Cancer: restriction of chemical energy by fatty acids as the common pathway whereby various anti-tumour procedures selectively damage malignant cells in situ.
Harmful effects may be inflicted upon cancer cells in vivo by a variety of means, for example, by the administration of bacterial endotoxins or alkylating agents, and by radiation treatment. These different procedures appear to act on tumours indirectly, and are also capable of inducing shock. The suggestion is made that the deleterious actions on cancer cells are mediated by the tissues of the host, and involve raising the levels of non-esterified fatty acids (NEFAs) in the plasma. Fatty acids may restrict the availability of chemical energy within cancer cells in at least two ways, either by modulating the activity of the mitochondrial adenine nucleotide translocase through the agency of their coenzyme A derivatives (LCFACoAs), or by uncoupling oxidative phosphorylation through the activation of phospholipase A2. The effectiveness of fatty acids in the former respect is theoretically and qualitatively examined on the basis of the affinity constants for LCFACoAs of the translocase and of certain enzymes concerned with beta-oxidation. The development of a new form of cancer chemotherapy by selectively harnessing and stimulating the lipotropic response of the host to a tumour is discussed in terms of the administration of fatty acids which possess specific properties while as the same time raising plasma NEFA concentrations and maintaining them at an elevated level.
D003065:Coenzyme A / Q000378:metabolism; D005227:Fatty Acids / Q000378:metabolism*; D006801:Humans; D008099:Liver / Q000378:metabolism; D008954:Models, Biological; D009369:Neoplasms / Q000188:drug therapy / Q000378:metabolism*
D005227:Fatty Acids; D003065:Coenzyme A