ABSTRACT
A review of the current state of knowledge on the effect of hyperthemmia on molecular aspects of the killing of cancer cells by imntunocytolysis is presented. The effect of hypenherthermia, fractionated heat and the synthesis of heat shock proteins, following heat or chemical stress, was examined on the density and lateral diffusion of murine cell surface histucompatibility antigens [H-2K]. These two properties of cell surface antigens are essential for the cell mediated killing of tumour cells. The results suggest that: [1] after an initial decrease following a heat shock, there is an increase in the antigen density of surviving cells. A remarkable 10-25 fold increase of antigens was observed in a sub-population of heat treated cells: [2] heat induced membrane modification, as shown by antigen protection; is far more rapid than the development of thermotoleranee; [3] heat shock proteins do not affect the thermal response of these antigens; [4] an unexpected observation was that CH-1 cells do not synthesize heat shock proteins under chemical or thermal stress-.cs. Heat effects on the diffusion patterns of membrane antigens of all the cell lines showed a temperature dependent decrease in the mobile fraction of the membrane. This "freezing" phenomenon was unaffected by the presence or absence of heat or chemically induced heat shock proteins. After 48-60 hr. following a heat shock, the diffusion patterns of the heat shocked cells were similar to those of unheated control cells. These data show that immediately after heat treatment, cells may be refractory to immnnumocytolysis. However, 96 hr. after heating, a striking increase in antigen density and normalization of the mobility properties of the membrane should render them susceptible to cytolysis. This review presents an explanation for the conflicting claims from different laboratories around the world regarding cancer cures and the susceptibility of tumours to inutuumocytolysis after heat treatment