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Targeting the Immune Checkpoint in Cancer: Is This a Viable Treatment Option for AML?

Coles, Steven (2018) Targeting the Immune Checkpoint in Cancer: Is This a Viable Treatment Option for AML? Open Access Journal of Oncology and Medicine, 1 (2). pp. 1-2.

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Abstract

The immune suppressive mechanisms displayed by malignant cells are considered a central process in the pathogenesis of cancer. Research in this area has gained significant momentum over the past 20 years, with several immune checkpoints identified, including; CTLA-4, CD200/CD200R, Tim-3/Galectin-9 and PD-L1/PD-1 (Figure 1). Whilst characterising the molecular basis of leukaemia for risk stratification remains at the forefront of AML research; this must now extend to understating how these immune checkpoint pathways fit into the equation. A good example of why this is important is to consider CD200 expression level in AML, which is a negative prognostic indicator [1]. CD200 is an immunosuppressive ligand, that when engaged with its receptor CD200R, has the capacity to attenuate T-cell and NK-cell anti-tumour activity. Interestingly, most cases of CBF AML express high levels of CD200, yet CBF AML performs relatively well clinically. This paradox suggests there is a complex interplay between AML molecular heterogeneity and immune surveillance. Given the recent development and FDA approval of several immune checkpoint therapies, a full understanding of these processes and integration with standard molecular risk stratification is warranted.

Item Type: Article
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Uncontrolled Keywords: AML, acute myeloidleukaemia, core binding factor, myeldysplastic syndrome
Subjects: Q Science > Q Science (General)
R Medicine > RC Internal medicine > RC0254 Neoplasms. Tumors. Oncology (including Cancer)
Divisions: Academic Departments > Institute of Science and the Environment
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Depositing User: Steven Coles
Date Deposited: 08 May 2018 13:50
Last Modified: 03 Aug 2018 14:23
URI: https://eprints.worc.ac.uk/id/eprint/6609

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