phenylbutazone--propyphenazone-drug-combination and Neoplasms

A hypothesis on blocking factor formation in carcinogenesis is discussed. Destabilisation of cell membranes and increased levels of proteolytic enzymes in tumor tissue are considered to be the trigger mechanism. Protease level in large bowel tumor was found to be higher than in normal tissue. Plasminogen level in cancer patients was significantly higher than in healthy subjects. Application of different experimental schemes of treatment with membrane-stabilizing drugs and an inhibitor of protease was followed by antitumor and antiblocking effects. Sorption of rheumatoid factor and immune complexes from plasma led to a decrease in the blocking activity of plasma in vitro. In cases of rectal cancer, plasmapheresis was followed by tumor regression and a fall in immune complex concentration.

Topics: 2,3-Diketogulonic Acid; Alloxan; Aminopyrine; Animals; Antigens, Neoplasm; Drug Combinations; Ferric Compounds; Fibrinolysis; Humans; Immunotherapy; Mefenamic Acid; Mice; Mice, Inbred BALB C; Mice, Inbred C3H; Neoplasms; Peptide Hydrolases; Phenylbutazone; Rheumatoid Factor