Gut-associated neuroendocrine tumors grow slowly. Throughout most of their natural history, their ill-effects are due to secretion of biologically-active products rather than to tumor burden alone [4, 7]. Specific therapy to reduce tumor peptide secretion therefore has considerable theoretical appeal as an adjunct to tumor mass reduction by surgical debulking, embolization or cytotoxic drugs. The recent introduction of somatostatin analogues for clinical use has translated this theoretical hope into reality [1, 3].
