Article
Mechanisms of resistance against PKC412 in resistant FLT3-ITD positive human acute myeloid leukemia cells.
Annals of hematology - 1 Jul 2010
Stölzel Friedrich, Steudel Christine, Oelschlägel Uta, Mohr Brigitte, Koch Sina, Ehninger Gerhard, Thiede Christian
Abstract excerpt
Treatment of acute myeloid leukemia (AML) remains challenging with many patients harboring unfavorable prognostic parameters such as FLT3 internal tandem duplication (FLT3-ITD) mutations leading to a constitutively activated FLT3-receptor tyrosine kinase (RTK). Activation of proteins by phosphorylation of tyrosine residues is a common mechanism in leukemia development. Therefore, specific tyrosine kinase...
Topics
- Cell Line, Tumor
- Chromosomes, Human, Pair 13
- Clinical Trials as Topic
- Drug Resistance, Neoplasm
- Gene Expression Profiling
- Gene Expression Regulation, Leukemic
- Humans
- Leukemia, Myeloid, Acute
- Mutation
- Oligonucleotide Array Sequence Analysis
- Prognosis
- Protein Kinase Inhibitors
- Staurosporine