Overcoming immunotherapeutic resistance by targeting the cancer inflammation cycle.

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ID: 83111
2020
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Abstract
Inflammation is a hallmark of cancer and supports tumor growth, proliferation, and metastasis, but also inhibits T cell immunosurveillance and the efficacy of immunotherapy. The biology of cancer inflammation is defined by a cycle of distinct immunological steps that begins during disease conception with the release of inflammatory soluble factors. These factors communicate with host organs to trigger bone marrow mobilization of myeloid cells, trafficking of myeloid cells to the tumor, and differentiation of myeloid cells within the tumor bed. Tumor-infiltrating myeloid cells then orchestrate an immunosuppressive microenvironment and assist in sustaining a vicious cycle of inflammation that co-evolves with tumor cells. This Cancer-Inflammation Cycle acts as a rheostat or "inflammostat" that impinges upon T cell immunosurveillance and prevents the development of productive anti-tumor immunity. Here, we define the major nodes of the Cancer-Inflammation Cycle and describe their impact on T cell immunosurveillance in cancer. Additionally, we discuss emerging pre-clinical and clinical data suggesting that intervening upon the Cancer-Inflammation Cycle will be a necessary step for broadening the potential of immunotherapy in cancer.
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wattenberg2020overcomingseminars Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Wattenberg, Max M;Beatty, Gregory L;
Journal seminars in cancer biology
Year 2020
DOI
S1044-579X(20)30003-1
URL
Keywords
Cancer inflammation macrophage t cells immunotherapy myeloid cells inflammostat

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