期刊
LEUKEMIA
卷 30, 期 9, 页码 1805-1815出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/leu.2016.161
关键词
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资金
- Italian Association for Cancer Research (AIRC) [10007]
- ImmOnc [BIO F.E.S.R. 2007/13, LR 34/2004]
- Oncology Program of Compagnia di San Paolo, Torino
- Ricerca Finalizzata, Ministero della Salute
- Gelu Foundation (Switzerland)
- Oncoethix
- PIQUR Therapeutics AG
- EMD Serono
- Bayer AG
- Sigma Tau
- Italfarmaco
- CTI Life Sciences and Celgene
The acquisition of a complete neoplastic phenotype requires cancer cells to develop escape mechanisms from the host immune system. This phenomenon, commonly referred to as 'immune evasion,' represents a hallmark of cancers and results from a Darwinian selection of the fittest tumor clones. First reported in solid tumors, cancer immunoescape characterizes several hematological malignancies. The biological bases of cancer immunoescape have recently been disclosed and include: (i) impaired human leukocyte antigen-mediated cancer cell recognition (B2M, CD58, CTIIA, CD80/CD86, CD28 and CTLA-4 mutations); (ii) deranged apoptotic mechanisms (reduced pro-apoptotic signals and/or increased expression of anti-apoptotic molecules); and (iii) changes in the tumor microenvironment involving regulatory T cells and tumor-associated macrophages. These immune-escape mechanisms characterize both Hodgkin and non-Hodgkin (B and T cell) lymphomas and represent a promising target for new anti-tumor therapies. In the present review, the principles of cancer immunoescape and their role in human lymphomagenesis are illustrated. Current therapies targeting these pathways and possible applications for lymphoma treatment are also addressed.
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