ABSTRACT
Although burning o tumors with ablative temperatures is an attractive option, lower temperatures of about 41-42°C (mild temperature hyperthermia) are ecacious as adjuncts to radiation therapy and chemotherapy. is is largely driven by an increase in blood flow (oen sustained for 1 to 2 days) and oxygen delivery and a decrease in oxygen demand (due to hyperthermia-induced cell death and metabolic suppression resulting in a shi toward anaerobic metabolism) that converge to increase tumor tissue oxygenation. Hyperthermia can also activate immunological responses. e molecular mechanisms of these eects of hyperthermia are being unraveled, and we now have a greater understanding of the subcellular events that render cells susceptible to various forms of damage (Fuller et al. 1994; Harmon et al. 1991). It is now known that there is no basic dierence among tumor cells, tumor vascular endothelial cells, and normal cells in their sensitivity to heat-induced cytotoxicity. However, inecient blood ow and oxygen transport through disordered tumor neovasculature results in an acidotic and nutrient-deprived environment within the tumor that makes them more thermosensitive (Bass et al. 1978). e greater sensitivity of hypoxic areas to heat allows for synergy with radiation therapy since hypoperfused areas within the tumor core are less sensitive to radiation-induced cytotoxicity, which depends on the generation of oxygen free radicals within well perfused regions. Increased perfusion also improves the delivery of chemo therapeutic drugs to the poorly vascularized tumor cores.
