Somatostatin receptors have been shown to be present at all main sites of its action, such as the anterior pituitary gland, the exocrine and endocrine pancreas, the mucosa of the gastrointestinal tract and the central nervous system (1, 2). Somatostatin receptors can be measured by two different approaches (3). First by direct biochemical techniques, i.e. binding studies on tissue homogenates in vitro, which allow precise characterization of the affinities and kinetics of these receptors. Secondly, receptors can also be visualized in tissue sections with autoradiography. This last method has the advantage of identifying histologically the tissues containing these receptors. High numbers of high affinity somatostatin receptors have been found on most growth hormone secreting pituitary tumors, as well as on many endocrine pancreatic tumors and carcinoids (4, 5). These receptors probably form the pathophysiological basis for the successful control of hormonal hypersecretion by most of these tumors during treatment with octreotide (Sandostatin). Several other human tumor types have also been recognized to contain large numbers of high affinity somatostatin receptors. All 27 meningiomas investigated contained these receptors, while well-differentiated glia-derived brain tumors like most oligo-dendrogliomas and (low-grade) astrocytomas, but not glioblastomas contain somatostatin receptors (6-9). Somatostatin receptors have also been found on 20-40% of human breast cancers (10).