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Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (show ERBB3 Antibodies) associated with alcohol dependence in humans and behavioral responses to ethanol in mice.
ALKR1275Q cooperated with MYCN (show MYCN Antibodies) in the development of aggressive NB, possibly by downregulating the expression of ECM (show MMRN1 Antibodies)/BM-associated genes and by conferring malignant potentials to MYCN (show MYCN Antibodies)-expressing cells.
ALK inhibitor alectinib inhibits tumor growth in a TH-MYCN (show MYCN Antibodies) transgenic neuroblastoma (show ARHGEF16 Antibodies) 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 (show MDK Antibodies)) 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 (show ARHGEF16 Antibodies).
Th-MYCN (show MYCN Antibodies) genetically-engineered murine models of neuroblastoma (show ARHGEF16 Antibodies) using MRI (show C7ORF49 Antibodies), we have identified a marked ALK(F1174L)-driven vascular phenotype.
The treatment of patients with anaplastic lymphoma receptor tyrosine kinase (ALK)-positive, metastatic non-small cell lung cancer.
The unique, potent, and pan (show SUPT6H Antibodies)-ALK mutant activity of brigatinib could be rationalized by structural analyses.
The results of our analysis indicate that C1156Y mutation alters the conformation of the ALK binding pocket residues which results in a marked decrease in hydrogen bond interactions between crizotinib and ALK.
Alectinib (Alecensa; Roche/Genentech), a second-generation, orally active, potent, and highly selective inhibitor of anaplastic lymphoma kinase (ALK).
The discovery of gain-of-function mutations in the ALK receptor tyrosine kinase (show RET Antibodies) gene as the major cause of familial neuroblastoma (show ARHGEF16 Antibodies) led to the discovery of identical somatic mutations and rapid advancement of ALK as a tractable therapeutic target. Inactivating mutations in a master regulator of neural crest development, PHOX2B (show PHOX2B Antibodies), have also been identified in a subset of familial neuroblastomas.
The prevalence of STRN (show STRN Antibodies)-ALK kinase fusions were determined in papillary thyroid cancer of an adult population
Colorectal carcinoma harboring ALK fusions represent a rare aggressive subtype of colorectal carcinoma with distinct clinicopathologic features. This report provides the first clinical evidence that such patients may benefit from targeted monotherapy with ALK inhibitors.
NSCLCs harboring EGFR (show EGFR Antibodies) mutations or ALK rearrangements are associated with low ORRs to PD-1 (show PDCD1 Antibodies)/PD-L1 (show CD274 Antibodies) inhibitors. Low rates of concurrent PD-L1 (show CD274 Antibodies) expression and CD8 (show CD8A Antibodies)(+) TILs within the tumor microenvironment may underlie these clinical observations.
The ROS1 S1986Y/F and ALK C1156Y mutations are homologous and displayed similar sensitivity patterns to ALK/ROS1 TKIs.
RT-PCR together with Sanger sequencing verified the presence of the FN1 (show FN1 Antibodies)-ALK fusion transcripts
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