Direct Growth Inhibitory Action of Sandostatin on Rat Pituitary 7315b Tumor Cells in Vitro

Abstract

With the introduction of somatostatin analogs that are more stable in the circulation than the hormone itself, an additional tool has been found in the treatment of (neuro-)endocrine tumors, i.e. the use of Sandostatin (SMS 201–995) in the treatment of acromegaly (1). The full mechanisms by which somatostatin and its analogs exert their tumor growth inhibition remains to be elucidated. Two remaining questions can be formulated: 1) In some of the acromegalic patients treated with Sandostatin, an actual shrinkage of the tumor is observed in addition to a reduction of the circulating levels of growth hormone and somatomedin-C (IGF-I) (2); does this represent a direct antiproliferative action of the hormone (-analog) or a secondary effect which results from the action of the hormone on growth hormone secretion? 2) In some patients with metastatic endocrine pancreatic or gastro-intestinal tumors, the tumors escape from Sandostatin treatment with regard to hormone secretion (3); can this phenomenon be prevented by different regimes of Sandostatin administration?