Use your antibodies-online credentials, if available.
Anaplastic lymphoma kinase (ALK) is a receptor tyrosine kinase (显示 ERBB3 抗体) associated with alcohol dependence in humans and behavioral responses to ethanol in mice.
ALKR1275Q cooperated with MYCN (显示 MYCN 抗体) in the development of aggressive NB, possibly by downregulating the expression of ECM (显示 MMRN1 抗体)/BM-associated genes and by conferring malignant potentials to MYCN (显示 MYCN 抗体)-expressing cells.
ALK inhibitor alectinib inhibits tumor growth in a TH-MYCN (显示 MYCN 抗体) transgenic neuroblastoma (显示 ARHGEF16 抗体) 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 (显示 MDK 抗体)) 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 (显示 ARHGEF16 抗体).
Th-MYCN (显示 MYCN 抗体) genetically-engineered murine models of neuroblastoma (显示 ARHGEF16 抗体) using MRI (显示 C7ORF49 抗体), we have identified a marked ALK(F1174L)-driven vascular phenotype.
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 (显示 ESRP1 抗体).
This computational investigation in-sighted the molecular factors involved in crizotinib resistance which enhanced in the identification of new ALK drugs that brings individualized medicine to treat ALK positive NSCLC patients with specific mutations.
Case Report: inflammatory myofibroblastic tumor (IMT) of the urinary bladder with a novel HNRNPA1 (显示 HNRNPA1 抗体)-ALK fusion.
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.
Results show no apparent association between environmental tobacco smoke exposure and ALK translocation.
Our results suggest that the ALK RGQ RT-PCR test could be useful in clinical practice as a complementary assay in multi-test diagnostic algorithms or even, if our data will be confirmed in independent studies, as a standalone or screening test for the selection of patients to be treated with ALK inhibitors.
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.
Recent preclinical models and translational efforts have provided critical insights into the molecular mechanisms of resistance to EGFR (显示 EGFR 抗体) 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 (显示 EGFR 抗体)-mutant and ALK-rearranged lung cancers
c-Met overexpression, HER-2 (显示 ERBB2 抗体) gene amplification, and SPTBN1 (显示 SPTBN1 抗体)-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.
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.
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