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Cancer-related inflammation.

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TLDR
The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.

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Citations
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Hallmarks of cancer: the next generation.

TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.
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Immunity, Inflammation, and Cancer

TL;DR: The principal mechanisms that govern the effects of inflammation and immunity on tumor development are outlined and attractive new targets for cancer therapy and prevention are discussed.
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Macrophage plasticity and polarization: in vivo veritas

TL;DR: The identification of mechanisms and molecules associated with macrophage plasticity and polarized activation provides a basis for Macrophage-centered diagnostic and therapeutic strategies.
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Macrophage Diversity Enhances Tumor Progression and Metastasis

TL;DR: There is persuasive clinical and experimental evidence that macrophages promote cancer initiation and malignant progression, and specialized subpopulations of macrophage may represent important new therapeutic targets.
References
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“Re-educating” tumor-associated macrophages by targeting NF-κB

TL;DR: A new role for NF-κB in cancer in maintaining the immunosuppressive phenotype of tumor-associated macrophages (TAMs), and the potential to “re-educate” the tumor-promoting macrophage population may prove an effective and novel therapeutic approach for cancer that complements existing therapies.
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De novo carcinogenesis promoted by chronic inflammation is B lymphocyte dependent.

TL;DR: It is reported that genetic elimination of mature T and B lymphocytes in a transgenic mouse model of inflammation-associated de novo epithelial carcinogenesis, e.g., K14-HPV16 mice, limits neoplastic progression to development of epithelial hyperplasias that fail to recruit innate immune cells.
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Ras-induced interleukin-8 expression plays a critical role in tumor growth and angiogenesis

TL;DR: Using a tumor xenograft model, it is shown that Ras-dependent CXCL-8 secretion is required for the initiation of tumor-associated inflammation and neovascularization and a novel mechanism by which the Ras oncogene can elicit a stromal response that fosters cancer progression.
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Effect of aspirin on long-term risk of colorectal cancer: consistent evidence from randomised and observational studies

E Flossmann, +1 more
- 12 May 2007 - 
TL;DR: Regular use of aspirin or NSAID was consistently associated with a reduced risk of colorectal cancer, especially after use for 10 years or more, with no difference between aspirin and other NSAIDs, or in relation to age, sex, race, or family history, site or aggressiveness of cancer.
Journal ArticleDOI

Aspirin and the Risk of Colorectal Cancer in Relation to the Expression of COX-2

TL;DR: Regular use of aspirin appears to reduce the risk of colorectal cancers that overexpress COX-2 but not the risk for cancers with weak or absent expression of COx-2.
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How LPS related to cancer?

LPS (lipopolysaccharide) is a molecule that can induce inflammation and is associated with cancer-related inflammation.