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Titolo:
Inflammation, carcinogenesis and cancer
Autore:
Fitzpatrick, FA;
Indirizzi:
Univ Utah, Huntsman Canc Inst, Salt Lake City, UT 84112 USA Univ Utah Salt Lake City UT USA 84112 Inst, Salt Lake City, UT 84112 USA
Titolo Testata:
INTERNATIONAL IMMUNOPHARMACOLOGY
fascicolo: 9-10, volume: 1, anno: 2001,
pagine: 1651 - 1667
SICI:
1567-5769(200109)1:9-10<1651:ICAC>2.0.ZU;2-9
Fonte:
ISI
Lingua:
ENG
Soggetto:
NONSTEROIDAL ANTIINFLAMMATORY DRUGS; P53 TUMOR-SUPPRESSOR; PROSTAGLANDIN-H SYNTHASE-2; OXIDATIVE DNA-DAMAGE; WILD-TYPE P53; PROTEASOME-MEDIATED DEGRADATION; BETA-CAROTENE SUPPLEMENTATION; EPITHELIAL OVARIAN-CANCER; SQUAMOUS-CELL CARCINOMA; HUMAN COLON-CANCER;
Keywords:
inflammation; carcinogenesis; cancer;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
224
Recensione:
Indirizzi per estratti:
Indirizzo: Fitzpatrick, FA Univ Utah, Huntsman Canc Inst, 2000 Circle Hope, Salt LakeCity, UT 84112 USA Univ Utah 2000 Circle Hope Salt Lake City UT USA 84112 USA
Citazione:
F.A. Fitzpatrick, "Inflammation, carcinogenesis and cancer", INT IMMUNO, 1(9-10), 2001, pp. 1651-1667

Abstract

To fulfill their role in host-defense, granulocytes secrete chemically reactive oxidants, radicals, and electrophilic mediators. While this is an effective way to eradicate pathogenic microbes or parasites, it inevitably exposes epithelium and connective tissue to certain endogenous genotoxic agents. In ordinary circumstances, cells have adequate mechanisms to reduce the genotoxic burden imposed by these agents to a negligible level. However, inflammation persisting for a decade eventually elevates the risk of cancer sufficiently that it is discernible in case control epidemiological studies. Advances in our understanding of tumor suppressors and inflammatory mediators offer an opportunity to assess the molecular and cellular models used to guide laboratory investigations of this phenomenon. Disappointing resultsfrom recent clinical trials with anti-oxidant interventions raise questions about the risks from specific endogenous agents such as hydrogen peroxideand oxy radicals. Simultaneously, the results from the anti-oxidant trialsdraw attention to an alternate hypothesis, favoring epigenetic inactivation of key tumor suppressors, such as p53, and the consequent liability this places on genomic integrity. (C) 2001 Elsevier Science BN. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/07/20 alle ore 12:41:48