Treatment with Secretin and a Cholecystokinin-Like Peptide in Patients with Pancreatic Cancer

Steffensrud, S.; Erichsen, H; Røysland, P.; Halvorsen, Tore; Klepp, Ragnhild; Klepp, Olbjørn; Wünsch, Erich; Petersen, H

doi:10.1080/00365521.1984.12005831

Cited by 4 publications

(1 citation statement)

References 11 publications

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“…There was no increase in side effects including pancreatitis, and there was no evidence of increased tumor growth induced by CCK and not compensated for by FAM. 18 Further studies are warranted to determine the role of CCK and its antagonists in the adjuvant treatment of pancreatic cancer.…”

Section: Gastrointestinal Hormones That May Promote Pancreatic Cancer Growthmentioning

confidence: 99%

Regulation of Pancreatic Cancer Growth by Gastrointestinal Hormones: A Clinically Useful Strategy?

Fisher¹,

Berger²

M. D. Anderson Solid Tumor Oncology Series

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atic islets. It has been characterized as the "universal off switch" because it inhibits the release of growth hormone and essentially all gastrointestinal hormones. Somatostatin is known to inhibit not only pancreatic endocrine and exocrine secretion but also DNA synthesis. 5 Somatostatin has been shown to inhibit carcinogenesis in animal models (Table 34.1). Somatostatin receptors have been 378 W.E. Fisher and D.H. Berger TABLE 34.1. Gastrointestinal hormones that may inhibit pancreatic cancer growth. Somatostatin References Somatostatin and its analog, RC-160, decreased preneoplastic changes and tumor formation in hamsters exposed to a pancreatic carcinogen. 30-31 RC-160 decreased tumor weight and prolonged survival of hamsters with pancreatic cancer. 32 Somatostatin and 5-FU inhibited preneoplastic changes and tumor formation in hamsters. 33 Somatostatin receptors were demonstrated in the normal exocrine pancreas and in pancreatic cancer specimen.34 Somatostatin receptors were demonstrated on normal human pancreas and pancreatic cancer cells. 35 Growth of human pancreatic cancer (MIA PaCa-2) cells was inhibited in cell culture by somatostatin-14. 36 Growth of human pancreatic cancer (MIA PaCa-2) cells was inhibited in cell culture by three long-acting 37 analogs of somatostatin. Colony formation of human pancreatic cancer BxPc-3, but not SOJ-6, cells was decreased by somatostatin. 38 Growth of human pancreatic cancer (MIA PaCa-2) cells implanted in nude mice was inhibited by octreotide. 39 A somatostatin analog, RC-160, inhibited the growth of human pancreatic cancer (MIA PaCa-2) tumors in 40 nude mice. A somatostatin analog containing methotrexate enhanced inhibition of human pancreatic cancer (MIA PaCa-2) 41 growth. Human pancreatic cancer (MIA PaCa-2 & Panc-1) cells did not have somatostatin receptors & somatostatin-14 42 did not affect growth of the cells in culture. Somatostatin inhibited the growth of human pancreatic cancer cells, SKI, in nude mice but not PGER. The SKI, 43-44 but not PER, cell line was shown to have somatostatin receptors. Somatostatin inhibited the growth of human pancreatic cancer cells (SKI & CAV) in nude mice. 45 Sandostatin, a long acting somatostatin analog, had no effect on 14 patients with metastatic pancreatic cancer 46 treated for 7 weeks. No survival benefit was seen in 19 patients with advanced exocrine pancreatic carcinoma given the somatostatin 47 analog BIM 23014 for 2 months. No benefit was seen in a randomized prospective trial of somatostatin vs. placebo in 86 pancreatic cancer patients. 48 The human pancreatic cancer cell line, MIA PaCa-2 was inhibited by somatostatin & octreotide in vitro and in 49 vivo. Other human pancreatic cancer cell lines (Capan-1, Capan-2, CAV, & Panc-1) were not inhibited. Vasoactive Intestinal Peptide (VIP) VIP receptors were demonstrated on human pancreatic cancer cells. 50 VIP receptors were demonstrated on human pancreatic cells (Capan-1) but no inhibition of cell proliferation in 51 culture was seen. VIP inhibited growth of hamster pan...

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Section: Gastrointestinal Hormones That May Promote Pancreatic Cancer Growthmentioning

confidence: 99%

Regulation of Pancreatic Cancer Growth by Gastrointestinal Hormones: A Clinically Useful Strategy?

Fisher¹,

Berger²

M. D. Anderson Solid Tumor Oncology Series

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Gastrointestinal hormones as potential adjuvant treatment of exocrine pancreatic adenocarcinoma

et al. 1998

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Secretin and Cholecystokinin

Mutt¹

1988

Advances in Metabolic Disorders

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Treatment with Secretin and a Cholecystokinin-Like Peptide in Patients with Pancreatic Cancer

Cited by 4 publications

References 11 publications

Regulation of Pancreatic Cancer Growth by Gastrointestinal Hormones: A Clinically Useful Strategy?

Regulation of Pancreatic Cancer Growth by Gastrointestinal Hormones: A Clinically Useful Strategy?

Gastrointestinal hormones as potential adjuvant treatment of exocrine pancreatic adenocarcinoma

Secretin and Cholecystokinin

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