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Clinical Oncology/Epidemiology

Treatment of patients with metastatic pancreatic and gastrointestinal tumours with the somatostatin analogue Sandostatin: a phase II study including endocrine effects

Abstract

Somatostatin analogues can suppress the secretion of some gastrointestinal hormones and growth factors involved in the growth regulation of gastrointestinal cancers and can inhibit the growth of experimental pancreatic tumours. Therefore, in a phase II study 34 patients with metastatic pancreatic (n = 14), colorectal (n = 16) and gastric cancer (n = 4) were treated with three daily subcutaneous injections of 100-200 micrograms of the somatostatin analogue Sandostatin (SMS 201-995). All patients had an extensive tumour load and 13 were pretreated with chemotherapy. Before Sandostatin treatment the patients with pancreatic cancer showed a higher mean plasma concentration of GH (P less than 0.05) and a lower concentration of 'total' somatomedin-C (P less than 0.005) compared with patients with colorectal cancer; there was no significant difference between these two groups in plasma levels of directly assayable somatomedin-C, EGF/TGF-alpha, insulin and prolactin. Within 3 days after start of treatment, somatomedin-C levels initially decreased (without a change in basal plasma GH levels), but returned to pretreatment levels within 4-13 weeks. Plasma insulin levels also were suppressed but only during the first 3-5 days of treatment. Plasma EGF-TGF-alpha levels increased significantly at day 5 of treatment only in the pancreatic cancer patients. Twenty-seven per cent of the patients showed stable disease for 3-9 months, but most patients experienced subjective improvement in the absence of serious side-effects. However, the overall survival remained disappointing, emphasising the need for better treatment regimens.

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Klijn, J., Hoff, A., Planting, A. et al. Treatment of patients with metastatic pancreatic and gastrointestinal tumours with the somatostatin analogue Sandostatin: a phase II study including endocrine effects. Br J Cancer 62, 627–630 (1990). https://doi.org/10.1038/bjc.1990.343

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