Abstract
Human acute myeloid leukemia (AML) derives from rare leukemic stem cells (LSCs). Relapse of disease can be ascribed to LSCs to some degree. Currently, a number of surface markers of AML LSCs have been identified, including CD123, CD44, CLL-1, CD96, CD47, CD32, CD25 and TIM-3. Moreover, monoclonal antibodies targeting some markers have demonstrated efficacy in xenotransplantation models. In our recent work, we found that N-cadherin and Tie2 positive CD34 + CD38 - CD123 + populations could develop acute myeloid leukemia more effectively in NOD/SCID mice than their negative counterparts at the same doses. Meanwhile, the blast cells from the bone marrow of leukemic mice are transplantable. It is speculated that FLT3-ITD mutation could make the LSCs more capable of expanding in the environment. These data suggested that N-cadherin and Tie2 were very important in development of leukemia as LSC markers.
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