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Article: Chemoprevention of gastric cancer by celecoxib in rats

TitleChemoprevention of gastric cancer by celecoxib in rats
Authors
Issue Date2004
PublisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/
Citation
Gut, 2004, v. 53 n. 2, p. 195-200 How to Cite?
AbstractBackground: Overexpression of cyclooxygenase 2 (COX-2) is frequently detected in gastric cancer and is believed to play a crucial role in gastric carcinogenesis. Aim: We examined the chemopreventive effect of a COX-2 inhibitor in an animal model of stomach carcinogenesis. Methods: Eighty six male Wistar rats were divided into six different treatment groups: group A, water alone (n = 5); group B, N-methyl-N′-nitro-N-nitrosoguanidine (MNNG 100 μg/ml) (n = 16); group C, indomethacin (3 mg/kg/day) (n = 16); group D, celecoxib (5 mg/kg/day) (n = 17); group E, celecoxib (10 mg/kg/day) (n = 16); and group F, celecoxib (20 mg/kg/day) (n = 16). Group B-F animals were treated with 10% sodium chloride (in the initial six weeks) and MNNG in drinking water to induce adenocarinoma in the stomach. All animals received treatment for 40 weeks, and were sacrificed after death or at 48 weeks. Gastric neoplasm was evaluated by histology. Results: The incidences of gastric cancer were 0% in group A, 75% in group B, 68.8% in group C, 70.6% in group D, 18.8% in group E, and 31.3% in group F (p = 0.002, ANOVA). Compared with MNNG controls, treatment with celecoxib 10 mg/kg/day also showed lower tumour multiplicity (0.19 (0.40) v 1.00 (0.73); p = 0.004) and lower mean tumour volume (2.4 v 2805 mm 3; p = 0.02). Although tumours had significantly higher COX-2 expression than their adjacent normal tissues (p<0.02), there was no significant difference in COX-2 levels among tumours in the different treatment groups. The lowest tumour prostaglandin E2 level was found in the indomethacin treated group, suggesting that the chemopreventive effect of celecoxib may be mediated by a COX independent pathway. Conclusion: While treatment with indomethacin had no significant effect on tumour development, treatment with celecoxib reduced gastric cancer incidence and growth in rats.
Persistent Identifierhttp://hdl.handle.net/10722/162813
ISSN
2015 Impact Factor: 14.921
2015 SCImago Journal Rankings: 6.474
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHu, PJen_US
dc.contributor.authorYu, Jen_US
dc.contributor.authorZeng, ZRen_US
dc.contributor.authorLeung, WKen_US
dc.contributor.authorLin, HLen_US
dc.contributor.authorTang, BDen_US
dc.contributor.authorBai, AHCen_US
dc.contributor.authorSung, JJYen_US
dc.date.accessioned2012-09-05T05:23:52Z-
dc.date.available2012-09-05T05:23:52Z-
dc.date.issued2004en_US
dc.identifier.citationGut, 2004, v. 53 n. 2, p. 195-200en_US
dc.identifier.issn0017-5749en_US
dc.identifier.urihttp://hdl.handle.net/10722/162813-
dc.description.abstractBackground: Overexpression of cyclooxygenase 2 (COX-2) is frequently detected in gastric cancer and is believed to play a crucial role in gastric carcinogenesis. Aim: We examined the chemopreventive effect of a COX-2 inhibitor in an animal model of stomach carcinogenesis. Methods: Eighty six male Wistar rats were divided into six different treatment groups: group A, water alone (n = 5); group B, N-methyl-N′-nitro-N-nitrosoguanidine (MNNG 100 μg/ml) (n = 16); group C, indomethacin (3 mg/kg/day) (n = 16); group D, celecoxib (5 mg/kg/day) (n = 17); group E, celecoxib (10 mg/kg/day) (n = 16); and group F, celecoxib (20 mg/kg/day) (n = 16). Group B-F animals were treated with 10% sodium chloride (in the initial six weeks) and MNNG in drinking water to induce adenocarinoma in the stomach. All animals received treatment for 40 weeks, and were sacrificed after death or at 48 weeks. Gastric neoplasm was evaluated by histology. Results: The incidences of gastric cancer were 0% in group A, 75% in group B, 68.8% in group C, 70.6% in group D, 18.8% in group E, and 31.3% in group F (p = 0.002, ANOVA). Compared with MNNG controls, treatment with celecoxib 10 mg/kg/day also showed lower tumour multiplicity (0.19 (0.40) v 1.00 (0.73); p = 0.004) and lower mean tumour volume (2.4 v 2805 mm 3; p = 0.02). Although tumours had significantly higher COX-2 expression than their adjacent normal tissues (p<0.02), there was no significant difference in COX-2 levels among tumours in the different treatment groups. The lowest tumour prostaglandin E2 level was found in the indomethacin treated group, suggesting that the chemopreventive effect of celecoxib may be mediated by a COX independent pathway. Conclusion: While treatment with indomethacin had no significant effect on tumour development, treatment with celecoxib reduced gastric cancer incidence and growth in rats.en_US
dc.languageengen_US
dc.publisherBMJ Publishing Group. The Journal's web site is located at http://gut.bmjjournals.com/en_US
dc.relation.ispartofGuten_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCyclooxygenase 2en_US
dc.subject.meshCyclooxygenase 2 Inhibitorsen_US
dc.subject.meshCyclooxygenase Inhibitors - Administration & Dosage - Therapeutic Useen_US
dc.subject.meshDinoprostone - Analysisen_US
dc.subject.meshDrug Administration Scheduleen_US
dc.subject.meshIndomethacin - Therapeutic Useen_US
dc.subject.meshIsoenzymes - Analysisen_US
dc.subject.meshMaleen_US
dc.subject.meshMethylnitronitrosoguanidineen_US
dc.subject.meshModels, Animalen_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Analysisen_US
dc.subject.meshPyrazolesen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshSodium Chlorideen_US
dc.subject.meshStomach Neoplasms - Prevention & Controlen_US
dc.subject.meshSulfonamides - Administration & Dosage - Therapeutic Useen_US
dc.titleChemoprevention of gastric cancer by celecoxib in ratsen_US
dc.typeArticleen_US
dc.identifier.emailLeung, WK:waikleung@hku.hken_US
dc.identifier.authorityLeung, WK=rp01479en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1136/gut.2003.021477en_US
dc.identifier.pmid14724149-
dc.identifier.scopuseid_2-s2.0-1642451874en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1642451874&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume53en_US
dc.identifier.issue2en_US
dc.identifier.spage195en_US
dc.identifier.epage200en_US
dc.identifier.isiWOS:000188098100009-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridHu, PJ=7201989582en_US
dc.identifier.scopusauthoridYu, J=35351306800en_US
dc.identifier.scopusauthoridZeng, ZR=7402647305en_US
dc.identifier.scopusauthoridLeung, WK=7201504523en_US
dc.identifier.scopusauthoridLin, HL=8950219500en_US
dc.identifier.scopusauthoridTang, BD=7402560876en_US
dc.identifier.scopusauthoridBai, AHC=7006523130en_US
dc.identifier.scopusauthoridSung, JJY=35405352400en_US

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