This paper reviews the evidence linking prostaglandin E (PGE) with the growth of neoplastic tissue. PGE2 is present in high concentrations in many natural and experimentally produced cancers. The immunosuppressive effect of some tumors in mice is due at least in part to a prostaglandin mechanism. The growth of these same tumors can be slowed and in some cases the tumor eliminated by administration of PG synthetase inhibitors. It is not yet clear whether the antitumor properties of these PG synthetase inhibitors are due to their releasing the hostimmune system from the chronic prostaglandin-mediated suppression of the tumor, resulting in an effective immune response to the tumor, or whether another mechanism is responsible. In humans overproduction of PGE2 by macrophages is partly responsible for the depressed PHA response in patients with Hodgkin's disease.
ASJC Scopus subject areas
- Cancer Research