Effect of CCK receptor antagonist on growth of pancreatic adenocarcinoma

Shivaram, S; Crist, Keith A.; Chaudhuri, B. K.; Mucci, Samuel J.; Chaudhuri, P. K.

doi:10.1016/0022-4804(92)90040-7

Cited by 6 publications

(2 citation statements)

References 6 publications

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“…Asperlin, a competitive, non‐peptide CCK receptor antagonist, significantly inhibited the growth of SKI tumors 71. A high‐fat diet treatment promoted the proliferation of SW‐1990 human pancreatic cancer,67 whereas a CCK‐A receptor‐specific antagonist suppressed human and hamster pancreatic adenocarcinomas 67,72,73. In addition, gastrin stimulated the growth of PANC‐1 human pancreatic cancer cells 74.…”

Section: Cck and The Growth Of Pancreatic Cancermentioning

confidence: 99%

Roles of gastrointestinal hormones in pancreatic cancer

Guo

Townsend

2000

Journal of Hepato-Biliary-Pancreatic Surgery

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Several gastrointestinal (GI) hormones, such as gastrin, cholecystokinin, and bombesin, have been reported to affect the development of pancreatic cancer. The receptors for these hormones are found in normal and neoplastic pancreatic cells. Activation of these receptors enhances pancreatic carcinogenesis and promotes the growth of established pancreatic carcinoma either in vitro or in vivo. On the other hand, some studies have shown that these GI hormones may have no effect or may play an inhibitory role in the development of pancreatic cancer. The reasons for the apparent discrepancies in the published literature are discussed in this review. In recent years, increasing emphasis has been placed on the effects of GI hormones on cancer invasion and metastasis. As the transition from noninvasion to the invasive state is the crucial event in cancer development, further investigation of the way in which GI hormones affect the invasion and metastasis of pancreatic cancer may be important for the development of new therapeutic approaches with eventual clinical utility.

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Section: Cck and The Growth Of Pancreatic Cancermentioning

confidence: 99%

Roles of gastrointestinal hormones in pancreatic cancer

Guo

Townsend

2000

Journal of Hepato-Biliary-Pancreatic Surgery

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“…These findings are in agreement with other reports: Watanapa et al [19] showed that lorglumide inhibited azaserine pancreatic carcinogenesis after pancreatobiliary diversion in rats; Morimoto et al [20] reported that loxiglumide (CR-1505), another specific CCK receptor antagonist, significantly inhibited the in vivo and in vitro growth of human pancreatic cancer, suggesting that its antitumor activity may be independent of the actual stimulation with CCK or anyway another agonist, and Shivaram et al [21] studied another CCK receptor antagonist, L-364,718, (a nonpeptide compound) that exhibited only a limited activity on the growth of transplantable pancreatic carcinoma in the Syrian hamster.…”

Section: Well-differentiated Duct Adenocarcinorna That Arose In a Fibmentioning

confidence: 99%

Effect of cholecystokinin analogue caerulein and cholecystokinin antagonist lorglumide on pancreatic carcinogenesis in the rat

Sperti

Militello

Rovati³

et al. 1994

Journal of Surgical Oncology

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The effects of the cholecystokinin (CCK)-analogue, caerulein, and CCK-receptor antagonist lorglumide (CR-1409) on pancreatic carcinogenesis induced by 7,12-dimethylbenz(a)anthracene (DMBA) were studied. One hundred thirty rats were divided into the following 10 treatment groups: group 1, DMBA (2-3 mg); group 2, DMBA + caerulein (5 micrograms/kg); group 3, DMBA + caerulein + CR-1409 (12 mg/kg); group 4, caerulein + DMBA; group 5, caerulein + CR-1409 + DMBA; group 6, DMBA + CR-1409; group 7, CR-1409 + DMBA; group 8, caerulein; group 9, CR-1409; and group 10, sham operation + saline. DMBA was surgically implanted into the pancreas. Caerulein and/or CR-1409 was administered twice daily for 15 days after (in groups 2, 3, and 6) or before (in groups 4, 5, and 7) DMBA implantation. Six months after carcinogen administration, all rats were sacrificed and autopsied. The incidence of pancreatic cancer appeared significantly (P < 0.001) increased when caerulein was administered following DMBA implantation. CR-1409 significantly inhibited (P < 0.02) caerulein effects and reduced tumor growth when injected after carcinogen exposure.

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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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Effect of CCK receptor antagonist on growth of pancreatic adenocarcinoma

Cited by 6 publications

References 6 publications

Roles of gastrointestinal hormones in pancreatic cancer

Roles of gastrointestinal hormones in pancreatic cancer

Effect of cholecystokinin analogue caerulein and cholecystokinin antagonist lorglumide on pancreatic carcinogenesis in the rat

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

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