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Leukemia-associated antigens are critical for the proliferation of acute myeloid leukemia cells

Leukemia-associated antigens are critical for the proliferation of acute myeloid leukemia cells
Leukemia-associated antigens are critical for the proliferation of acute myeloid leukemia cells
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
Acute myeloid leukemia (AML), cancer vaccines, Leukemia-associated antigens (LAAs), peptide vaccination, dendritic cells (DC)
1078-0432
7161-7166
Greiner, Jochen
8c8d50c3-bf3a-4913-8d80-ef8d4e5d2cd8
Bullinger, Lars
5a395588-dc36-4850-bd2c-5f66a0ca643b
Guinn, Barbara-ann
728d28c9-a23d-413a-ba1d-4531005705d7
Dohner, Hartmut
4abd8398-69e6-427a-8987-8345f825ef34
Schmitt, Michael
17c42a41-f6f9-41a4-a2a0-1085adab2079
Greiner, Jochen
8c8d50c3-bf3a-4913-8d80-ef8d4e5d2cd8
Bullinger, Lars
5a395588-dc36-4850-bd2c-5f66a0ca643b
Guinn, Barbara-ann
728d28c9-a23d-413a-ba1d-4531005705d7
Dohner, Hartmut
4abd8398-69e6-427a-8987-8345f825ef34
Schmitt, Michael
17c42a41-f6f9-41a4-a2a0-1085adab2079

Greiner, Jochen, Bullinger, Lars, Guinn, Barbara-ann, Dohner, Hartmut and Schmitt, Michael (2008) Leukemia-associated antigens are critical for the proliferation of acute myeloid leukemia cells. Clinical Cancer Research, 14, 7161-7166. (doi:10.1158/1078-0432.CCR-08-1102).

Record type: Article

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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More information

Published date: 15 November 2008
Keywords: Acute myeloid leukemia (AML), cancer vaccines, Leukemia-associated antigens (LAAs), peptide vaccination, dendritic cells (DC)

Identifiers

Local EPrints ID: 71031
URI: http://eprints.soton.ac.uk/id/eprint/71031
ISSN: 1078-0432
PURE UUID: 4eb619af-b6b8-4b19-b069-563dc2e0d7f1

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Date deposited: 14 Dec 2009
Last modified: 13 Mar 2024 20:17

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Contributors

Author: Jochen Greiner
Author: Lars Bullinger
Author: Barbara-ann Guinn
Author: Hartmut Dohner
Author: Michael Schmitt

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