Mechanism of regression of mammary adenocarcinomas in rats following plasma adsorption over protein A-containing Staphylococcus aureus.

The plasma from 7,12-dimethylbenz(a)anthracene-induced mammary tumor-bearing rats was adsorbed ex vivo with nonviable protein A-containing Staphylococcus aureus Cowan I and then injected into the rats, along with its original blood cells. Tumors in the treated rats showed significant (p less than 0.005) growth inhibition. There were fewer metastatic nodules; cellular cytotoxicity in the presence of plasma was augmented, and there was increased antitumor cytotoxic antibody activity in treated rats. Plasma from sham-treated rats, however, showed blocking activity. It appears that plasma perfusion over S. aureus decreases blocking activity and augments antitumor immunoreactivity of plasma. The exact mechanism by which growth of 7,12-dimethylbenz(a)anthracene-induced mammary tumors was inhibited in these treated Sprague-Dawley rats is not known. However, it is hypothesized that the observed tumor regression is at least partly attributable to the augmentation of antitumor immunoreactivity in the treated animals.