| Oncogenic EML4-ALK assemblies suppress growth factor perception and modulate drug tolerance. | Oncogenic EML4-ALK assemblies suppress growth factor perception and modulate drug tolerance.
Gonzalez-Martinez D, Roth L, Mumford TR, Guan J, Le A, Doebele RC, Huang B, Tulpule A, Niewiadomska-Bugaj M, Bivona TG, Bugaj LJ., Free PMC Article | 11/7/2024 |
| Malignant pleural mesothelioma with an EML4-ALK fusion: Expect the unexpected! | Malignant pleural mesothelioma with an EML4-ALK fusion: Expect the unexpected!
Cordier F, Van der Meulen J, van Roy N, De Wilde J, van Dijck H, Vanhoenacker F, Lambrechts M, Noyez V, Van de Vijver K, Ferdinande L, Dendooven A, Van Dorpe J, Creytens D. | 04/2/2022 |
| Phase-separated foci of EML4-ALK facilitate signalling and depend upon an active kinase conformation. | Phase-separated foci of EML4-ALK facilitate signalling and depend upon an active kinase conformation.
Sampson J, Richards MW, Choi J, Fry AM, Bayliss R., Free PMC Article | 03/19/2022 |
| An unusual fusion gene EML4-ALK in a patient with congenital mesoblastic nephroma. | An unusual fusion gene EML4-ALK in a patient with congenital mesoblastic nephroma.
Misove A, Vicha A, Zapotocky M, Malis J, Balko J, Nemeckova T, Szabova J, Kyncl M, Novakova-Kodetova D, Stolova L, Jencova P, Broz P, Krskova L. | 03/19/2022 |
| The impact of the ALK fusion variant on clinical outcomes in EML4-ALK patients with NSCLC: a systematic review and meta-analysis. | The impact of the ALK fusion variant on clinical outcomes in EML4-ALK patients with NSCLC: a systematic review and meta-analysis.
Wang S, Luo R, Shi Y, Han X. | 03/5/2022 |
| A novel break site of EML4-ALK report and a rare PRKAR1A-ALK report analyzed by different ALK detection platforms in non-small cell lung cancer patients. | A novel break site of EML4-ALK report and a rare PRKAR1A-ALK report analyzed by different ALK detection platforms in non-small cell lung cancer patients.
Du X, Zhang J, Gao H, Tai Y., Free PMC Article | 02/5/2022 |
| Identification of a EML4-ALK exon 19 fusion variant in lung adenocarcinoma and alectinib resistance. | Identification of a EML4-ALK exon 19 fusion variant in lung adenocarcinoma and alectinib resistance.
Liu D, Xu X, Wen J, Zhang C, Fan M. | 10/30/2021 |
| Clinicopathological and Prognostic Significance of the EML4-ALK Translocation and IGFR1, TTF1, Napsin A Expression in Patients with Lung Adenocarcinoma.", trans "Clinicopathological and Prognostic Significance of the EML4-ALK Translocation and IGFR1, TTF1, Napsin A Expression in Patients with Lung Adenocarcinoma. | Clinicopathological and Prognostic Significance of the EML4-ALK Translocation and IGFR1, TTF1, Napsin A Expression in Patients with Lung Adenocarcinoma.
Bulutay P, AkyÜrek N, MemiŞ L., Free PMC Article | 10/16/2021 |
| Investigation on the prognostic impact of concurrent genomic alterations in crizotinib-treated EML4-ALK-rearranged advanced non-small cell lung cancer patients. | Investigation on the prognostic impact of concurrent genomic alterations in crizotinib-treated EML4-ALK-rearranged advanced non-small cell lung cancer patients.
Zheng J, Zhu Y, Sun K, Shen Q, Wang Y, Cao H, Lizaso A, Yu B, Lin J, Chen S, Zhou J, Zhou J. | 08/7/2021 |
| The Prevalence of the EML4-ALK Fusion Gene in Cytology Specimens from Patients with Lung Adenocarcinoma. | The Prevalence of the EML4-ALK Fusion Gene in Cytology Specimens from Patients with Lung Adenocarcinoma.
Heriyanto DS, Trisnawati I, Kumara EG, Laiman V, Yuliani FS, Sumpono ASB, Cempaka R, Marcellus, Budiono E., Free PMC Article | 08/7/2021 |
| EML4-ALK V3 oncogenic fusion proteins promote microtubule stabilization and accelerated migration through NEK9 and NEK7. | EML4-ALK V3 oncogenic fusion proteins promote microtubule stabilization and accelerated migration through NEK9 and NEK7.
O'Regan L, Barone G, Adib R, Woo CG, Jeong HJ, Richardson EL, Richards MW, Muller PAJ, Collis SJ, Fennell DA, Choi J, Bayliss R, Fry AM., Free PMC Article | 06/26/2021 |
| EML4-ALK induces cellular senescence in mortal normal human cells and promotes anchorage-independent growth in hTERT-transduced normal human cells. | EML4-ALK induces cellular senescence in mortal normal human cells and promotes anchorage-independent growth in hTERT-transduced normal human cells.
Miyanaga A, Matsumoto M, Beck JA, Horikawa I, Oike T, Okayama H, Tanaka H, Burkett SS, Robles AI, Khan M, Lissa D, Seike M, Gemma A, Mano H, Harris CC., Free PMC Article | 05/8/2021 |
| Effective RNA Knockdown Using CRISPR-Cas13a and Molecular Targeting of the EML4-ALK Transcript in H3122 Lung Cancer Cells. | Effective RNA Knockdown Using CRISPR-Cas13a and Molecular Targeting of the EML4-ALK Transcript in H3122 Lung Cancer Cells.
Saifullah, Sakari M, Suzuki T, Yano S, Tsukahara T., Free PMC Article | 03/6/2021 |
| Identification of anaplastic lymphoma kinase fusions in clear cell renal cell carcinoma. | Identification of anaplastic lymphoma kinase fusions in clear cell renal cell carcinoma.
Chen W, Li W, Bai B, Wei H., Free PMC Article | 09/26/2020 |
| Mitotic phosphorylation by NEK6 and NEK7 reduces the microtubule affinity of EML4 to promote chromosome congression. | Mitotic phosphorylation by NEK6 and NEK7 reduces the microtubule affinity of EML4 to promote chromosome congression.
Adib R, Montgomery JM, Atherton J, O'Regan L, Richards MW, Straatman KR, Roth D, Straube A, Bayliss R, Moores CA, Fry AM. | 08/15/2020 |
| The prevalence of EML4-ALK, EGFR status and KRAS mutations in 208 Chinese patients with non-small cell lung cancer, is reported. | Clinical significance of EML4-ALK fusion gene and association with EGFR and KRAS gene mutations in 208 Chinese patients with non-small cell lung cancer.
Li Y, Li Y, Yang T, Wei S, Wang J, Wang M, Wang Y, Zhou Q, Liu H, Chen J., Free PMC Article | 04/10/2020 |
| The study uncovered miR-100-5p to confer resistance to Crizotinib and Lorlatinib in EML4-ALK non-small cell lung cancer cells and to be a potential therapeutic target in drug resistance. | miR-100-5p confers resistance to ALK tyrosine kinase inhibitors Crizotinib and Lorlatinib in EML4-ALK positive NSCLC.
Lai Y, Kacal M, Kanony M, Stukan I, Jatta K, Kis L, Norberg E, Vakifahmetoglu-Norberg H, Lewensohn R, Hydbring P, Ekman S. | 12/28/2019 |
| The study reports a fusion circRNA (F-circEA) produced from the EML4-ALK fusion gene mainly located in the cytoplasm. Moreover, F-circEA, independent of the EML4-ALK linear transcript and fusion protein, can promote cell migration and invasion, thus contributing to tumor development. | Circular RNA F-circEA produced from EML4-ALK fusion gene as a novel liquid biopsy biomarker for non-small cell lung cancer.
Tan S, Gou Q, Pu W, Guo C, Yang Y, Wu K, Liu Y, Liu L, Wei YQ, Peng Y., Free PMC Article | 10/5/2019 |
| associated with Infantile hypertrophic pyloric stenosis risk | Genome-wide meta-analysis identifies BARX1 and EML4-MTA3 as new loci associated with infantile hypertrophic pyloric stenosis.
Fadista J, Skotte L, Geller F, Bybjerg-Grauholm J, Gørtz S, Romitti PA, Caggana M, Kay DM, Matsson H, Boyd HA, Hougaard DM, Nordenskjöld A, Mills JL, Melbye M, Feenstra B., Free PMC Article | 06/8/2019 |
| a novel circRNA F-circEA-2a produced from the EML4-ALK fusion gene was identified and mainly located in the cytoplasm to promote cell migration and invasion in lung cancer cells. | Circular RNA F-circEA-2a derived from EML4-ALK fusion gene promotes cell migration and invasion in non-small cell lung cancer.
Tan S, Sun D, Pu W, Gou Q, Guo C, Gong Y, Li J, Wei YQ, Liu L, Zhao Y, Peng Y., Free PMC Article | 04/27/2019 |
| EML4-ALK fusion variant V3 is a high-risk feature for anaplastic lymphoma kinase-driven non-small cell lung cancer | EML4-ALK fusion variant V3 is a high-risk feature conferring accelerated metastatic spread, early treatment failure and worse overall survival in ALK(+) non-small cell lung cancer.
Christopoulos P, Endris V, Bozorgmehr F, Elsayed M, Kirchner M, Ristau J, Buchhalter I, Penzel R, Herth FJ, Heussel CP, Eichhorn M, Muley T, Meister M, Fischer JR, Rieken S, Warth A, Bischoff H, Schirmacher P, Stenzinger A, Thomas M. | 12/22/2018 |
| The EML4-ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma. | Clinicopathological features of younger (aged ≤ 50 years) lung adenocarcinoma patients harboring the EML4-ALK fusion gene.
Kometani T, Sugio K, Osoegawa A, Seto T, Ichinose Y., Free PMC Article | 12/22/2018 |
| lung adenocarcinoma in Asian patients aged </=50 years had a higher gene mutation rate than in those aged >50 years, especially EML4-ALK and ROS1 fusion. Mutation analysis may be helpful in determining targeted therapy for the majority of these patients | Driver mutations of young lung adenocarcinoma patients with malignant pleural effusion.
Wu SG, Liu YN, Yu CJ, Yang JC, Shih JY. | 10/27/2018 |
| Our analysis indicated that ALK-EML4 positive non-small-cell lung cancers comprised a unique subgroup of adenocarcinomas with distinct clinicopathological characteristics. Incidence of ALK positivity was found to be higher in females and never smokers. | New insights into anaplastic lymphoma kinase-positive nonsmall cell lung cancer.
Dubey AP, Pathi N, Viswanath S, Rathore A, Pathak A, Sud R. | 07/14/2018 |
| Mutation testing at diagnosis is feasible in the vast majority of patients with Stage IV adenocarcinoma of the lung. Patients with EGFR or EML4ALK mutation and those who received pemetrexed maintenance had better clinical outcomes. | Clinical profile and outcomes of patients with Stage IV adenocarcinoma of lung: A tertiary cancer center experience.
Paliwal P, Rajappa S, Santa A, Mohan M, Murthy S, Lavanya N. | 07/14/2018 |