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( Department of Surgery, Laboratory of Surgical Research, and the Department of Pathology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania)
Previous studies demonstrated that liver damage produced by a variety of modalities enhanced the incidence and growth of experimentally induced hepatic metastases. Search for possible mechanisms responsible for this augmentation provided no evidence that a humoral factor related to hepatic damage or regeneration was responsible. It was considered, however, that direct contact of damaged cells with tumor cells could be a factor. Since little information was available relevant to the effect of normal or damaged cells upon adjacent neoplastic elements, studies were carried out, with tissue homogenates, to provide an environment for tumor cells somewhat akin to that in damaged liver.
Homogenates of various organs from adult animals given injections either simultaneously with tumor cells or at separate sites accelerated the onset and subsequent growth of tumor. Freezing or heating of tissues failed to eliminate this response, and species specificity was not a factor.
Injection of homogenate in one member of a parabiotic pair had a similar growth-promoting effect upon tumor growing in the other parabiont. Of particular interest was the occurrence of tumor at the site of homogenate injection in both single and parabiotic animals when this was separate from the location of tumor cell inoculation.
Speculation as to mechanisms responsible for these observations is entertained, and it is suggested that the tumor growth-promoting factor is a product of dead or dying normal cells rather than a humoral factor associated with regeneration.
* Supported by American Cancer Society Grant No. P-142 and U.S.P.H. Grants CA-05716 and CA-05949.
Received 5/15/63.
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