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Leukemia-Associated Antigens Are Critical for the Proliferation of Acute Myeloid Leukemia Cells

Authors' Affiliations: ¹ Department of Internal Medicine III, University of Ulm, Ulm, Germany and ² Department of Haematological Medicine, The Rayne Institute, London, United Kingdom

Requests for reprints: Jochen Greiner, Department of Internal Medicine III, University of Ulm, Robert-Koch-Str.8, 89081 Ulm, Germany. Phone: 49-731-500-45709; Fax: 49-731-500-45855; E-mail: jochen.greiner{at}uniklinik-ulm.de.

Abstract

Acute myeloid leukemia (AML) is the most common acute leukemia in adults. With intensive induction therapy, most patients younger than 60 years achieve complete remission. However, even if these younger patients were treated intensively, more than 50% will relapse. Clinical results of patients older than 60 years are more unfavorable. Therefore, in all patients with AML, the overall survival is still low. In the past decade, several leukemia-associated antigens (LAA) have been identified in patients with acute myeloid leukemia. BAGE, BCL-2, OFA-iLRP, FLT3-ITD, G250, hTERT, PRAME, proteinase 3, RHAMM, survivin, and WT-1 are all LAAs that have been shown to induce CD8⁺ T-cell recognition and for some antigens also humoral immune responses. Interestingly, most of these LAAs are linked to cell cycle or proliferation. This article discusses the balance between LAA-driven leukemia cell expansion and the elimination of these cells through attacks on LAAs by the immune system. Current knowledge of the function and CD8⁺ T-cell recognition of LAAs is reviewed and an outlook is given on how to improve T-cell responses to LAAs in acute myeloid leukemia cells.

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