Controlled and predictable interference with hormonal feed back mechanisms has become a major direction of preclinical and clinical research. There is a steadily increasing number of hormonal pep tides detected and characterized that are re sponsible for endo-, para-, and autocrine cellular actions. Naturally, these peptides have been studied with regard to their cell growth stimulatory action and, in parallel, the re spective antagonists are being investigated in terms of their antiproliferative (antineoplastic) function. Among the numerous pep tides of interest in this respect, somatostatin (somatotropin release inhibitory factor) and bombesin antagonizing factors have been the topic of inten sive research during recent years. No presentation of the role of pep tides in oncology would be complete without a compre hensive treatise of their physiological, preclinical and clinical functions in the context of their antineoplastic mechanism of action. Somatostatin and its various short- and long-acting analogs have the unique feature of suppressing and inhibiting a wide range of cellular processes including cell proliferation. Recep tors for these peptides, which belong in a wider sense to the family of neuropeptides or neurotransmitters, are widely dis tributed, a feature which is not in keeping with the general view of a growth hormone regulatory system. Thus, these substances are found in the gut in a variety of endocrine and exocrine glands including breast, pancreas, and prostate, and in the nervous system.
