Somatostatin receptor-dependent growth inhibition of liver metastases by octreotide

Abstract

Rats were administered the somatostatin analogue octreotide 15 micrograms intraperitoneally twice daily for 4 weeks after intraportal injection of somatostatin receptor-positive pancreatic tumour cells (CA-20948) and somatostatin receptor-negative colonic tumour cells (CC531). Octreotide significantly inhibited the growth and development of somatostatin receptor-positive tumour cells in the liver. The median number of liver tumours was 286 (range 146 to greater than 500) in the treated animals and more than 500 (range 250 to in excess of 500) in the controls (P < 0.05). This significant difference in tumour load was also represented in the mean(s.e.m.) liver weight (14.5(3.7) g in animals given octreotide versus 17.9(3.0) g in the controls). No effect of octreotide treatment was found on the growth and development of somatostatin receptor-negative tumour cells in the liver. The median (range) number of tumours was 6.5 (0-425) in the treated animals and 11.0 (0-475) in the controls. Mean(s.e.m.) liver weights were 14.0(5.7) g and 11.8(4.5) g respectively. There was no difference in serum levels of growth hormone, prolactin and insulin-like growth factor between control and octreotide-treated rats. The growth inhibition of somatostatin receptor-positive tumour cells was unlikely to be the result of suppressed secretion of one of these tumour growth factors. Octreotide may be useful for the treatment of patients with somatostatin receptor-positive hepatic metastases, which can be demonstrated by somatostatin receptor scintigraphy.

Prospective study of the antitumor efficacy of long‐term octreotide treatment in patients with progressive metastatic gastrinoma

“…To our knowledge, other antitumor modalities such as hepatic embolization, chemoembolization, or treatment with radiolabeled somatostatin analogues have not been clearly shown to improve survival by inhibiting tumor growth in patients with malignant PETs 10, 40. Third, numerous studies have demonstrated that somatostatin analogues can inhibit the growth of NETs in animal studies 18, 45. Furthermore, a number of studies have demonstrated that treatment with somatostatin analogues has an antitumor growth effect in patients with malignant gastrointestinal NETs (i.e., carcinoids or PETs), resulting in stabilization of the tumor growth in 37–80% of patients to the point that no additional growth occurred (i.e., tumoristatic effect) as well as a decrease in tumor size in 0–17% of patients (i.e., tumoricidal effect) 18, 26, 40, 46–49.…”

Effect of octreotide on cell-cycle kinetics and serum carcinoembryonic antigen level in hepatic metastases of colonic adenocarcinoma

“…(3) Somatostatin also exerts an inhibitory effect on DNA synthesis in tumor cells. And (4) Furthermore, somatostatin analogues can also inhibit the angiogenesis of neoplasm [6][7][8] .…”

Pre-clinical evaluation of [111In-DTPA-Pro1, Tyr4]bombesin, a new radioligand for bombesin-receptor scintigraphy

“…Experiment E: 2 groups of 3 male WAGRIJ rats inoculated with CC531 colon-carcinoma cells in the vena porta (Van Eijck et al, 1994) and 2 groups of 3 male Lewis rats inoculated with CA20948 pancreatic-tumour cells in the hindleg (Bakker et al, 1991b) were injected with 2 MBq (0.1 µg) [ 111 In-DTPA-Pro 1 ,Tyr 4 ]BN with or without 100 µg [Tyr 4 ]BN. Tissue distribution was determined after 24 hr.…”