The development of the genetic studies on acute myeloid leukemias (AMLs) has led to the identification of some recurrent genetic abnormalities. Their discovery was of fundamental importance not only for a better understanding of the molecular pathogenesis of AMLs, but also for the identification of new therapeutic targets. In this context, it is essential to identify AML-associated "driver" mutations, which have a causative role in leukemogenesis. Evidences accumulated during the last years indicate that activating internal tandem duplication mutations in FLT3 (FLT3-ITD), detected in about 20% of AMLs, represents driver mutations and valid therapeutic targets in AMLs. Furthermore, the screening of FLT3-ITD mutations has also considerably helped to improve the identification of more accurate prognostic criteria and of the therapeutic selection of patients.
Keyphrases
- acute myeloid leukemia
- allogeneic hematopoietic stem cell transplantation
- liver failure
- end stage renal disease
- tyrosine kinase
- bone marrow
- chronic kidney disease
- high resolution
- respiratory failure
- signaling pathway
- bioinformatics analysis
- peritoneal dialysis
- dendritic cells
- immune response
- acute lymphoblastic leukemia
- dna methylation