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Antigenic targets for the immunotherapy of acute myeloid leukaemia

Khan, Ghazala; Orchard, Kim; Guinn, Barbara-ann


Ghazala Khan

Kim Orchard


One of the most promising approaches to preventing relapse is the stimulation of the body's own immune system to kill residual cancer cells after conventional therapy has destroyed the bulk of the tumour. In acute myeloid leukaemia (AML), the high frequency with which patients achieve first remission, and the diffuse nature of the disease throughout the periphery, makes immunotherapy particularly appealing following induction and consolidation therapy, using chemotherapy, and where possible stem cell transplantation. Immunotherapy could be used to remove residual disease, including leukaemic stem cells from the farthest recesses of the body, reducing, if not eliminating, the prospect of relapse. The identification of novel antigens that exist at disease presentation and can act as targets for immunotherapy have also proved useful in helping us to gain a better understand of the biology that belies AML. It appears that there is an additional function of leukaemia associated antigens as biomarkers of disease state and survival. Here, we discuss these findings.


Khan, G., Orchard, K., & Guinn, B. (2019). Antigenic targets for the immunotherapy of acute myeloid leukaemia. Journal of Clinical Medicine, 8(2), 134.

Journal Article Type Article
Acceptance Date Jan 20, 2019
Online Publication Date Jan 23, 2019
Publication Date Jan 23, 2019
Deposit Date Jan 30, 2019
Publicly Available Date Jan 30, 2019
Journal Journal of Clinical Medicine
Print ISSN 2077-0383
Publisher MDPI
Peer Reviewed Peer Reviewed
Volume 8
Issue 2
Pages 134
Series Title Special Issue Immunotherapies for Acute Myeloid Leukemia
Keywords Acute myeloid leukaemia; Cancer-testis antigen; Human; Clinical trial; Immunotherapy
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Copyright Statement
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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