) significantly influenced T790M status.
|
28866043 |
2018 |
rs121434569
|
|
|
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
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Osimertinib was approved by the US Food & Drug Administration in November 2015 for patients whose tumors exhibited T790M mutation and for those with progressive disease on other EGFR TKIs.
|
28367058 |
2017 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
A total of 4 of the 5 patients with a history of T790M positivity based on plasma DNA levels had PD.
|
28588734 |
2017 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
T790M was detected in 14/29 patients (48.3%) with a partial response to afatinib, 1/4 patients (25%) with stable disease, and 1/4 patients (25%) with progressive disease as the best response.
|
28978102 |
2017 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Almost half of the T790M ctDNA positive patients were identified at a median time of 2.2 months prior to clinically progressive disease (PD).
|
26867973 |
2016 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
Dividing into four periods (before PD, at PD, at discontinuation of EGFR-TKI and subsequently), T790M was detected in 10, 19, 24 and 27% of patients, respectively.
|
26577492 |
2016 |
rs121434569
|
|
|
0.100 |
GeneticVariation |
BEFREE |
EGFR T790M was identified from plasma DNA in 54% (15 of 28) of patients with prior clinical response to gefitinib/erlotinib, 29% (4 of 14) with prior stable disease, and in 0% (0 of 12) that had primary progressive disease or were untreated with gefitinib/erlotinib.
|
19351754 |
2009 |
rs113488022
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Additionally, the presence of BRAFV600E was tested in peripheral mononuclear blood cells (PBMCs) as well as brain biopsies from LCH-ND patients, and the response to BRAF-V600E inhibitor was evaluated in 4 patients with progressive disease.
|
29624648 |
2018 |
rs121913377
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Additionally, the presence of BRAFV600E was tested in peripheral mononuclear blood cells (PBMCs) as well as brain biopsies from LCH-ND patients, and the response to BRAF-V600E inhibitor was evaluated in 4 patients with progressive disease.
|
29624648 |
2018 |
rs113488022
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Quantitative imaging analysis revealed progressive disease and a lack of response to conventional chemotherapy in most patients with BRAF V600E PLGG.
|
28727518 |
2017 |
rs121913377
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Quantitative imaging analysis revealed progressive disease and a lack of response to conventional chemotherapy in most patients with BRAF V600E PLGG.
|
28727518 |
2017 |
rs113488022
|
|
|
0.050 |
GeneticVariation |
BEFREE |
In the cohort of WDTC with distant metastasis, patients with wild-type BRAF and TERT promoter had a significantly higher response rate after radioiodine therapy (p = 0.024), whereas the BRAF V600E mutation was significantly correlated with progressive disease (p = 0.025).
|
26857243 |
2016 |
rs121913377
|
|
|
0.050 |
GeneticVariation |
BEFREE |
In the cohort of WDTC with distant metastasis, patients with wild-type BRAF and TERT promoter had a significantly higher response rate after radioiodine therapy (p = 0.024), whereas the BRAF V600E mutation was significantly correlated with progressive disease (p = 0.025).
|
26857243 |
2016 |
rs113488022
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Vemurafenib induces tumour regression in most patients with BRAF(V600E)-mutant melanoma; eventually, most experience progressive disease (PD).
|
25980594 |
2015 |
rs121913377
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Vemurafenib induces tumour regression in most patients with BRAF(V600E)-mutant melanoma; eventually, most experience progressive disease (PD).
|
25980594 |
2015 |
rs113488022
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Six had V600E-positive tumours (n=4 had PD; n=1 had SD; n=1 unevaluable for response), and 11 had tumours containing wild-type BRAF (n=9 PD; n=1 SD; n=1 unevaluable for response).
|
16880785 |
2006 |
rs121913377
|
|
|
0.050 |
GeneticVariation |
BEFREE |
Six had V600E-positive tumours (n=4 had PD; n=1 had SD; n=1 unevaluable for response), and 11 had tumours containing wild-type BRAF (n=9 PD; n=1 SD; n=1 unevaluable for response).
|
16880785 |
2006 |
rs1057519847
|
|
|
0.040 |
GeneticVariation |
BEFREE |
Here, we conducted a retrospective study to assess 375 patients whose initial biopsy indicated a TKI-sensitizing mutation (either EGFR 19del or L858R) and who developed PD after treatment with first-generation TKIs, and assayed for T790M status.
|
30927306 |
2019 |
rs1057519848
|
|
|
0.040 |
GeneticVariation |
BEFREE |
Here, we conducted a retrospective study to assess 375 patients whose initial biopsy indicated a TKI-sensitizing mutation (either EGFR 19del or L858R) and who developed PD after treatment with first-generation TKIs, and assayed for T790M status.
|
30927306 |
2019 |
rs121434568
|
|
|
0.040 |
GeneticVariation |
BEFREE |
Here, we conducted a retrospective study to assess 375 patients whose initial biopsy indicated a TKI-sensitizing mutation (either EGFR 19del or L858R) and who developed PD after treatment with first-generation TKIs, and assayed for T790M status.
|
30927306 |
2019 |
rs1057519847
|
|
|
0.040 |
GeneticVariation |
BEFREE |
Patients with EGFR-activating mutations (del19 and L858R) that progressed using first-line gefitinib treatment were enrolled and treated with gefitinib beyond PD plus pemetrexed 500 mg/m<sup>2</sup> q3w.
|
30268482 |
2018 |