PUBLICATION

Overexpression of FLT3-ITD driven by spi-1 results in expanded myelopoiesis with leukemic phenotype in zebrafish

Authors
Lu, J.W., Hou, H.A., Hsieh, M.S., Tien, H.F., Lin, L.I.
ID
ZDB-PUB-160610-15
Date
2016
Source
Leukemia   30(10): 2098-2101 (Journal)
Registered Authors
Lin, Liang-In, Lu, Jeng-Wei
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Myelopoiesis/genetics*
  • Phenotype
  • Proto-Oncogene Proteins/physiology*
  • Trans-Activators/physiology*
  • Zebrafish/embryology
  • fms-Like Tyrosine Kinase 3/genetics
  • fms-Like Tyrosine Kinase 3/metabolism*
PubMed
27271227 Full text @ Leukemia
Abstract

Acute myeloid leukemia (AML) is a clonal hematologic malignancy that shows great variability with regard to pathogenesis and treatment outcomes. The class III receptor tyrosine kinase of FMS-like tyrosine kinase 3 (FLT3) has an important role in normal hematopoiesis and internal tandem duplications of FLT3 (FLT3-ITD), which disrupts the autoinhibitory juxtamembrane domain, is one of the most common mutations in AML. The FLT3-ITD mutation is typically associated with poor prognosis and significantly increased relapse rates. Indeed, FLT3-ITD can induce growth factor-independent proliferation in leukemia cell lines and fetal myeloproliferative neoplasm (MPN) in murine models. Therefore, FLT3-ITD is considered a key driver of AML pathogenesis and may be an ideal therapeutic target for AML patients. Nucleophosmin (NPM1) is a multifunctional nucleus-cytoplasm shuttling protein known to be involved in the regulation of cell growth and proliferation.

Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes