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 subset of lung cancers, lymphomas, and neuroblastomas that harbor genomic ALK alterations may be clinically responsive to pharmacologic ALK inhibition.

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

the anaplastic lymphoma kinase, originally identified as a fusion kinase in a subtype of non-Hodgkin's lymphoma (NPM-ALK) and more recently in adenocarcinoma of lung (EML4-ALK), is also a frequent target of genetic alteration in advanced neuroblastoma

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

Anaplastic lymphoma kinase immunoreactivity in non-small cell lung carcinomas was associated with transcriptional up-regulation, ALK locus rearrangement, and the presence of EML4-ALK fusion transcript.

lung adenocarcinomas with ALK rearrangements are uncommon in the western population and represent a distinct entity of carcinomas with unique characteristics.

ALK gene rearrangements are associated with non-small cell lung cancer.

frequent rearrangement in lung signet-ring cell carcinoma

Increased ALK gene copy number and amplification are frequent in non-small cell lung cancer.

EML4-ALK fusion gene mutations are widely recognized alterations involved in biology and the clinical management of lung adenocarcinoma.This review reports the molecular bases that have led clinical application of detection for such genetic impairments.

ALK gene rearrangement is associated with non-small cell lung carcinoma.

ALK gene rearrangement is associated with non-small cell lung carcinoma.

ALK gene rearrangement is associated with response to pemetrexed therapy in patients with non-small cell lung cancer.

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

High ALK is associated with poor tumor responses to EGFR tyrosine kinase inhibitors in pulmonary adenocarcinoma.

ALK gene rearrangement is associated with non-small cell lung cancer.

Anaplastic lymphoma kinase translocation is associated with pemetrexed efficacy in non-small cell lung cancer.

The discovery of the novel KIF5B-ALK variant further consolidated the role of aberrant anaplastic lymphoma kinase signaling in lung carcinogenesis.

ALK gene rearrangement is associated with nonsmall cell lung cancer.

Report comprehensive histologic analysis of ALK-rearranged lung carcinomas.

ALK translocation is associated with non-small cell lung cancer.

ALK rearrangement is strongly associated with ALK immunoreactivity, and was seen only in lung tumours with pure signet-ring morphology and solid growth pattern.

In patients with advanced, ALK-positive non-small cell lung cancer, crizotinib therapy is associated with improved survival.

ALK gene rearrangement is associated with lung adenocarcinomas.

findings are important because they provide a molecular basis of ALK-positive lung adenocarcinomas and triple-negative lung adenocarcinomas and further stratify more or less aggressive subgroups of triple-negative lung ADC

Echinoderm microtubule-associated protein like 4-ALK fusion gene is associated with longer overall survival of lung adenocarcinoma patients with wild-type epidermal growth factor receptor mutations.

Data indicate that PIK3CA mutations occur in lung adenocarcinomas, usually concurrently with EGFR, KRAS, and anaplastic lymphoma kinase (ALK).

rearrangement for ALK locus by fluorescence in situ hybridization was found in one lung and in two central nervous system samples of inflammatory myofibroblastic tumor

in patients with nonsmall cell lung cancer, ALK gene rearrangement was significantly associated with pericardial disease and pleural disease; patients with ALK gene rearrangements and patients with EGFR mutations were predisposed to liver metastasis compared to triple negative cohort

identified at least one clinically relevant genomic alteration in 59% of the samples and revealed two gene fusions, C2orf44-ALK in a colorectal cancer sample and KIF5B-RET in a lung adenocarcinoma.

ALK mutation is not associated with crizotinib resistance in Non-Small Cell lung cancer.

nonsmall cell lung cancers (NSCLC) harboring activating EGFR mutations were more likely to express low ERCC1 and thymidylate synthetase (TS) mRNA levels; patients with NSCLC who had ALK rearrangement were more likely to express low TS mRNA levels

ALK gene amplification is a nonrandom and clonally related event in a subset of pulmonary sarcomatoid carcinoma.

Report histologic subtypes and distinctive cytomorphologic features of ALK-rearranged lung adenocarcinomas.

ALK rearrangement is associated with response to therapy in metastatic non-small-cell lung cancer.

Discordance between anaplastic lymphoma kinase status occurred in primary non-small-cell lung cancers and their corresponding metastases.

Anaplastic lymphoma kinase gene rearrangement is associated with Hepatoid carcinoma of the lung.

ALK gene rearrangement is associated with metastasis in 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.

ALK rearrangement is associated with crizotinib resistance in non-small-cell lung cancer.

The prevalence of ALK translocation in an unselected population of European patients with advanced non-small-cell lung carcinomas was 10%.

Anaplastic lymphoma kinase (ALK) gene rearrangements are present in a small subset of non-small-cell lung cancers. ALK-positive cancers are highly sensitive to small-molecule ALK kinase inhibitors, such as crizotinib.

ALK protein overexpression and ALK gene rearrangement is associated with lung adenocarcinomas.

ALK gene rearrangement is associated with non-small-cell lung cancer.

Targeted resequencing reveals ALK fusions in non-small cell lung carcinomas detected by FISH, immunohistochemistry, and real-time RT-PCR: a comparison of four methods.

ALK rearrangement is associated with response to therapy in non-small-cell lung cancer.

ALK gene rearrangement is associated with metastatic lung adenocarcinoma.

Detection of ALK rearrangement using ICC on routine Papanicolau cytology slides is considered to be advantageous for lung cancer treatments.

ALK gene rearrangement is associated with lung adenocarcinoma.

ALK rearrangement is associated with early pneumothorax as a feature of response to crizotinib therapy in lung adenocarcinoma.

ALK rearrangement and EML4-ALK variation is associated with lung adenocarcinoma.

ALK gene rearrangment is associated with advanced non-small-cell lung cancer.

Profiling of 100 non-small cell lung cancers identified numerous genetic alterations impacting fibroblast growth factor receptor 3 (FGFR3) in lung squamous cell carcinoma and a novel ALK fusion partner in lung adenocarcinoma.

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

Chromogenic in situ hybridization is a highly reliable, sensitive and specific method for the detection of ALK gene rearrangements in pulmonary adenocarcinomas.

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

44 cases of ALK-rearranged samples were identified by fluorescent in-situ hybridization (FISH), immunohistochemistry (IHC), and reverse transcription polymerase chain reaction (RT-PCR) in a large number of surgically resected lung cancers

The frequencies of somatic EGFR, KRAS, and ALK gene abnormalities reflect the diverse ethnicity and smoking patterns of non-small-cell lung cancers patients in the United States.

in lung adenocarcinomas, KRAS mutations are prevalent in male smokers; EGFR mutations are associated with female sex, nonsmoking and lepidic and micropapillary growth; TTF1 has a role in survival; BRAF mutations have roles in survival

Data indicate that coexistence of EML4-ALK fusion or ALK copy number increase and EGFR, MET, and KRAS mutations in tumor tissue from two treatment-naive Chinese non-small cell lung cancer (NSCLC) patients.

Chromogenic in situ hybridisation is a very reliable, convenient and inexpensive method to detect ALK-positive non-small cell lung carcinomas.

gene rearrangement has no prognostic relevance in patients with resected non-small cell lung cancer

ALK gene rearrangement is associated with spinal cord metastasis and leptomeningeal carcinomatosis in non-small-cell lung cancer.

Increased ALK gene copy number is associated with response to chemotherapy in lung adenocarcinoma.

ALK rearrangement is associated with response to chemotherapy in brain metastases of non-small-cell lung cancer.

Findings indicate that ASP3026 has potential efficacy for non-small cell lung cancer (NSCLC) and is expected to improve the therapeutic outcomes of patients with cancer with anaplastic lymphoma receptor tyrosine kinase (ALK) abnormality.

ALK kinase splicing isoform is not associated with non-small-cell lung cancer.

poorer disease-free survival in fusion-positive lung adenocarcinoma patients after curative surgery

ALK rearrangement and transcriptional up-regulation is associated with non-small-cell lung cancers.

ALK rearrangement is associated with non-small-cell lung cancers.

ALK rearrangement is associated with crizotinib responsiveness in non-small-cell lung cancer.

ALK, ROS1 and RET fusions are associated with pathological features of lung adenocarcinoma and are more prevalent in solid-predominant adenocarcinoma.

Anaplastic lymphoma kinase gene rearrangements is associated with non-small cell lung cancer.

ALK gene rearrangements are associated with lung cancer.

ALK G1202R mutation confers high-level resistance to alectinib in ALK-rearranged non-small-cell lung cancer patients who progressed on crizotinib.

TPR-ALK fusion is associated with lung adenocarcinoma.

data argue against PDGFRB activation in association with ALK gene aberrations in metastatic NSCLC and seem to imply differential pathobiological roles of ALK alterations in lung cancer and lymphoma, possibly depending on different fusion partner genes.

ALK translocation, occurring at a frequency of 6.8% in Chinese patients, defines a unique molecular subgroup of lung tumors.

ALK rearrangement is a prognostic factor of tumor recurrence in completely resected non-small cell lung cancer of any stage.

This is the first report of ALK rearrangement in an octogenarian patient with pleomorphic carcinoma of the lung.

identification of ALK rearrangements in non-small cell lung cancer

ALK rearrangement is rare in lung cancer with nodular ground-glass opacity, but is associated with advanced stage and larger tumor size, suggesting its association with aggressive progression of lung adenocarcinoma.

ALK fusion-positive lung lesions were significantly smaller and had a lower tumor disappearance rate than ALK fusion-negative lesions when using high-resolution computed tomography.

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

ALK fusion is an infrequent alteration in Finnish non-small cell lung cancer patients.

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.

study identified a novel V1180L gatekeeper mutation from the cell line model and a second novel I1171T mutation from the non-small cell lung cancer patient who developed resistance to alectinib; both ALK mutations conferred resistance to alectinib as well as to crizotinib, but were sensitive to ceritinib and other next-generation ALK-TKIs

ALK positive lung adenocarcinomas are more likely than EGFR mutant lung adenocarcinomas to be associated with larger volume, multifocal thoracic lymphadenopathy.

Two patients with non-small-cell lung cancer developed acquired resistance to alectinib with the presence of a mutation in amino acid residue 1171 located in the hydrophobic regulatory spine of the ALK kinase.

ALK protein expression is not a rare molecular event in lung squamous cell carcinoma.

ALK gene rearrangement is associated with lung adenocarcinomas.

ALK gene rearrangement is associated with non-small cell lung carcinoma.

The ALK gene fuses with echinoderm microtubule-associated protein-like 4 in the majority of ALK-positive lung cancer cases.

Brain metastases are frequent in advanced EGFR-mutated or ALK-rearranged non-small-cell lung cancers.

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.

ALK expression was correlated with ALK translocation, but not with ALK gene copy number gain. ALK translocation was also mutually exclusive with EGFR mutation in Taiwanese non-small cell lung cancer

The novel 1A4 antibody represents a promising candidate for screening lung tumors for the presence of ALK rearrangements.

KRAS and EGFR co-mutation was detected in one case. PPMA patients with ALK rearrangements or KRAS mutation represent a unique subtype in Non-Small-Cell lung Carcinoma

analysis of anaplastic lymphoma kinase (ALK) gene rearrangements in lung adenocarcinoma

Case Report: lung adenocarcinoma with different histological types between primary tumor and metastasis, but both haboring ALK-rearrangement.

ALK and ROS1 rearrangements found in advanced non-small cell lung cancer patients

Cystic Brain Metastases Occurring in Anaplastic Lymphoma Kinase Gene Rearranged Non-Small-Cell lung cancer Patients Receiving Crizotinib.

Intratumoral genetic heterogeneity was demonstrated to coexist with histologic heterogeneity in both single-driver and ALK/EGFR coaltered lung adenocarcinomas (LADCs).

Intratumor Heterogeneity of ALK-Rearrangements and Homogeneity of EGFR-mutations in Mixed lung Adenocarcinoma

this study shows that anaplastic lymphoma kinase variants might have no correlation with clinical response to crizotinib in non-small-cell lung cancer patients

Data identified several cases of complex EGFR mutations, and concomitant EGFR mutations and ALK rearrangements in non-small cell lung cancer

COPD-related NSCLC patients exhibited low prevalences of EGFR mutations and ALK rearrangements compared with the non-COPD group. Further studies are required regarding the molecular mechanisms underlying lung cancer associated with COPD

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

ALK rearrangements are associated with non-small-cell lung cancer.

There is a high prevalence of ALK positivity in wild-type EGFR non-small cell lung cancer

our study suggested that the prevalence of ALK, ROS1 and RET fusions is very rare in lung squamous cell carcinoma patients.

ALK point mutations are associated lung cancer.

Anaplastic lymphoma kinase gene rearrangement is associated with non-small cell lung cancer.

mutation in ALK-fusion genes are associated with tyrosine kinase inhibitor resistance in lung cancer.

Durable benefits with pemetrexed-based therapies in RET-rearranged lung cancers are comparable with ALK- and ROS1-rearranged lung cancers. When selecting therapies for patients with RET-rearranged lung cancers, pemetrexed-containing regimens should be considered.

ALK oncogenic activity is involved in the regulation of an epithelial mesenchymal transition phenotype in a subset of non-small cell lung carcinomas by repression of the epithelial splicing regulatory protein 1.

ALK gene rearrangement is associated with pulmonary adenocarcinoma.

or patients with non-small cell lung cancer with a EGFR mutation and an anaplastic lymphoma kinase mutation(ALK) with brain metastases, several agents have shown intracranial activity. Lapatinib has been tested for patients with brain metastases from breast cancer harboring a HER2 mutation. molecular targeted therapies have shown efficacy in BRAF-positive melanoma brain metastasis

ALK Rearrangement is associated with lung cancer.

The treatment of patients with anaplastic lymphoma receptor tyrosine kinase (ALK)-positive, metastatic non-small cell lung cancer.

ALK-positive lung adenocarcinoma who test immunohistochemistry-positive and FISH-negative may still respond to crizotinib therapy.

Ambiguous ALKpositive lung cancers are challenging tumors with diagnosis.

c-Met overexpression, HER-2 gene amplification, and SPTBN1-ALK gene fusion can coexist in lung adenocarcinoma and may become a potential biomarker of cancer refractory to crizotinib, chemotherapy, and radiotherapy as well as of a relatively poor prognosis.

EML4-ALK Rearrangement Along with Resistance mutation is associated with lung Adenocarcinoma.

mutation in ALK gene is associated with Advanced lung Adenocarcinoma.

We report the first case of an ALK-positive Non Small Cell lung Carcinoma patient who benefited from pemetrexed rechallenge after developing ALK inhibitor resistance. This strategy may be an option for some patients who suffer from acquired resistance to ALK inhibitors but responded to previous pemetrexed chemotherapy

A high ALK-gene copy number gain pattern might be associated with smoking status and theoretically it might mirror genomic instability in non-small lung cancer.

ALK rearrangement was not observed in lung adenocarcinoma arising in long-term ex-smokers

ALK kinase domain mutations seem to be uncommon events in ALK inhibitor-naive ALK rearranged lung adenocarcinomas but their effect on intrinsic resistance to achievable doses of clinically-available ALK inhibitors should be better evaluated in preclinical models and clinical cases.

ALK Fusion Patterns are associated with Response to Crizotinib Treatment in lung cancer.

The frequencies of ALK, ROS1 and RET rearrangements are low in non-adenocarcinoma NSCLC patients. And their clinical characteristics are similar to those in lung adenocarcinoma. Fusions of the above 3 genes are not prognostic factor for non-adnocarcinoma NSCLC patients.

This review summarizes the current understanding of the pathologic features, diagnostic approach, treatment options, resistance mechanisms, and future research areas for ALK-positive non-small cell lung cancer.

EMT was reversed by miR200c, which suggests that miR200c may serve a role in mediating the sensitivity of NCI2228/CRI cells to crizotinib. The present study may therefore contribute to improving the sensitivity of ALK positive lung cancer cells to crizotinib

ALK fluorescence in situ hybridization alone may not be the most reliable assay for detection of ALK gene rearrangements, and probably should be used in parallel with ALK immunohistochemistry and next generation sequencing for detection of gene fusions and mutations in lung adenocarcinoma.

ALK fusions occur in approximately 5% of lung adenocarcinoma and typically occur in a mutually exclusive manner to EGFR mutations.

ALK gene Rearrangement is associated with Venous Thromboembolism in Non-Small-Cell lung cancer.

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

ALK gene copy number gains occurred most due to unspecific polyploidy (whole DNA reduplication) rather than locus specific gene amplification in lung cancer.

Report accurate detect ALK gene rearrangements which could be used for diagnostic screening of lung cancer patients.

microRNA expression profiles had clinicopathological implications that were related to EGFR and KRAS mutations, as well as ALK-rearrangement in lung adenocarcinoma.

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.

we reviewed the literature related to characteristics of metastatic ovarian malignancies that form from lung tumors, the utility of ALK inhibition for treating ALK-positive NSCLC, the molecular diagnosis of ALK rearrangement and the role of next generation sequencing for ALK rearrangement detection.

Data suggest that ALK rearrangement in lung adenocarcinoma is associated with specific and distinct clinical-pathological characters compared to other genotypes.

Our results suggest that the dynamic change in the numbers of circulating tumor cells (CTC) with ALK-CNG may be a predictive biomarker for crizotinib efficacy in ALK-rearranged non-small cell lung cancer (NSCLC)patients. Serial molecular analysis of CTC shows promise for real-time patient monitoring and clinical outcome prediction in this population.

Reverse transcription-polymerase chain reaction is a suitable method for detecting ALK translocations using cytology samples from patients with primary lung cancer.

Detection of Gene Rearrangements in Circulating tumor Cells: Examples of ALK-, ROS1-, RET-Rearrangements in Non-Small-Cell lung cancer and ERG-Rearrangements in Prostate cancer.(

Recent preclinical models and translational efforts have provided critical insights into the molecular mechanisms of resistance to EGFR and ALK inhibitors. In this review, we present a framework for understanding resistance to targeted therapies. We also provide overviews of the molecular mechanisms of resistance and strategies to overcome resistance among EGFR-mutant and ALK-rearranged lung cancers

there are many treatment options for targeting ALK+ non-small-cell lung cancerbut the best treatment sequence remains unanswered

ALK and KRAS mutations are associated with acquired resistance to crizotinib in ALK-positive non-small cell lung cancer

the present study suggests that HER2 has an important role in the regulation of the cancer stem-like cells phenotype in ALK translocated lung cancers that is mainly orchestrated by HER2/HER3 heterodimers.

Detection of ALK expression by immunohistochemistry is reliable and the most practical way of identifying Non-small cell lung cancer patients likely to benefit from crizotinib treatment.

Case Reports: inflammatory myofibroblastic tumors of the lung containing a chimeric A2M-ALK gene categorized as a specific type of inflammatory myofibroblastic tumor that develops exclusively in neonates and infants.

Novel oncogenic ALK fusion transcripts have been found in non-small cell lung cancer patients using next-generation sequencing approaches.

Our data suggest that targeting Src signaling may be an effective approach to the treatment of ALK-non-small cell lung cancer (NSCLC) with acquired resistance to ALK inhibitors.

In xenografts in mice, trametinib inhibited the growth of EML4-ALK-positive non-small cell lung cancer and RAS-mutant neuroblastoma but not ALK-addicted neuroblastoma.

Here, we report our experience with ceritinib in terms of its efficacy and safety among ALK-positive nonsmall cell lung cancer patients who were previously exposed to crizotinib.

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.

We report higher frequency of ALK positivity (10.9%) in patients with adenocarcinoma of the lung. ALK by immunohistochemistry is more sensitive than FISH for ALK detection with high concordance. These patients had good clinical outcome with TKIs targeting ALK fusion protein.

in 24 ALK+ lung adenocarcinoma cases, 15 rearrangements detected (gene partner: EML4 in all cases)

This gene has been found to be rearranged, mutated, or amplified in a series of tumours including anaplastic large cell lymphomas, neuroblastoma, and non-small cell lung cancer.

The study reviews the drug-resistance mechanism of lung neoplasm cells with rearranged ALK. The resultant ALK fusion protein is aberrantly overexpressed and dimerized through the oligomerization domains, such as the coiled-coil domain, in the fusion partner that induces abnormal constitutive activation of ALK tyrosine kinase. Gene amplification or mutation confers tumor resistance to kinase inhibitors. [review]

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

In this paper, we reviewed fusion partner genes with ALK, detection methods for ALK-rearrangement (ALK-R), and the ALK-tyrosine kinase inhibitor, crizotinib, used in non-small-cell lung cancer patients.

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

this study describes response to crizotinib in advanced ALK-rearranged non-small cell lung cancers with different ALK-fusion variants

Baseline Circulating tumor cell count could be a predictive biomarker for EGFR-mutated and ALK-rearranged non-small cell lung cancer , which allows for better guidance and monitoring of patients over the course of molecular targeted therapies.

Our findings suggest that high integrin b3 expression in ALK-rearranged non-small cell lung cancer (NSCLC) is associated with tumor progression and a worse prognosis. This finding demonstrates the prognostic value of integrin b3 and provides a rationale for combination treatment with ALK and integrin b3 inhibitors in patients with ALK-rearranged NSCLC.

TP53 mutations define a subset of ALK-translocated non-small cell lung carcinoma tumours with recurrent MYC amplication that harbour chromosomal instability, leading to the co-occurrence of pathogenic aberrations.

ALK Rearrangement is associated with lung Adenocarcinoma.

Study systematically explored the mutational effects of ALK mutations on non-small cell lung cancer drug resistance properties and found that the activation of ALK was increased by substitution with destabilizing mutations, creating the capacity to confer drug resistance to inhibitors.

characteristics of the expression of epidermal growth factor receptor (EGFR), anaplastic lymphoma kinase (ALK), V-Ki-ras2 Kirsten rat sarcoma viral oncogene homologue (KRAS) in non-small cell lung cancer

Non-Small Cell lung cancers positive for ALK mutation by immunohistochemistry but not detected by Fluorescence in situ Hybridization show good response to crizotinib and merit treatment with the same

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

Double mutations of EGFR and ALK Gene in Non-small Cell lung cancer

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.

There were 35 patients with ALK-positive non-small cell lung cancer , nine of whom received ceritinib after alectinib. The overall response rate to ceritinib was 44%. It was 16% in patients who received ceritinib immediately after alectinib, and 100% in patients who received chemotherapy before ceritinib.

For appropriate molecular testing of primary ALK (+) lung cancer.

ALK gene rearrangements are associated with non-small cell lung cancer.

ALK-rearrangement can be detected in Circulating tumor cells collected from advanced non small cell lung cancer patients.

this study reveals 3.5% of ALK rearrangement rate in the cytology specimens from the patients with primary or metastatic lung non-small cell carcinoma

The incidence of both EGFR and ALK1 mutations is higher in the adenocarcinoma of the lung population studied and seem to correlate with a well differentiated, acinar pattern on morphology.

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.

Findings suggest that the measurement of C-terminal ALK or ROS1 protein could be a reliable diagnostic method for each fusion in lung cancer.

Results found ALK rearrangement not associated with survival of patients with lung adenocarcinoma.

Efficacy of brigatinib in ALK+ non-small-cell lung cancer.

Rearrangements of ALK/ROS1 were quantified using circulating tumor cells (CTCs) mRNA and matched with those identified in biopsy specimens from 12 patients with late-stage non-small cell lung cancer. Moreover, CTC counts and copy numbers of ALK/ROS1 rearrangements could be used together for evaluating treatment responses and disease progression.

constitutively active ALK induces tumorigenic phenotypes, such as increased cancer cell proliferation/colony formation via YAP/TAZ and elevated immune evasion via YAP/TAZ-programmed death-ligand 1 in breast and lung cancer cells.

Relationship between serum tumor markers and Anaplastic Lymphoma Kinase mutations in stage IV lung adenocarcinoma in Hubei province, Central China.

ALK-Rearranged lung Adenocarcinoma is associated with Krukenberg tumors.

Low frequency of mutation of epidermal growth factor receptor (EGFR) and arrangement of anaplastic lymphoma kinase (ALK) in primary pulmonary lymphoepithelioma-like carcinoma.

Brain metastases from non-small cell lung cancer with EGFR or ALK mutations: A systematic review and meta-analysis of multidisciplinary approaches.

Low ALK FISH positive metastatic non-small cell lung cancer (NSCLC) patients have shorter progression-free survival after treatment with ALK inhibitors.

Detection of ALK Gene Rearrangement in Cell-free RNA from lung cancer Malignant Pleural Effusion.

Alteration in the sensitivity to crizotinib by Na(+)/H(+) exchanger regulatory factor 1 is dependent to its subcellular localization in ALK-positive lung cancers.

Efficacy and safety of ceritinib in anaplastic lymphoma kinase-rearranged non-small cell lung cancer: A systematic review and meta-analysis.

Frequency of anaplastic lymphoma kinase rearrangements in Moroccan patients with non small cell lung cancer: a multi-institutional national retrospective study.

[Epidemiology and diagnosis of mutations in the ALK gene in patients with non-small cell lung cancer in the Moscow region].", trans "Epidemiologiya i diagnostika mutatsii v gene ALK u patsientov s nemelkokletochnym rakom legkogo v Moskovskoi oblasti.

Cost-effectiveness analysis comparing companion diagnostic tests for EGFR, ALK, and ROS1 versus next-generation sequencing (NGS) in advanced adenocarcinoma lung cancer patients.

Concomitant echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase rearrangement and epidermal growth factor receptor mutation in non-small cell lung cancer patients from eastern India.

High prevalence of ROS1 gene rearrangement detected by FISH in EGFR and ALK negative lung adenocarcinoma.

Beyond EGFR, ALK and ROS1: Current evidence and future perspectives on newly targetable oncogenic drivers in lung adenocarcinoma.

Individualized nomogram for predicting ALK rearrangement status in lung adenocarcinoma patients.

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

Impact of STAT1 polymorphisms on crizotinib-induced hepatotoxicity in ALK-positive non-small cell lung cancer patients.

[Clinicopathological significance in non-small cell lung cancer with mutations and co-mutations of EGFR, ALK and ROS1].

Immunocytochemical Detection of ALK and ROS1 Rearrangements in lung cancer Cytological Samples.

CT radiomics-based prediction of anaplastic lymphoma kinase and epidermal growth factor receptor mutations in lung adenocarcinoma.

[Semiquantitative parameters of (18)F-FDG PET/CT, gene mutation states of epidermal growth factor receptor and anaplastic lymphoma kinase in prognosis evaluation of patients with lung adenocarcinoma].