Prostaglandins in Immunotherapy of Cancer

Abstract

Since prostaglandins (PGs) act as modulators in many biological systems, for some years many researchers have been carefully examining a possible association between PGs and cancer (for review and general aspects see Jaffe 1974; Honn et al. 1981; Powels et al. 1982; Thaler-Dao et al. 1984). Two approaches have been employed, one using inhibitors of cyclooxygenase (NSAIA), the other using the natural PGs or synthetic analogs with prolonged activity. The results of these experiments have been contradictory. In fact, some authors have concluded that Pgs accelerate tumor growth and decrease the survival time of tumor-bearing animals (Humes et al. 1974; Bennett et al. 1979; Lynch and Salomon 1979), while others have published data suggesting opposite results, i.e., that PGs inhibit tumor growth and prolong the survival time (Santoro et al. 1977; Santoro and Jaffe 1979; Tutton and Barkla 1980). The only concordant datum is that tumor cells produce a very large amount of PGs (Thomas et al. 1974). Some authors have supposed that these prostaglandins can be responsible for tumor dissemination (Mahan et al. 1985) and for immunosuppression causing an enhancement in tumor growth (Plescia et al. 1975). But not everyone agrees on the fact that PGs are immunosuppressive; in fact, there are some data suggesting their immunostimulating effect (Mertin et al. 1984;Hacker-Shahin and Droge 1985).