gopubmed logo
find other proteinsAll proteins
GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Echinoderm microtubule associated protein like 4

EML4, echinoderm microtubule-associated protein-like 4
Top mentioned proteins: ALK, EGFR, KRAS, HAD, CAN
Papers on EML4
A novel acquired ALK F1245C mutation confers resistance to crizotinib in ALK-positive NSCLC but is sensitive to ceritinib.
Ou et al., The Woodlands, United States. In Lung Cancer, Feb 2016
Here we described the emergence of an ALK F1245C mutation in an advanced ALK+ NSCLC patient (EML4-ALK variant 3a/b) who developed slow disease progression after a durable response to crizotinib.
ALK-positive large B-cell lymphoma: identification of EML4-ALK and a review of the literature focusing on the ALK immunohistochemical staining pattern.
Takeuchi et al., Tokyo, Japan. In Int J Hematol, Feb 2016
Here, we examined an ALK+LBCL case showing a unique diffuse cytoplasmic ALK staining pattern and identified EML4-ALK, which has not previously been reported in ALK+LBCL.
Molecular mechanisms that underpin EML4-ALK driven cancers and their response to targeted drugs.
Richards et al., Seoul, South Korea. In Cell Mol Life Sci, Feb 2016
UNASSIGNED: A fusion between the EML4 (echinoderm microtubule-associated protein-like) and ALK (anaplastic lymphoma kinase) genes was identified in non-small cell lung cancer (NSCLC) in 2007 and there has been rapid progress in applying this knowledge to the benefit of patients.
[News about targeted therapies in non-small-cell lung cancer in 2015 (except immuno-therapy)].
Wislez et al., Paris, France. In Ann Pathol, Feb 2016
The EML4-ALK translocation is found in about 5% of NSCLC and more particularly in adenocarcinoma of young non-smoking patients.
Overcoming crizotinib resistance in ALK-rearranged NSCLC with the second-generation ALK-inhibitor ceritinib.
Peters et al., Amsterdam, Netherlands. In Expert Rev Anticancer Ther, Feb 2016
UNASSIGNED: In up to 5% of non-small cell lung cancer (NSCLC) patients, the EML4-ALK translocation drives tumor progression.
EML4-ALK translocation is associated with early onset of disease and other clinicopathological features in Chinese female never-smokers with non-small-cell lung cancer.
Zhang et al., Zhengzhou, China. In Oncol Lett, Dec 2015
UNASSIGNED: Non-small-cell lung cancer (NSCLC) with echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) translocation is resistant to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs), including gefitinib and erlotinib, but responds to the ALK-TKI crizotinib.
Role of circulating-tumor DNA analysis in non-small cell lung cancer.
Zhou et al., Shanghai, China. In Lung Cancer, Nov 2015
The discovery of actionable driver mutations such as epidermal growth factor receptor (EGFR) and microtubule-associated protein-like 4 anaplastic lymphoma kinase (EML4-ALK) and their highly responses to EGFR and ALK tyrosine kinase inhibitors (TKIs) in patients with advanced non-small-cell lung cancer (NSCLC) allowed precise medicine into reality.
RAS-MAPK dependence underlies a rational polytherapy strategy in EML4-ALK-positive lung cancer.
Bivona et al., San Francisco, United States. In Nat Med, Sep 2015
Here we demonstrate in models of lung adenocarcinoma harboring the oncogenic fusion of ALK and EML4 that the GTPase RAS-mitogen-activated protein kinase (MAPK) pathway, but not other known ALK effectors, is required for tumor-cell survival.
PF-06463922, an ALK/ROS1 Inhibitor, Overcomes Resistance to First and Second Generation ALK Inhibitors in Preclinical Models.
Smeal et al., San Diego, United States. In Cancer Cell, Aug 2015
Furthermore, PF-06463922 treatment led to regression of EML4-ALK-driven brain metastases, leading to prolonged mouse survival, in a superior manner.
In vivo engineering of oncogenic chromosomal rearrangements with the CRISPR/Cas9 system.
Ventura et al., New York City, United States. In Nature, 2015
A recently discovered example is a fusion between the genes echinoderm microtubule-associated protein like 4 (EML4) and anaplastic lymphoma kinase (ALK), generated by an inversion on the short arm of chromosome 2: inv(2)(p21p23).
Personalized treatment options for ALK-positive metastatic non-small-cell lung cancer: potential role for Ceritinib.
Shackelford et al., Shreveport, United States. In Pharmgenomics Pers Med, 2014
The fusion of echinoderm microtubule-associated protein-like 4 with the anaplastic lymphoma kinase (EML4-ALK) is found in 3%-7% of non-small-cell lung cancer (NSCLC) cases and confers sensitivity to crizotinib, the first United States Food and Drug Administration (FDA)-approved ALK inhibitor drug.
Non-Small Cell Lung Cancer in a Very Young Woman: A Case Report and Critical Review of the Literature.
Pasello et al., Padova, Italy. In Am J Case Rep, 2014
CASE REPORT: We report here a case of a very young woman with diagnosis of early-stage lung adenocarcinoma harboring EML4-ALK rearrangement; she underwent radical surgery and adjuvant chemotherapy according to the pathologic stage.
ROS1 mutation and treatment with crizotinib in a 30-year old Caucasian woman with stage IV non-small cell lung cancer/adenocarcinoma and complete remission.
Studnicka et al., Salzburg, Austria. In Thorac Cancer, 2014
We enrolled the patient in an off-label program for the treatment of ROS1 rearranged adenocarcinomas with the EML4/anaplastic lymphoma kinase inhibitor crizotinib.
Cost effectiveness of EML4-ALK fusion testing and first-line crizotinib treatment for patients with advanced ALK-positive non-small-cell lung cancer.
Leighl et al., Hamilton, Canada. In J Clin Oncol, 2014
PURPOSE: ALK-targeted therapy with crizotinib offers significant improvement in clinical outcomes for the treatment of EML4-ALK fusion-positive non-small-cell lung cancer (NSCLC).
MED12 controls the response to multiple cancer drugs through regulation of TGF-β receptor signaling.
Bernards et al., Amsterdam, Netherlands. In Cell, 2012
Inhibitors of the ALK and EGF receptor tyrosine kinases provoke dramatic but short-lived responses in lung cancers harboring EML4-ALK translocations or activating mutations of EGFR, respectively.
A novel EML4-ALK variant: exon 6 of EML4 fused to exon 19 of ALK.
Warth et al., Heidelberg, Germany. In J Thorac Oncol, 2012
EML4-ALK variant is associated with lung cancer.
A novel mass spectrometry-based assay for diagnosis of EML4-ALK-positive non-small cell lung cancer.
Nishio et al., Ōsaka, Japan. In J Thorac Oncol, 2012
EML4-ALK-variations are associated with non-small cell lung cancer.
Successful long-term treatment with pemetrexed of NSCLC associated with EML4-ALK and low thymidylate synthase expression.
Nakagawa et al., Ōsaka, Japan. In Clin Lung Cancer, 2012
EML4-ALK and low thymidylate synthase expression is associated with treatment outcome with pemetrexed in Non-Small Cell Lung Cancer.
EML4-ALK translocation predicts better outcome in lung adenocarcinoma patients with wild-type EGFR.
Yang et al., Yün-lin, Taiwan. In J Thorac Oncol, 2012
EML4-anaplastic lymphoma kinase (ALK) fusion gene is associated with longer overall survival of lung adenocarcinoma patients with wild-type epidermal growth factor receptor mutations.
[Lung cancer in never smoker: Epidemiology, molecular profiles and treatment].
Planchard et al., Villejuif, France. In Presse Med, 2011
New molecular targets are on investigation, such as EML4-ALK translocation.
share on facebooktweetadd +1mail to friends