نتایج جستجو برای: anaplastic lymphoma kinase
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Description 1620 amino acids; 177 kDa; after glycosylation, produces a 200 kDa mature glycoprotein; composed of an extracellular domain, a transmembrane domain, a tyrosine kinase domain, and an intracytoplasmic domain in C-term; dimerization. Expression Is tissue specific; mainly in: brain, gut and testis; not in the lymphocytes. Localisation Cell membrane. Function Membrane associated tyrosine...
Background: Patients with non-small cell lung cancer (NSCLC) harboring anaplastic lymphoma kinase (ALK) fusions may benefit from ALK-tyrosine inhibitors (ALK-TKIs). However, few studies have analyzed the clinical outcome in patients multiple ALK fusions, including double or triple fusions. Here, our study aimed to analyze impact of on efficacy receiving ALK-TKIs NSCLC patients.
on chromosome 2p23, and codes for a protein that is expressed in some cells of the central nervous system, but in virtually no other normal human cells. Interest in this protein among diagnostic pathologists has been related to its utility in recognizing a subset of CD30+ anaplastic large cell lymphomas (ALCL's), that show a characteristic t(2;5)(p23;q35) translocation. This translocation resul...
BACKGROUND The role of β-catenin in cancer has been most studied in tumors of epithelial cell origin. The functional status and biological significance of this protein in anaplastic lymphoma kinase (ALK)-positive anaplastic large cell lymphoma is unknown. DESIGN AND METHODS ALK-positive anaplastic large cell lymphoma cell lines and patients' tumor samples were examined for status of β-catenin...
primary cutaneous anaplastic large cell lymphoma is a t-cell malignancy with atypical cd30 positive lymphocytes. pseudoepitheliomatous hyperplasia is an uncommon finding in primary cutaneous anaplastic large cell lymphoma, and may mimic squamous cell carcinoma as pseudomalignancy. careful attention of a pathologist to correct diagnosis of pseudoepitheliomatous hyperplasia and its underlying cau...
Herein, we have reviewed and analysed recent literature, published in 2013 and early 2014, in the context of pre-existing data. Considered target therapies were tyrosine kinase inhibitors of active epidermal growth factor receptor mutations (e.g. erlotinib, gefinitib and afatinib), anaplastic lymphoma kinase rearrangements (e.g. crizotinib) or angiogenesis (drugs under development), or monoclon...
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