EML4-ALK fusion gene product is involved in the carcinogenesis in non-small cell lung carcinomas

EML4-ALK fusions occur in less than 3% of non-small cell lung cancers samples; EML4 and/or ALK amplifications also occur.

A lung cancer cell line expressing endogenous variant 3 of EML4-ALK underwent cell death on exposure to a specific inhibitor of ALK catalytic activity.

EML4-ALK fusion gene is expressed in lung cancer

Genomic rearrangements accompanying the EML4-ALK fusion is associated with non-small cell lung cancer.

The EML4-ALK transcript cannot be regarded as a specific diagnostic tool for non-small cell lung cancer.

EML4-ALK fusion genes are associated with non-small-cell lung cancer.

It was discovered that about 5% of cases with non-small cell lung cancer, a new active fused kinase EMLA4-ALK is generated.Its use in molecular targeted therapy is promising.

frequent rearrangement in lung signet-ring cell carcinoma

EML4-ALK fusion variants have a role in non-small cell lung cancer

EML4-ALK and low thymidylate synthase expression is associated with treatment outcome with pemetrexed in Non-Small Cell lung cancer.

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.

EML4-ALK variant is associated with lung cancer.

EML4-ALK-variations are associated with non-small cell lung cancer.

variations in EML4-ALK fusion is associated with small-cell lung cancer with adenocarcinoma.

EML4-ALK fusion variant is associated with non-small-cell lung cancer.

The prevalence of EML4-ALK, EGFR status and KRAS mutations in 208 Chinese patients with non-small cell lung cancer, is reported.

EML4-ALK rearrangements are associated with lung carcinomas.

EML4-ALK rearrangement is associated with response to therapy in lung adenocarcinoma.

The first report concerning the presence of the EML4-ALK fusion gene in a sarcomatoid carcinoma of the lung.

evaluated mutations in four driver genes, epidermal growth factor receptor (EGFR), Kirsten ras oncogene (KRAS), c-MET, and echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK), in Chinese lung adenocarcinoma patients

EGFR gene mutations and the EML4-ALK fusion gene were detected in 92 lung adenocarcinoma patients in China.

Results suggest that heat shock protein 90 (Hsp90) inhibitors may overcome ligand-triggered resistance in microtubule associated protein-like 4 (EML4)--anaplastic lymphoma kinase (ALK) lung cancer cells.

Letter/Case Report: lung adenocarcinoma where EML4-ALK gene rearrangement was missed by FISH techniques but detected using reverse transcriptase PCR.

It was revealed that the EML4-ALK fusion gene was observed predominantly in adenocarcinoma, non-smoking and non-small-cell lung cancers (NSCLC) patients, especially those diagnosed in the advanced clinical stage of NSCLC.

The FISH-based method of detecting EML4-ALK rearrangement in lung cancer may miss a significant number of patients who could benefit from targeted ALK therapy. IHC should be strongly considered, and NGS is recommended in borderline cases.

case report in which the EML4-ALK fusion gene was identified as a second primary lung cancer after surgically resecting EGFR mutation-positive adenocarcinoma

EML4-ALK-positive lung cancer is often highly progressive.

identified EML4-ALK gene rearrangement in expanded circulating tumor cells from a patient with ALK-positive lung adenocarcinoma

We assessed the prevalence of EML4-ALK rearrangement gene measured by immunohistochemistry in an unselected population-based consecutive cohort of patients with adenocarcinoma of the lung (ACL), and the correlation with smoking history, thyroid transcription factor 1 (TTF1), gender and age

Our findings show that group EML4-ALK variants 3a/b in non-small cell lung cancer may be a major source of ALK inhibitor resistance in the clinic.

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.

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.

EML4-ALK fusion variant V3 is a high-risk feature for anaplastic lymphoma kinase-driven non-small cell lung cancer

The EML4-ALK fusion gene may be a strong oncogene in younger patients with lung adenocarcinoma.

lung adenocarcinoma in Asian patients aged 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

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.

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.

Effective RNA Knockdown Using CRISPR-Cas13a and Molecular Targeting of the EML4-ALK Transcript in H3122 lung cancer Cells.