Abstract
An increasing number of leukemia-associated antigens (LAAs) have been identified in acute myeloid leukemia (AML) patients such as BAGE, BCL - 2, OFA-iLRP, FLT3 -ITD, G250, hTERT, PR AME, RHAMM, proteinase 3, survivin and WT -1 [1]. All of these LAAs can elicit specific T -cell responses in AML patients. RHAMM and WT -1 induce both serologic and cellular immune reactions. In vitro experiments demonstrated that epitopes in these LAAs are able to induce cell lysis of autologous leukemic blasts by specific cytotoxic T cells [2]. Specific cytotoxic T- lymphocyte transfusion activated against PR -1, a peptide derived from proteinase 3, reduced leukemia burden in a mouse AML xenograft model [3]. Posttransplant graft-versus-leukemia effect was found to be associated with cytotoxic CD8 + T cells against WT -1 [4]. The LAAs RHAMM, proteinase 3 and WT -1 were tested in clini1 were tested in clini
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