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Titolo:
The effect of bombesin, cholecystokinin, gastrin, and their antagonists onproliferation of pancreatic cancer cell lines
Autore:
Ohlsson, B; Fredang, N; Axelson, J;
Indirizzi:
Univ Hosp, Dept Surg, Lund, Sweden Univ Hosp Lund SwedenUniv Hosp, Dept Surg, Lund, Sweden
Titolo Testata:
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
fascicolo: 12, volume: 34, anno: 1999,
pagine: 1224 - 1229
SICI:
0036-5521(199912)34:12<1224:TEOBCG>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR ANTAGONIST; STIMULATES GROWTH; RAT PANCREAS; EXPRESSION; ADENOCARCINOMA; PEPTIDE;
Keywords:
bombesin; cell lines; cell proliferation; cholecystokinin; devazepide; gastrin; L-365,260; pancreatic cancer;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Ohlsson, B Univ Hosp, Dept Surg, Lund, Sweden Univ Hosp Lund SwedenUniv Hosp, Dept Surg, Lund, Sweden
Citazione:
B. Ohlsson et al., "The effect of bombesin, cholecystokinin, gastrin, and their antagonists onproliferation of pancreatic cancer cell lines", SC J GASTR, 34(12), 1999, pp. 1224-1229

Abstract

Background: The role of cholecystokinin (CCK) and gastrin in the development and growth of pancreatic cancer cells is controversial. The aim of this study was to evaluate the role of CCK-8S, gastrin-17, bombesin, and their antagonists on cell lines from patients with pancreatic cancer. Methods: Cell Lines were established from pancreatic cancers operated on at our department. The cells were grown in 10% fetal calf serum (FCS). The effects of CCK-8S, gastrin-17, bombesin, and their antagonists in different concentrations and for different time intervals were studied. The cell number was evaluated with the XTT method. Results: The cell line LN 36 responded with increased cell number to stimulation by gastrin-17 and decreased cell number to inhibition by the CCK-B receptor antagonist L-365,260. In contrast, LPC I responded with increased cell number to CCK-8S and decreased cell number to the CCK-A receptor antagonist devazepide. LPC 2, 6, and 7 were stimulated byCCK-8S, gastrin-17, and their antagonists. LPC 3 showed decreased cell number after inhibition by the antagonists, and LPC 5 and 10 showed increased cell number after stimulation by CCK-8S and gastrin-17. LPC 4 was stimulated by CCK-8S, and LPC 8 was stimulated by all substances except gastrin-17. Intermittent administration of the substances to LN 36 led to a greater effect on the cell number than administration every day, which was not the case with LPC 1 and LPC 3. Bombesin led to an increased growth in LPC 5 but not in LPC 3. Conclusion: CCK-8S and gastrin-17 led to an increased cell number in some cell lines. A blockade of the CCK-A and CCK-B receptors by theirantagonists led to an increased, an unaffected, or a decreased cell numberof the cell lines. The effect of bombesin on different cell lines also varied. This shows a great heterogenicity among pancreatic cancer cells from different patients.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 16:56:35