|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Circulating cell-free DNA has a high degree of specificity to detect exon 19 deletions and the single-point substitution mutation L858R in non-small cell lung cancer.
|
27081078 |
2016 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Circulating tumor DNA (ctDNA) is released into the circulation by tumor cell turnover and has been shown to be detectable in urine.<b>Experimental Design:</b> We tested the hypothesis that dynamic changes in EGFR activating (exon 19del and L858R) and resistance (T790M) mutation levels detected in urine could inform tumor response within days of therapy for advanced non-small cell lung cancer (NSCLC) patients receiving osimertinib, a second-line third-generation anti-EGFR tyrosine kinase inhibitor.<b>Results:</b> Eight of nine evaluable NSCLC patients had detectable T790M-mutant DNA fragments in pretreatment baseline samples.
|
28420725 |
2017 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Clinical features of epidermal growth factor receptor (EGFR) mutations, L858R, deletions in exon 19, T790M, and insertions in exon 20, in non-small cell lung cancer (NSCLC) are well known.
|
21531810 |
2011 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Collectively, compound <b>13</b>, a novel hederagenin-NO donor hybrid with a different chemical structure from those of the current FDA-approved EGFR-targeted anti-NSCLC drugs, may be a promising lead compound for the treatment of NSCLC expressing gefitinib-resistant EGFR with a T790 M mutation or osimertinib-resistant EGFR-LTC with an L858R/T790M/C797S mutation.
|
31718182 |
2019 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Common EGFR-mutated subgroups (Del19/L858R) in advanced non-small-cell lung cancer: chasing better outcomes with tyrosine kinase inhibitors.
|
25629371 |
2015 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Common epidermal growth factor receptor (EGFR) mutations in non-small-cell lung cancer (NSCLC) predict sensitivity to EGFR tyrosine kinase inhibitors (TKIs), with exon 19 deletions being associated with better outcome compared to L858R mutations.
|
30473385 |
2019 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Compound 12k exhibited strong and selective EGFR L858R/T790M inhibitory activity (IC50 = 0.047 μM) and displayed antiproliferative effects on EGFR mutation NSCLC cell lines HCC827 (del E746_A750) and H1975 (L858R/T790M) with IC50 values of 0.007 and 0.029 μM, respectively.
|
23668441 |
2013 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Compound 23a displayed strong antiproliferative activity against the H1975 non-small cell lung cancer (NSCLC) cells bearing T790M/L858R.
|
29486953 |
2018 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Compound 8 exhibited good microsomes stabilities and pharmacokinetic properties and lower binding affinity to hERG ion channel than AZD9291 and displayed strong antiproliferative activity against the H1975 non-small cell lung cancer (NSCLC) cells bearing T790M/L858R and in vivo anticancer efficacy in a human NSCLC (H1975) xenograft mouse model.
|
28426996 |
2017 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Constitutively active EGFR mutations, including in-frame deletion in exon 19 and L858R point mutation in exon 21, contribute about 90% of all EGFR-activating mutations in NSCLC.
|
29398601 |
2018 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Distinct Benefit of Overall Survival between Patients with Non-Small-Cell Lung Cancer Harboring EGFR Exon 19 Deletion and Exon 21 L858R Substitution.
|
28110331 |
2017 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
E746-A750 deletion and L858R mutations were screened in 50 unselected NSCLC formalin-fixed paraffin-embedded (FFPE) tissue samples.
|
30092812 |
2018 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
EGFR tyrosine kinase inhibitors versus chemotherapy as first-line therapy for non-small cell lung cancer patients with the L858R point mutation.
|
27811976 |
2016 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
EGFR)-targeted drugs have been the first-line treatment for patients with <i>EGFR</i>-mutant non-small cell lung cancer (NSCLC), especially exon 19 deletions and L858R mutation in exon 21.
|
31686847 |
2019 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Eight patients received an EGFR TKI: three cases with G719X plus another mutation had partial responses (PRs) to erlotinib; of three cases with L858R plus another mutation, two displayed PRs and one (with EGFR-L858R+A871G) progressive disease (PD) to erlotinib; one NSCLC with EGFR-L861Q+E709A and one with delL747_T751+R776S had PRs to EGFR TKIs.
|
23242437 |
2013 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Eligible participants were adults (> 18 years) with NSCLC and EGFR mutations (exon 19 deletion or L858R mutation in exon 21) with no history of chemotherapy for metastatic disease (neoadjuvant or adjuvant chemotherapy ending ≥ 6 months before study entry was allowed).
|
22285168 |
2012 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Epidermal growth factor (EGFR) tyrosine kinase inhibitors (TKIs), such as gefitinib and erlotinib, show excellent clinical efficacy for patients with non-small cell lung cancer (NSCLC) with EGFR mutations, including Exon 19 deletion and single-point substitution, and L858R of exon 21.
|
29031620 |
2018 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Epidermal growth factor receptor (EGFR) gene mutations (G719X, exon 19 deletions/insertions, L858R, and L861Q) predict favorable responses to EGFR tyrosine kinase inhibitors (TKIs) in advanced non-small cell lung cancer (NSCLC).
|
24353160 |
2013 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Epidermal growth factor receptor 19Del and L858R exhibited distinct imaging phenotypes, which may help to guide the selection of more accurate and personalized treatment programs for patients with NSCLC.
|
31376283 |
2019 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exogenous expression of either the L858R point mutant or the DeltaE746-E750 deletion mutant form of EGFR in immortalized human bronchial epithelial cells, p53 WT NSCLC (A549), or p53-null NSCLC (NCI-H1299) resulted in dramatically increased sensitivity to IR.
|
17018617 |
2006 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exon 19 deletion and L858R mutation in exon 21 of the epidermal growth factor receptor (EGFR) are both common mutations that predict a good response to EGFR tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC).
|
26967328 |
2018 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exon 19 deletion mutations and the single-point substitution mutation L858R in exon 21 are the most frequent in NSCLC and are termed 'classical' mutations.
|
19680293 |
2009 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exon 19 deletions and L858R point mutation are the most commonly encountered active epidermal growth factor receptor (EGFR) mutations in non-small cell lung cancer (NSCLC), and they predict greater efficacy of gefitinib therapy.
|
25173459 |
2014 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exon 19 deletions and exon 21 L858R substitutions are the most common mutations, accounting for approximately 90% mutations in NSCLC; these are termed classic mutations and result in high sensitivity to tyrosine kinase inhibitors (TKIs).
|
31367543 |
2019 |
|
rs1057519848
|
|
|
0.800 |
GeneticVariation |
BEFREE |
Exon19 deletions and exon21 L858R mutations in EGFR were detected in 4 (12%) and 13 (38%) of 34 NSCLC cases, respectively.
|
18448998 |
2008 |