License: Creative Commons Attribution 4.0 PDF - Published Version (7MB) |
- URN to cite this document:
- urn:nbn:de:bvb:355-epub-568821
- DOI to cite this document:
- 10.5283/epub.56882
Abstract
Acute myeloid leukemia (AML) with mutations in the FMS-like tyrosine kinase (FLT3) is a clinically unresolved problem. AML cells frequently have a dysregulated expression and activity of epigenetic modulators of the histone deacetylase (HDAC) family. Therefore, we tested whether a combined inhibition of mutant FLT3 and class I HDACs is effective against AML cells. Low nanomolar doses of the FLT3 ...
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