Somatostatin receptors are present on most hormone-secreting tumours. They are the pathophysiological basis for the successful control of hormonal hypersecretion by pituitary adenomas, metastatic islet cell tumours and carcinoids during treatment with the long-acting somatostatin analogue octreotide. There is also evidence for inhibition of tumour growth in some of these patients. Visualization of somatostatin receptor-positive tumours is possible in vivo after the administration of ([111In]diethylenetriaminepentaacetic acid)octreotide. Primary tumours are detected and often metastases that were previously unrecognized. Tumours that secrete growth hormone or thyroid-stimulating hormone and non-functioning pituitary adenomas, islet cell tumours, carcinoids, paragangliomas, phaeochromocytomas, medullary thyroid carcinomas and small-cell lung cancers are visualized in 70-100% of cases. Meningiomas, renal cell cancers, breast cancers and malignant lymphomas are often somatostatin receptor positive, allowing their localization with this scanning procedure. In some of these tumours discrepancies have been noted between binding studies with somatostatin-14, somatostatin-28 and octreotide, which suggests the presence of somatostatin receptor subtypes on some tumours. Most hormone-secreting tumours react in vitro to octreotide with an inhibition of hormone release and growth. Cultured meningioma cells react to octreotide with a stimulation in growth, possibly by interference with the autocrine inhibitory growth control by interleukin 6. This suggests that the presence of somatostatin receptors on human tumours does not automatically imply a beneficial effect of somatostatin analogue therapy.