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Cancer Research Laboratory, Department of Chemical Engineering, Carnegie-Mellon University, Pittsburgh, Pennsylvania 15213
Participation of the host immune response in eradication of tumor by hyperthermia has been suspected for a long time. The effect of local tumor heating on the immunocompetence of rats bearing Mc7 sarcoma was studied. Following heat treatment of 1- to 1.5-ml foot tumors at 43° for 2 hr, regression of primary tumors resulted in host cure (15 of 21; 71%), and this was accompanied by an increased skin response to both 3 M KCl extract of Mc7 and dinitrochlorobenzene as well as in elevation of antibody to bovine serum albumin. Increased levels of antitumor antibody were not detected. Animals that were cured by hyperthermia showed no sign of metastatic tumor in lymph nodes and lungs; most control animals at the time of heat treatment had secondary tumor deposits in lymph nodes and lungs. Tumor regression after curative heating did not occur in rats (0 of 10) treated by whole-body X-rays (150 R; 3 times) plus cortisone acetate (60 mg/kg; 4 times; s.c.), and the tumor cure rate was reduced (9 of 21; 43%) by blocking macrophage activity with silica (1 g/kg; i.v. and i.p.). Also, these rats (43%) succumbed to tumor challenge with 2.5 x 106 Mc7 cells; 50% of the heat-cured animals not given silica consistently rejected this challenge dose. The results imply that immunostimulation comprising mainly T-cells and macrophages plays a major part in tumor regression by hyperthermia.
1 Work was supported by the North of England Council of the Cancer Research Campaign and by the National Science Foundation (ENG-78-25432).
Received 7/28/80. Accepted 2/ 2/81.
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