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Abstract
The influence of stress protein synthesis and thermotolerance on blood-borne (experimental) metastatic potential was examined in the 13762NF rat mammary adenocarcinoma model. Cloned cell populations with highly reproducible and well denned metastatic potential were treated by hyperthermia and sodium arsenite to induce a complete set of stress proteins and thermotolerance with minimal cell killing. The influence of these in vitro treatments on subsequent experimental metastasis in vivo was determined for location, frequency, size distribution and volume. Metastatic tumour burden generally decreased following induction of increased heat or arsenite stress proteins and thermotolerance; however, there was no evidence for altered size distribution or location of metastatic lesions.