Expression of receptors for gut peptides in pancreata of BOP-treated and control hamsters

The growth of pancreatic cancers may be influenced by certain gut peptides. However, the alteration of gut peptide receptors in the progress of pancreatic carcino-genesis is largely unknown. With storage phosphor auto-radiography, this study visualized and characterized receptors for cholecystokinin...

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Veröffentlicht in:Carcinogenesis (New York) 1996-10, Vol.17 (10), p.2171-2175
Hauptverfasser: Tang, Chengwei, Biemond, Izãk, Appel, Marko J., Visser, Corjan J.T., Woutersen, Ruud A., Lamers, Cornelis B.H.W.
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Sprache:eng
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Zusammenfassung:The growth of pancreatic cancers may be influenced by certain gut peptides. However, the alteration of gut peptide receptors in the progress of pancreatic carcino-genesis is largely unknown. With storage phosphor auto-radiography, this study visualized and characterized receptors for cholecystokinin (CCK), somatostatin (SST), bombesin (BBS), secretin and vasoactive intestinal peptide (VIP) in pancreata of control hamsters (n = 7) and pancreatic preneoplastic lesions (n = 10) or adeno-carcinomas (n=10) of N-nitrosobis(2-oxopropyl)amine (BOP)-treated hamsters. The specific CCK-A and secretin receptors expressed in normal pancreata were markedly reduced in pancreatic preneoplastic lesions and absent in adenocarcinomas. In the development of pancreatic tumours, the subgroup of SST receptors did not change, but both the affinity and binding capacity declined. In comparison with the binding of VIP to normal pancreata, specific VIP binding was significantly lower in preneo-plastic lesions and almost absent in pancreatic adeno-carcinomas. No specific binding for BBS was detected in normal pancreas or (pre)neoplastic lesions of hamster pancreas. The reduction or absence of receptors for CCK, secretin, SST and VIP in hamster pancreas with the progress of carcinogenesis suggests that in BOP-treated hamsters, pancreatic adenocarcinomas have, to a large extent, lost the hormone-dependent characteristics of the original tissue.
ISSN:0143-3334
1460-2180
DOI:10.1093/carcin/17.10.2171