Inhibition of growth of pancreatic carcinomas in animal models by analogs of hypothalamic hormones (tumor weight and volume reduction/somatostatin analogs/luteinizing hormone-releasing hormone analogs)

TLDR: In this paper, the effect of analogs of hy- pothalamic hormones on tumor growth was investigated using animal models of acinar and ductal pancreatic cancer, using Wistar/Lewis rats bearing the acinar pancreatic tumor DNCP-322.

Abstract: Using animal models of acinar and ductal pancreatic cancer, we investigated the effect of analogs of hy- pothalamic hormones on tumor growth. In Wistar/Lewis rats bearing the acinar pancreatic tumor DNCP-322, chronic ad- ministration of (L-5-Br-Trp8)somatostatin-14 significantly de- creased tumor weights and volume. Somatostatin-28 and the cyclic hexapeptide analog of somatostatin cyclo(Pro-Phe-D- Trp-Lys-Thr-Phe) failed to influence the growth of this tumor. The agonistic analog of luteinizing hormone-releasing hor- mone (D-Trp6)LH-RH also significantly decreased tumor weight and volume in this model and reduced testosterone lev- els and the weights of the ventral prostate and testes. In Syrian hamsters bearing ductal type of pancreatic carcinoma, chronic administration of (L-5-Br-Trp8)somatostatin diminished tu- mor weights and volume. The percentage change in tumor vol- ume was significantly decreased when compared to control an- imals. In one experiment, cyclic hexapeptide of somatostatin also inhibited growth of this tumor. (D-Trp6)LH-RH, given twice daily or injected in the form of microcapsules for con- stant controlled release, significantly decreased tumor weight and volume and suppressed serum testosterone levels. Ham- sters castrated 4 days after transplantation of the pancreatic tumors showed a significant decrease in weight and volume of these tumors. This suggests that pancreatic cancers may, at least in part, be sex hormone sensitive. (D-Trp6)LH-RH may decrease the growth of pancreatic carcinomas by suppressing androgens. Somatostatin analogs reduce the growth of pancre- atic ductal and acinar cancers, probably by inhibiting the re- lease or stimulatory action of gastrointestinal hormones on tu- mor cells (or both). Inhibition of animal models of pancreatic tumors by chronic administration of somatostatin analogs and (D-Trp6)LH-RH suggests that these compounds should be con- sidered for the development of a new hormonal therapy for cancer of the pancreas.