期刊
IMMUNOLOGY AND CELL BIOLOGY
卷 95, 期 4, 页码 325-332出版社
WILEY
DOI: 10.1038/icb.2016.126
关键词
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资金
- Naito Foundation
- QIMR Berghofer Seed Grant
- National Health and Medical Research Council of Australia (NH&MRC) Senior Principal Research Fellowship [1078671]
- NH&MRC Development Grant [1093566]
- National Health and Medical Research Council of Australia [1093566] Funding Source: NHMRC
Recent advances in cancer immunotherapy, particularly immune checkpoint blockade therapy have dramatically changed the therapeutic strategy against advanced malignancies. Still, only a subset of patients shows a good response to any single therapy. Moreover, it remains largely unsolved how we can maintain durable clinical responses, or how we can successfully treat a broader range of cancers by immunotherapy. Growing evidence suggests that the major barrier to more successful cancer immunotherapy is the tumour microenvironment (TME), where chronic inflammation has a predominant role in tumour survival and proliferation, angiogenesis and immunosuppression. Over the past decades, our understanding of cancer-related inflammation has significantly evolved, and now we have various therapeutic options tailored to the TME. These therapeutic strategies include inhibiting inflammatory mediators or their downstream signalling molecules, blocking the recruitment of myeloid cells, modulating immunosuppressive functions in myeloid cells and re-educating the TME. In this review, we discuss the role of cancer-related inflammation as a potential target in the era of immunotherapy.
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