|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
"Caged" reagents for miRNA research (siRNA targeting EGFR, involved in miRNA maturation, and mimics of miR-20a, playing a key role in tumor formation and metastasis) were prepared.
|
27484612 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Background:</b> Papulopustular rash is the most common cutaneous adverse effect during targeted tumour therapy particularly with epidermal growth factor receptor inhibitors (EGFRIs).
|
31010330 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<b>BI-4020</b> potently inhibits the above-described EGFR variants and induces tumor regressions in a cross-resistant EGFR<sup>del19 T790M C797S</sup> xenograft model.
|
31689114 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Conclusion</b>: IRDye800CW-labeled 8708 (scFv)<sub>2</sub> and 8709 scFv-Fc had desirable binding affinities, clearance times, and tumor accumulation to be used for imaging in combination with current EGFR targeted therapies.
|
30867810 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<b>Conclusion:</b> Our results indicate that EGFR mutations may drive different metabolic tumor phenotypes that are captured in PET images, whereas KRAS-mutated tumors do not.
|
27688480 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Conclusion:</b> The 3 <sup>64</sup>Cu-repebody complexes demonstrated specific and rapid uptake in EGFR-expressing tumors within 1 h and may have potential as novel EGFR imaging agents for PET.
|
28916621 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Conclusions:</b> CAL<sup>R</sup> xenografts established from HNSCC cells resistant to EGFR TKIs are more hypoxic, poorly perfused and glycolytic than sensitive CAL<sup>S</sup> tumors.
|
30083516 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Expert commentary</b>: The expanding armamentarium of EGFR TKIs, improvements in the understanding of resistance mechanisms and technological developments in the molecular analysis of tumors may help render <i>EGFR</i> mutation-positive NSCLC a chronic disease in many patients by facilitating optimal sequential therapy.
|
30913927 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<b>Methods:</b> In this study, 52 lung adenocarcinoma patients were enrolled, and EGFR mutation status was detected with tumor tissues as well as cell blocks and exosomes in MPEs.
|
31608233 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Objectives:</b> Tumor pathology examination especially epidermal growth factor receptor (<i>EGFR</i>) mutations molecular testing has been integral part of lung cancer clinical practices.
|
31555581 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<b>Purpose:</b> To identify molecular factors that determine duration of response to EGFR tyrosine kinase inhibitors and to identify novel mechanisms of drug resistance, we molecularly profiled <i>EGFR</i>-mutant tumors prior to treatment and after progression on EGFR TKI using targeted next-generation sequencing.<b>Experimental Design:</b> Targeted next-generation sequencing was performed on 374 consecutive patients with metastatic <i>EGFR</i>-mutant lung cancer.
|
29530932 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<b>Results:</b> Both types of EGFR-targeting QLs showed enhanced delivery to target cancer cells, resulting in more effective gene silencing and enhanced tumor imaging compared to non-targeting control QLs.
|
30809312 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<i>EGFR</i> and <i>KRAS</i> mutation, expression of EGFR family members and of cMET and PTEN and <i>EGFR</i> and <i>ABCG2</i> germline polymorphisms were tested on tumor tissue or blood samples to either confirm previously proposed predictive role or describe it in an explorative setting.
|
28915692 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<i>RAS</i> status and tumor location (sidedness) are predictive markers of patients' response to anti-EGFR mAbs.
|
30952636 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
<i>TP53, KRAS, APC</i>) has limited diagnostic sensitivity (40-60%), however, methylated DNA including <i>SEPT9, SFRP1, SDC2</i> can be applied with higher sensitivity (up to 90%) for CRC.Circulating miRNAs (e.g. miR-21, miR-92, miR-141) provide comparably high sensitivity for CRC as the circulating tumor cell mRNA markers (e.g.EGFR, CK19, CK20, CEA).
|
31046485 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<sup>64</sup>Cu-Labeled Trastuzumab Fab-PEG<sub>24</sub>-EGF Radioimmunoconjugates Bispecific for HER2 and EGFR: Pharmacokinetics, Biodistribution, and Tumor Imaging by PET in Comparison to Monospecific Agents.
|
28049295 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<sup>89</sup>Zr-DFO-nimotuzumab was evaluated <i>in vivo</i> by microPET and <i>ex vivo</i> by biodistribution in healthy and EGFR-positive tumor bearing mice.
|
29682209 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
(89)Zr-DFO-ZEGFR:2377 provides higher tumour-to-organ ratios than anti-EGFR antibody (89)Zr-DFO-cetuximab at 48 h after injection.
|
26847636 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
(i) hERG1 was expressed at high levels in 59% of primary PDAC; (ii) hERG1 blockade decreased PDAC cell growth and migration; (iii) hERG1 was physically and functionally linked to the Epidermal Growth Factor-Receptor pathway; (iv) in transgenic mice, ERG1 was expressed in PanIN lesions, reaching high expression levels in PDAC; (v) PDAC patients whose primary tumour showed high hERG1 expression had a worse prognosis; (vi) the α-hERG1-MoAb could detect PDAC in vivo.
|
25719829 |
2015 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
- To develop a timely and cost-effective assay that can accurately detect EGFR mutations in circulating tumor DNA and to evaluate the analytic and clinical performance of the assay.
|
28537806 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
1) Association of Grb2 to EGFR in BxPC-3 induced by EGF in the presence of Erbitux indicates an alternate pathway of Ras-MAPK activation, which may be related with the tumor resistance to treatment; 2) transactivation of EGFR downstream Ras-MAPK pathway by FGF contributes the resistance to treatment; and 3) downregulation of EGFR may increase the response to therapy.
|
12850474 |
2003 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
123 newly diagnosed GBMs were analyzed for the tumor cell expression of 23 pre-identified proteins and EGFR amplification, together allowing for the subclassification of 65% of the tumors.
|
25546404 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
127 lung adenocarcinomas were examined.30 (24%) tumors harbored ALK rearrangements, 97 (76%) tumors harbored EGFR mutations.
|
25312988 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
129 microRNAs were significantly differentially expressed in lung adenocarcinomas compared with normal lung tissue, and 17 microRNAs were differentially expressed between EGFR-mutated and EGFR wildtype tumors.
|
24599520 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
9 (15%) cases presented with ERBB1 amplification, which was correlated with lymph node involvement (P = 0.04), poorly differentiated tumours (P = 0.03) and a hypopharyngeal primary site (P = 0.035).
|
8943688 |
1996 |