A sustained and chronically-inflamed environment is characterized by the presence of heterogeneous inflammatory cellular components, including neutrophils, macrophages, lymphocytes and fibroblasts. These infiltrated cells produce growth stimulating mediators (inflammatory cytokines and growth factors), chemotactic factors (chemokines) and genotoxic substances (reactive oxygen species and nitrogen oxide) and induce DNA damage and methylation. Therefore, chronic inflammation serves as an intrinsic niche for carcinogenesis and tumor progression. In this article, we summarize the up-to-date findings regarding definitive/possible causes and mechanisms of inflammation-related carcinogenesis derived from experimental and clinical studies. We also propose 10 strategies, as well as candidate agents for the prevention of inflammation-related carcinogenesis.
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Purpose: The MHC-unrestricted activity of cytokine-induced killer (CIK) cells against chemo-surviving melanoma cancer stem cells (mCSC) was...
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Publication date: 18 April 2017 Source: Cell Reports, Volume 19, Issue 3 Author(s): David Estoppey, Chia Min Lee, Marco Janoschke, Boon He...
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from #AlexandrosSfakianakis via Alexandros G.Sfakianakis on Inoreader http://ift.tt/2oLOayI via IFTTT
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Abstract Functionalised electrospun polyamide-6 (PA-6) nanofibres incorporating gadolinium oxide nanoparticles conjugated to zinc tetracar...
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Cytokine-dependent renewal of stem cells is a fundamental requisite for tissue homeostasis and regeneration. Spermatogonial progenitor cells...
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Vol.20 No.1 from #AlexandrosSfakianakis via Alexandros G.Sfakianakis on Inoreader http://ift.tt/2seUCMY via IFTTT
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Abstract This paper addresses the hybrid consensus-based formation keeping problem for nonholonomic mobile robots in the presence of a nov...
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Current treatments for generalized pustular psoriasis are unsatisfactory. We applied recently-developed techniques for transcriptomic analys...
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Downregulation of mouse CCR3 by lentiviral shRNA inhibits proliferation and induces apoptosis of mouse eosinophils. Mol Med Rep. 2016 ...
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