SOMATOSTATIN RECEPTOR-DEPENDENT GROWTH-INHIBITION OF LIVER METASTASESBY OCTREOTIDE

Rats were administered the somatostatin analogue octreotide 15 mu g in traperitoneally 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). Octreoti de significantly inhibited the growth and development of somatostatin receptor-positive tumour cells in the liver. The median number of live r tumours was 286 (range 146 to greater than 500) in the treated anima ls 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 represent ed in the mean(s.e.m) liver weight (14.5(3.7) g in animals given octre otide versus 17.9(3.0) g in the controls). No effect of octreotide tre atment was found on the growth and development of somatostatin recepto r-negative tumour cells in the liver. The median (range) number of tum ours was 6.5 (0-425) in the treated animals and 11.0 (0-475) in the co ntrols. Mean(s.e.m.) liver weights were 14.0(5.7) g and 11.8(4.5) g re spectively. There was no difference in serum levels of growth hormone, prolactin and insulin-like growth factor between control and octreoti de-treated rats. The growth inhibition of somatostatin receptor-positi ve tumour cells was unlikely to be the result of suppressed secretion of one of these tumour growth factors. Octreotide may be useful for th e treatment of patients with somatostatin receptor-positive hepatic me tastases, which can be demonstrated by somatostatin receptor scintigra phy.