van Eijck C H, Slooter G D, Hofland L J, Kort W, Jeekel J, Lamberts S W, Marquet R L
Department of Surgery, University Hospital Dijkzigt, Rotterdam, The Netherlands.
Br J Surg. 1994 Sep;81(9):1333-7. doi: 10.1002/bjs.1800810925.
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.
