Abstract
Although standard therapy for AML has been relatively constant over the past 2 decades, this may be changing with enhanced technologies allowing for the classification of acute myeloid leukemia (AML) into molecularly distinct subsets. Some specific subsets of AML have an excellent prognosis in response to standard therapy, whereas the poor prognosis of AML associated with specific sets of mutations or chromosomal anomalies requires the development of new therapies. Elucidation of the molecular pathogenesis of AML has led to the development of therapies that affect signaling, apoptosis, protein and intermediate metabolism, the surface of the leukemia cell, leukemia cell/stromal interaction, and epigenetic regulation of gene expression.
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