|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
After targeted RNA-sequencing, dual FISH fusion and array-CGH analysis, 7 of 13 tumors exhibited NTRK rearrangements (6 TPM3-NTRK1 and 1 EML4-NTRK3) and 3 a COL1A1-PDGFB fusion; in the other 3 neoplasms, all of which were positive with S100 (2 diffuse, 1 focal), we identified no rearrangement.
|
30877273 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
In another case, EML4-ALK fusion detected in the primary tumor was associated with ALK G1202R secondary resistance mutation in the post-treatment metastasis.
|
30946933 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
YAP silencing suppressed tumor growth in resistant cells, patient-derived xenografts, and EML4-ALK transgenic mice, whereas YAP overexpression decreased the responsiveness of parental cells to ALK inhibitor.
|
31633304 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The EML4-NTRK3 fusion was identified in two cases of infantile fibrosarcoma (one of which was previously described), and in one case of congenital mesoblastic nephroma, demonstrating that the EML4-NTRK3 fusion is a recurrent genetic event in these related tumors.
|
29099503 |
2018 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The ALK-EML4 translocation was found in 10% (2/20 tested); there was no patient with HER2 or BRAF mutated tumor.
|
28631135 |
2018 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Only 1 tumor had the coexistence of L858R mutation and EML4-ALK fusion.
|
27438512 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
EML4-ALK tumor developed after 1 week of tamoxifen treatment.
|
27836576 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CRISPR/Cas9 Technology-Based Xenograft Tumors as Candidate Reference Materials for Multiple EML4-ALK Rearrangements Testing.
|
28732214 |
2017 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Historically the coexistence of <i>EGFR</i> mutations and <i>EML4-ALK</i> rearrangements in the same tumor has been described as virtually impossible.
|
28938691 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We prepared formalin-fixed, paraffin-embedded samples derived from the xenograft tumor tissue of three non-small cell lung cancer cell lines with different EML4-ALK rearrangements and used PTs to evaluate the detection performance of laboratories in China.
|
26988569 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Echinoderm microtubule-associated protein-like 4 (EML4)-ALK fusions represent the majority of ALK rearrangements in lung adenocarcinomas and were, until recently, thought to be exclusive to that tumour type.
|
26880345 |
2016 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
RNA sequencing identified a kinase fusion in five of the six sequenced tumors: TPM3-NTRK1 (2 tumors), complex rearrangements involving TPM3, ALK, and IL6R (1 tumor), BAIAP2L1-BRAF (1 tumor), and EML4-BRAF (1 disseminating tumor).
|
26892443 |
2016 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The never smoker whose tumor harbored de novo EML4-ALK-E5;A20+ALK-S1206F only achieved a 4-month radiographic response to crizotinib 250mg twice daily.
|
27565908 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
By and large, the oncogenic activation of ALK in human tumors is known to occur by gene rearrangement (e.g.EML4-ALK, NMP-ALK, etc.).
|
25714698 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The median overall survival was 22.4 months (95% CI, 8.8-36.0) for the 17 patients with RET-rearranged tumors, compared with 21.3 months (95% CI, 18.7-23.9; P=0.57) for the 451 patients with EGFR-mutant tumors, 5.4 months (95% CI, 2.7-8.1; P=0.002) for the 13 patients with KRAS-mutant tumors, 18.9 months (95% CI, 10.7-27.1; P=0.82) for the 51 patients with EML4-ALK-rearranged tumors, and 12.0 months (95% CI, 9.0-15.0; P=0.07) for the 190 patients with quadri-negative tumors.
|
25773866 |
2015 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We apply TRUP to RNA-seq data of different tumor types, and find it to be more sensitive than alternative tools in detecting chimeric transcripts, such as secondary rearrangements in EML4-ALK-positive lung tumors, or recurrent inactivating rearrangements affecting RASSF8.
|
25650807 |
2015 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Alectinib led to tumor size reduction in EML4-ALK-positive xenograft tumors that failed to regress fully during the treatment with crizotinib.
|
24887559 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
ASP3026 also showed potent antitumor activities, including tumor shrinkage to a nondetectable level, in hEML4-ALK transgenic mice and prolonged survival in mice with intrapleural NCI-H2228 xenografts.
|
24419060 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The oncogenic driver for this tumor is a translocation involving the genes for anaplastic lymphoma receptor tyrosine kinase (ALK) and echinoderm microtubule associated protein like 4 (EML4).
|
24633422 |
2014 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Although there is a possibility that the left lung cancer is de novo one with multiple metastases, detection of the same fusion gene of the very rare EML4-ALK variant 1 in both tumors suggests that the left cancer is a recurrence of the right lung cancer after an interval of 15 years.
|
25238939 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The EML4-ALK fusion defines a new molecular subset of NSCLC that has distinct clinical and bronchoscopic findings suggesting more proximal origin when compared to tumours harbouring EGFR mutations.
|
24361161 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In 2011, regulatory entities granted conditional approval to an anaplastic lymphoma kinase inhibitor (crizotinib) based on an impressive overall response rate in previously treated non-small cell lung cancer patients whose tumors harbored EML4/ALK translocations.
|
24598368 |
2014 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Alectinib showed potent efficacy against intracranial EML4-ALK-positive tumor.
|
25205428 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Furthermore, tumors with EML4-ALK fusions had significantly higher levels of ERCC1, a molecule with a key role in platinum drug efficacy, than tumors without EML4-ALK fusions.
|
23277484 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To further elucidate the role of PF02341066 in tumor inhibition, we examined its effects alone and in combination with radiation on downstream signaling, apoptosis, and radiosensitivity in two NSCLC cell lines in vitro: H3122, which harbors the EML4-ALK fusion, and H460, which does not.
|
23443800 |
2013 |