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Titolo:
Inhibition of rat colon tumors by sulindac and sulindac sulfone is independent of K-ras (codon 12) mutation
Autore:
De Jong, TA; Skinner, SA; Malcontenti-Wilson, C; Vogiagis, D; Bailey, M; Van Driel, IR; OBrien, PE;
Indirizzi:
Monash Univ, Sch Med, Dept Surg, Melbourne, Vic 3181, Australia Monash Univ Melbourne Vic Australia 3181 , Melbourne, Vic 3181, Australia Monash Univ, Sch Med, Dept Epidemiol & Prevent Med, Melbourne, Vic 3181, Australia Monash Univ Melbourne Vic Australia 3181 , Melbourne, Vic 3181, Australia Monash Univ, Sch Med, Dept Pathol & Immunol, Melbourne, Vic 3181, Australia Monash Univ Melbourne Vic Australia 3181 , Melbourne, Vic 3181, Australia
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY
fascicolo: 2, volume: 278, anno: 2000,
pagine: G266 - G272
SICI:
0193-1857(200002)278:2<G266:IORCTB>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
FAMILIAL ADENOMATOUS POLYPOSIS; NONSTEROIDAL ANTIINFLAMMATORY DRUGS; ABERRANT CRYPT FOCI; COLORECTAL ADENOMAS; MURINE MODEL; ASPIRIN USE; APOPTOSIS; CANCER; CARCINOGENESIS; SULFIDE;
Keywords:
colorectal cancer; 1,2-dimethylhydrazine dihydrochloride; nonsteroidal anti-inflammatory drugs;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Skinner, SA Monash Univ, Alfred Hosp, Dept Surg, Prahran, Vic 3181, Australia Monash Univ Prahran Vic Australia 3181 n, Vic 3181, Australia
Citazione:
T.A. De Jong et al., "Inhibition of rat colon tumors by sulindac and sulindac sulfone is independent of K-ras (codon 12) mutation", AM J P-GAST, 278(2), 2000, pp. G266-G272

Abstract

Nonsteroidal anti-inflammatory drug (NSAID) use reduces the risk of colorectal cancer by 40-50%. Previous studies suggest that effective inhibition of colorectal cancer by NSAIDs may be dependent on the presence or absence of a K-ras mutation. This study was aimed at determining the relationship between inhibition of colorectal cancer by sulindac and sulindac sulfone and the presence of activating K-ras mutations in the 1,2-dimethylhydrazine dihydrochloride rat model. Sulindac (20 mg.kg(-1).day(-1)), sulindac sulfone (40 mg.kg(-1).day(-1)), or vehicle was administered orally to male Sprague-Dawley rats for a 4-wk period beginning 20 wk after tumor induction. Tumor number and volume were measured before treatment by laparotomy and colonoscopy and again after treatment. Sulindac and sulindac sulfone treatment significantly reduced the number and volume of colorectal tumors compared with control rats. For K-ras (codon 12) mutation detection, frozen tumor tissue was collected at the endpoint. We found K-ras codon 12 mutations in 11 of 21(52%) control tumors. The proportion of tumors with K-ras mutations in thesulindac-treated group [5 of 8 (62%); odds ratio = 1.51 (95% confidence interval = 0.29, 8.33)] and the proportion of sulindac sulfone-treated tumors[9 of 14 (64%); odds ratio = 1.63 (95% confidence interval = 0.41, 6.66)] were not significantly different from controls. Tumor inhibition did not correlate with K-ras (codon 12) mutation status, which suggests that the mechanism of inhibition of rat colorectal cancer by sulindac and sulindac sulfone is independent of K-ras mutation.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/07/20 alle ore 17:47:06