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Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (zeige ERBB3 ELISA Kits) associated with alcohol dependence in humans and behavioral responses to ethanol in mice.
ALKR1275Q cooperated with MYCN (zeige MYCN ELISA Kits) in the development of aggressive NB, possibly by downregulating the expression of ECM (zeige MMRN1 ELISA Kits)/BM-associated genes and by conferring malignant potentials to MYCN (zeige MYCN ELISA Kits)-expressing cells.
ALK inhibitor alectinib inhibits tumor growth in a TH-MYCN (zeige MYCN ELISA Kits) transgenic neuroblastoma (zeige ARHGEF16 ELISA Kits) mouse model.
Alk -/- mice initially consume more ethanol and have increased basal and ethanol-stimulated GABA release in the central nucleus of the amygdala when compared to Alk +/+ mice. After chronic ethanol exposure, Alk +/+ mice escalate their ethanol consumption, whereas Alk -/- mice do not. Basal GABA release in Alk -/- mice is not enhanced by chronic intermittent ethanol-two bottle choice drinking as it is in Alk +/+ mice.
An oral anaplastic lymphoma kinase (ALK) inhibitor.
ALK knock out male mice exhibit hypogonadotropic hypogonadism.
Ethanol activates ALK (and MDK (zeige MDK ELISA Kits)) signaling in the brain which regulates behaviors related to alcohol abuse.
Hyperactivation of Alk induces neonatal lethality in knock-in AlkF1178L mice.
Mutations in the ALK gene is associated with neuroblastoma (zeige ARHGEF16 ELISA Kits).
Th-MYCN (zeige MYCN ELISA Kits) genetically-engineered murine models of neuroblastoma (zeige ARHGEF16 ELISA Kits) using MRI (zeige C7ORF49 ELISA Kits), we have identified a marked ALK(F1174L)-driven vascular phenotype.
ALK Rearrangement is associated with resistant to crizotinib therapy in a metastatic abdominal nodule with Small Cell Carcinoma.
ALK Fusion Patterns are associated with Response to Crizotinib Treatment in Lung cancer.
High ALK expression is associated with Merkel cell carcinoma.
The aim was to investigate the prevalence of ALK fusion variants and to compare clinical outcomes according to ALK fusion variants.
Results demonstrate that the frequency and spectrum of ALK resistance mutations differs depending on the ALK inhibitor. Moreover, resistance profiles may evolve over time and in response to sequential ALK inhibitors.
Detection of Gene Rearrangements in Circulating Tumor Cells: Examples of ALK-, ROS1 (zeige ROS1 ELISA Kits)-, RET (zeige RET ELISA Kits)-Rearrangements in Non-Small-Cell Lung Cancer and ERG (zeige ERG ELISA Kits)-Rearrangements in Prostate Cancer.(
ALK-L1198F and ALK-G1201E mutations, originally identified in anaplastic thyroid cancer, do not result in ligand independent gain-of-function activity.
ALK+, LBCL cases display a dismal clinical outcome and can only be cured with conventional chemotherapy protocols at the stage of localized disease
Studies showed recurrent oncogenic alterations suche as chromosomal translocation and gene amplification of ALK in anaplastic large-cell lymphoma, inflammatory myofibroblastic tumor, and neuroblastoma (zeige ARHGEF16 ELISA Kits) and has highlighted the importance for ALK in histologically diverse pediatric cancers. [review]
Case Reports: inflammatory myofibroblastic tumors of the lung containing a chimeric A2M (zeige A2M ELISA Kits)-ALK gene categorized as a specific type of inflammatory myofibroblastic tumor that develops exclusively in neonates and infants.
This gene encodes a receptor tyrosine kinase, which belongs to the insulin receptor superfamily. This protein comprises an extracellular domain, an hydrophobic stretch corresponding to a single pass transmembrane region, and an intracellular kinase domain. It plays an important role in the development of the brain and exerts its effects on specific neurons in the nervous system. 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 chromosomal rearrangements are the most common genetic alterations in this gene, which result in creation of multiple fusion genes in tumourigenesis, including ALK (chromosome 2)\\/EML4 (chromosome 2), ALK\\/RANBP2 (chromosome 2), ALK\\/ATIC (chromosome 2), ALK\\/TFG (chromosome 3), ALK\\/NPM1 (chromosome 5), ALK\\/SQSTM1 (chromosome 5), ALK\\/KIF5B (chromosome 10), ALK\\/CLTC (chromosome 17), ALK\\/TPM4 (chromosome 19), and ALK\\/MSN (chromosome X).
ALK tyrosine kinase receptor
, anaplastic lymphoma kinase (Ki-1)
, CD246 antigen
, mutant anaplastic lymphoma kinase
, anaplastic lymphoma receptor tyrosine kinase
, anaplastic lymphoma kinase