Molecular variability of FLT3/ITD mutants and their impact on the differentiation program of 32D cells: implications for the biological properties of AML blasts
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19181379
DOI
10.1016/j.leukres.2009.01.004
PII: S0145-2126(09)00011-3
Knihovny.cz E-resources
- MeSH
- Leukemia, Myeloid, Acute genetics pathology MeSH
- Blast Crisis genetics pathology MeSH
- Cell Differentiation MeSH
- Cell Division MeSH
- Exons MeSH
- Genetic Variation * MeSH
- Cloning, Molecular MeSH
- Humans MeSH
- Molecular Sequence Data MeSH
- Mutation MeSH
- Mice genetics MeSH
- Cell Line, Tumor MeSH
- Reverse Transcriptase Polymerase Chain Reaction MeSH
- Retroviridae genetics MeSH
- Amino Acid Sequence MeSH
- Oligonucleotide Array Sequence Analysis MeSH
- Gene Expression Profiling MeSH
- Tandem Repeat Sequences genetics MeSH
- fms-Like Tyrosine Kinase 3 genetics MeSH
- Blotting, Western MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Mice genetics MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- FLT3 protein, human MeSH Browser
- fms-Like Tyrosine Kinase 3 MeSH
FLT3 is the most frequently mutated gene in acute myeloid leukemia (AML), with internal tandem duplications (ITDs) accounting for up to 30% of its mutations. To analyze the impact of individual ITDs on the expression profile of immature myeloid cells, we have established 32D cell lines expressing nine different FLT3/ITDs isolated from AML patients and subjected them to whole genome expression profiling and 2DE/LC/MS proteomics. Our data indicate that in comparison to the controls, FLT3/ITD-positive 32D cells exhibit less mature expression profiles resembling early hematopoietic progenitors. Moreover, our results suggest that there exist biological differences among individual ITD variants.
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