Genomic structure of the downstream part of the human FLT3 gene: exon/intron structure conservation among genes encoding receptor tyrosine kinases (RTK) of subclass III

Tandem duplication of the epidermal growth factor receptor tyrosine kinase and calcium internalization domains in A-172 glioma cells

“…In contrast, certain members of the subclass III receptor family, such as FLT3, c-kit, c-fms and members of the Janus (JAK) family of receptors have two separate tyrosine kinase domains separated by a KI or`kinase insert' region (Agnes et al, 1994). Small internal tandem duplication of nucleotide sequences within the juxtamembrane and TK-1 regions of the FLT3 gene have been reported in the cells of patients with acute myeloid leukemia .…”

Improved prognostic significance of cytokine-induced proliferation in vitro in patients with de novo acute myeloid leukemia of intermediate risk: impact of internal tandem duplications in the Flt3 gene

“…As cytogenetic aberrations are thought to be important prognostic factors for AML 20,21 patients were stratified in three groups, ie a good risk group consisting of patients defined by a karyotype of t(8;21), t(15;17) or inv(16) and a poor risk group defined by del(5), del(7), or deletions of the q arms of these chromosomes, t (6,9), alterations in the 11q23 region or the presence of multiple aberrations (more than three) in the karyotype. All other karyotypic aberrations and a normal karyotype were included in an intermediate risk group.…”

“…Adverse prognostic factors include (1) an age over 60 years, (2) AML resulting from a prior hematological disorder such as MDS and (3) a high white blood cell count. 2 The fms-like tyrosine kinase 3 (Flt3), also known as stem cell tyrosine kinase-1 (STK1) or fetal liver tyrosine kinase-2 (FLK-2), [3][4][5][6] belongs to the group of class III receptor tyrosine kinases (RTKs) which also include the receptors c-kit and cfms. Signals generated by ligand-induced dimerisation of these receptors involve tyrosine phosphorylation of certain regions of the receptor and activation of cellular tyrosine kinases.…”

Gene expression changes in normal haematopoietic cells

“…RTKs contain intrinsic kinases that drive intracellular signaling activity and are divided into more than 20 subclasses. 71 The RTK subclass III (the PDGFR family) is the best-studied in normal and abnormal hematopoiesis, and is composed of 5 homologous members (CSF1R, FLT3, KIT, PDGFRA, and PDGFRB). [71][72][73] The shared structure includes: five extracellular immunoglobulin-like domains (EMD), a transmembrane domain (TMD), juxtamembrane domain (JMD), two intracellular tyrosine kinase domains (TKD), and a hydrophilic insertion/linker domain between the TKDs (KID).…”

“…71 The RTK subclass III (the PDGFR family) is the best-studied in normal and abnormal hematopoiesis, and is composed of 5 homologous members (CSF1R, FLT3, KIT, PDGFRA, and PDGFRB). [71][72][73] The shared structure includes: five extracellular immunoglobulin-like domains (EMD), a transmembrane domain (TMD), juxtamembrane domain (JMD), two intracellular tyrosine kinase domains (TKD), and a hydrophilic insertion/linker domain between the TKDs (KID). 72,73 Compared to RTKs, CKRs do not have intrinsic tyrosine kinase activity and must recruit kinases to initiate intracellular signaling.…”