Author/Authors :
Deshpande، نويسنده , , Aniruddha J. and Cusan، نويسنده , , Monica and Rawat، نويسنده , , Vijay P.S. and Reuter، نويسنده , , Hendrik and Krause، نويسنده , , Alexandre and Pott، نويسنده , , Christiane and Quintanilla-Martinez، نويسنده , , Leticia and Kakadia، نويسنده , , Purvi and Kuchenbauer، نويسنده , , Florian and Ahmed، نويسنده , , Farid and Delabesse، نويسنده , , Eric and Hahn، نويسنده , , Meinhard and Lichter، نويسنده , , Peter and Kneba، نويسنده , , Michael and Hiddemann، نويسنده , , Wolfgang and Macintyre، نويسنده , , Elizabeth and Mecucci، نويسنده , , Cristina and Ludwig، نويسنده , , Wolf-Dieter and Humphries، نويسنده , , R. Keith and Bohlander، نويسنده , , Stefan K. and Feuring-Buske، نويسنده , , Michaela Feuring-Buske، نويسنده , , Christian، نويسنده ,
Abstract :
Summary
lenge for the development of therapies selectively targeting leukemic stem cells in acute myeloid leukemia (AML) is their similarity to normal hematopoietic stem cells (HSCs). Here we demonstrate that the leukemia-propagating cell in murine CALM/AF10-positive AML differs from normal HSCs by B220 surface expression and immunoglobulin heavy chain rearrangement. Furthermore, depletion of B220+ cells in leukemic transplants impaired development of leukemia in recipients. As in the murine model, human CALM/AF10-positive AML was characterized by CD45RA (B220)-positive, IG DH-JH rearranged leukemic cells. These data demonstrate in a murine leukemia model that AML can be propagated by a transformed progenitor with lymphoid characteristics, which can be targeted by antibodies that do not crossreact with normal HSCs.
