摘要
Acute myeloid leukemia (AML) is a clonal heterogeneous disease of the myeloid white blood cells. It is characterised by an accumulation of immature blast cells and a number of chromosomal and genetic mutations have been identified. In both de novo and therapy-related AML, defective DNA repair mechanisms are responsible for some of these genetic abnormalities. Targeting the DNA repair mechanism has been shown to be successful against certain forms of solid tumors and may represent a novel therapeutic approach for AML.
Acute myeloid leukemia (AML) is a clonal heterogeneous disease of the myeloid white blood cells. It is characterised by an accumulation of immature blast cells and a number of chromosomal and genetic mutations have been identified. In both de novo and therapy-related AML, defective DNA repair mechanisms are responsible for some of these genetic abnormalities. Targeting the DNA repair mechanism has been shown to be successful against certain forms of solid tumors and may represent a novel therapeutic approach for AML.
