Abstract

Somatostatin has been demonstrated in high concentrations in the hypothalamus, the cerebral cortex, the brain stem, the gastrointestinal tract, and the pancreas. In the central nervous system, it acts as a neurotransmitter, whereas its hormonal activities include the inhibition of the release of growth hormone, insulin, glucagon, and gastrin (for a review, see ref. 1). Also, antiproliferative effects have been reported, both in vitro on tumor cell lines, and in vivo on neuroendocrine human tumors. High-affinity somatostatin receptors have been identified in the brain and on many cells of neuroendocrine origin, like the somatotroph cells of the anterior pituitary and the pancreatic islet cell^.^.^ Also, cells not known classically as neuroendocrine, such as lymphocytes, may possess these receptor^.^ Besides, somatostatin receptors have been demonstrated on a variety of human tumors by classical biochemical binding techniques, as well as by in vitro autoradiography. These tumors include those with APUD (amine precursor uptake and decarboxylation) characteristics (pituitary tumors, endocrine pancreatic tumors, carcinoids, paragangliomas, small cell lung cancers, medullary thyroid carcinomas, pheochromocytomas} as well as meningiomas, well-differentiated brain tumors (astrocytomas), neuroblastomas, and some human breast cancers. Because of the short plasma half-life of somatostatin (2-4 min), analogues more suitable for medical treatment have been developed. The somatostatin analogue, octreotide, has been shown to bind to somatostatin receptors on both tumorous and nontumorous tissues. An 'In-labeled somatostatin analogue ([DTPA-D-Phe'l-octreotide] was developed for its use in scintigraphy. [DTPA-D-Phe'l-octreotide was shown to bind 'In efficiently in a single-step labeling procedure. The binding as well as the biological

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