Therapeutic hyperthermia: The old, the new, and the upcoming - Critical Reviews in Onco... - 1 views
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not well understood, but it is felt to be a combination of both heat-induced necrosis and of protein inactivation (e.g., repair enzymes) as opposed to DNA damage
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alterations in tumor cytoskeletal and membrane structures, which disrupt cell motility and intracellular signal transduction
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A common explanation for HT-enhancement of RT and CT involves inhibition of homologous recombination repair of double-strand DNA breaks, preventing cells from repairing sub-lethal damage
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it does appear to inhibit rejoining of RT-induced DNA breaks more than is commonly observed after RT alone
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HT damages cells and enhances RT and CT sensitivity as a function of both temperature and duration of treatment
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Cancer cells are particularly vulnerable to heating; in vivo studies have shown that temperatures in the range of 40–44 °C cause more selective damage to tumor cells
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selective cytotoxic effect on tumor cells include inhibition of key cancer cell-signaling pathways such as AKT, inducing apoptosis, suppression of cancer stem cell proliferation, and others
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increase in immunological attacks against tumors after HT, which were believed to be achieved through activation of HSPs and subsequent modulation of the innate and adaptive immune responses against tumor cells
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HT does lead to activation of the immune system and HSP-induced cell death through modification of the tumor cell surface
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These HSPs and tumor antigens are taken up by dendritic cells and macrophages and go on to induce specific anti-tumor immunity
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In vivo studies demonstrate HT-enhancement of NK cell activity, and HT has been shown to increase neutrophilic granulocytes with anti-tumor activity
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it has become increasingly clear that HT results in immune stimulation, through both direct heat-mediated cell killing as well as innate and adaptive immune system modulation
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The term hyperthermia is used in this review to refer to heating within the clinically accepted range of 40–45 °C
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temperatures above 42.5–43 °C the exposure time can be halved with each 1 °C increase while maintaining equivalent cell killing