Mechanisms of drug resistance in AML.

摘要: The acute myelogenous leukemias (AML) are diverse in their clinical presentation, molecular, biological and immunological characteristics, response to therapies. They encompass a wide spectrum of features, developing slowly from myelodysplastic syndromes (MDS) or presenting with dramatic features without prior warning, such as high circulating blast count resulting leucostastis bleeding, coagulopathies, cutaneous organ infiltration, sepsis due neutropenia, anemia. Morphological classification was initially codified the French-American-British (FAB) system1 recently modified World Health Organization (WHO) system.2 leukemic transformation is believed occur at an early stem cell level, based on ability CD34+38-leukemic cells repopulate NOD/scid mice3 exception promyelocytic (APL) that probably originate CD34-33+cells. However, were reported reside pre-CD34 “side-population” (SP) population,4 suggesting even more primitive origin