Journal
BLOOD CANCER JOURNAL
Volume 4, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/bcj.2014.14
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Funding
- Herlev University Hospital Research Council
- Danish Cancer Society
- Aase and Ejnar Danielsen's Foundation
- Betty and Valdemar van Hauen Foundation
- Inge and Jorgen Larsen's grant
- Prosektor Axel Soeborg Ohlsen's grant
- A.V. Lykfeldt and Wife's grant
- Novo Nordisk Fonden [NNF13OC0003435] Funding Source: researchfish
- The Danish Cancer Society [R72-A4531, R72-A4396] Funding Source: researchfish
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Treatment with the demethylating agent 5-Azacytidine leads to prolonged survival for patients with myelodysplastic syndrome, and the demethylation induces upregulation of cancer-testis antigens. Cancer-testis antigens are well-known targets for immune recognition in cancer, and the immune system may have a role in this treatment regimen. We show here that 5-Azacytidine treatment leads to increased T-cell recognition of tumor cells. T-cell responses against a large panel of cancer-testis antigens were detected before treatment, and these responses were further induced upon initiation of treatment. These characteristics point to an ideal combination of 5-Azacytidine and immune therapy to preferentially boost T-cell responses against cancer-testis antigens. To initiate such combination therapy, essential knowledge is required about the general immune modulatory effect of 5-Azacytidine. We therefore examined potential treatment effects on both immune stimulatory (CD8 and CD4 T cells and Natural Killer (NK) cells) and immune inhibitory cell subsets (myeloid-derived suppressor cells and regulatory T cells). We observed a minor decrease and modulation of NK cells, but for all other populations no effects could be detected. Together, these data support a strategy for combining 5-Azacytidine treatment with immune therapy for potential clinical benefit.
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