Neutralizing Tumor-Promoting Chronic Inflammation: A Magic Bullet?
By Lisa M. Coussens, Laurence Zitvoge, A. Palucka. Science, 2013
1,077 citations recorded by the source corpus.
A Shift in Cancer's Inflammatory Balance One of the many factors that contribute to the initiation and progression of cancer is inflammation. Inflammation can support tumor development, both directly and indirectly, and tumors can promote a chronic inflammatory environment that results in immunosuppression, which benefits the tumor. Coussens et al. (p. 286) review the components of the immune system that contribute to the chronic inflammation seen in tumors. Potential therapies might shift this inflammatory environment toward one more characteristic of an acute, resolving inflammation, similar to what is observed during a pathogenic infection. Such a shift would relieve immunosuppression and drive antitumor immunity that, when combined with other therapies, may ultimately result in tumor cell clearance. There have been substantial advances in cancer diagnostics and therapies in the past decade. Besides chemotherapeutic agents and radiation therapy, approaches now include targeting cancer cell–intrinsic mediators linked to genetic aberrations in cancer cells, in addition to cancer cell–extrinsic pathways, especially those regulating vascular programming of solid tumors. More recently, immunotherapeutics have entered the clinic largely on the basis of the recognition that several immune cell subsets, when chronically activated, foster tumor development. Here, we discuss clinical and experimental studies delineating protumorigenic roles for immune cell subsets that are players in cancer-associated inflammation. Some of these cells can be targeted to reprogram their function, leading to resolution, or at least neutralization, of cancer-promoting chronic inflammation, thereby facilitating cancer rejection.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/e3aa8ff002403995ccb0d07701c359b8c55a026c
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Citations in the corpus
- Autophagy in malignant transformation and cancer progression (2015, neutral): “At least in some cases, malignant transformation is stimulated by an inflammatory microenvironment, which contains high amounts of potentially genotoxic ROS as well as various mitogenic cytokines (Coussens et al , 2013).”
- Noninvasive imaging of immune responses (2015, neutral): “The approach described here obviates the need for the generation of panels of tumor-specific antibodies, if indeed such accumulation of myeloid cells is a general phenomenon, as suggested by the available evidence (2, 34).”
- Immunological Effects of Conventional Chemotherapy and Targeted Anticancer Agents. (2015, background): “Moreover, chronic inflammation (mostly supported by myeloid cells) can stimulate carcinogenesis (Coussens et al., 2013).”
- Immunity, inflammation, and cancer: an eternal fight between good and evil. (2015, positive): “Exposure of macrophages to IL-4 produced by CD4+ T cells and/or cancer cells (59, 63), growth factors such as colony stimulating factor-1 (CSF1) (64), GM-CSF (65), and TGFβ secreted by cancer cells, can also induce the M2 switch.”
- Cancer immunotherapy via dendritic cells (2012, positive): “Tumor-derived factors can alter DCs maturation so as to yield cells that indirectly help tumor growth (“pro-tumor” inflammation) [84].”
- Mechanism of action of conventional and targeted anticancer therapies: reinstating immunosurveillance. (2013, background): “…immunosuppressive mechanisms, encompassing the secretion of specific cytokines such as interleukin-10 (IL-10) and the accumulation of immunomodulatory cell types including FOXP3+ regulatory T (Treg) cells, myeloid-derived suppressor cells (MDSCs), and M2 macrophages (Coussens et al., 2013).”