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Titolo:
APC1638N - A MOUSE MODEL FOR FAMILIAL ADENOMATOUS POLYPOSIS-ASSOCIATED DESMOID TUMORS AND CUTANEOUS CYSTS
Autore:
SMITS R; VANOORDT WVH; LUZ A; ZURCHER C; JAGMOHANCHANGUR S; BREUKEL C; KHAN PM; FODDE R;
Indirizzi:
LEIDEN UNIV,FAC MED,DEPT HUMAN GENET,MED GENET CTR SW NETHERLANDS,WASSENAARSEWEG 72,POB 9503 NL-2300 RA LEIDEN NETHERLANDS LEIDEN UNIV,FAC MED,DEPT HUMAN GENET,MED GENET CTR SW NETHERLANDS NL-2300 RA LEIDEN NETHERLANDS LEIDEN UNIV,DEPT MOL CARCINOGENESIS NL-2300 RA LEIDEN NETHERLANDS GSF FORSCHUNGSZENTRUM UMWELT & GESUNDHEIT GMBH NEUHERBERG GERMANY DEPT PATHOL NEUHERBERG GERMANY UNIV UTRECHT,DEPT VET PATHOL UTRECHT NETHERLANDS
Titolo Testata:
Gastroenterology
fascicolo: 2, volume: 114, anno: 1998,
pagine: 275 - 283
SICI:
0016-5085(1998)114:2<275:A-AMMF>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
MULTIPLE INTESTINAL NEOPLASIA; APC GENE-PRODUCT; COLI GENE; MUTATION; PROTEIN; CELLS; APOPTOSIS; ALLELES; 3'-PART; CYCLE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
39
Recensione:
Indirizzi per estratti:
Citazione:
R. Smits et al., "APC1638N - A MOUSE MODEL FOR FAMILIAL ADENOMATOUS POLYPOSIS-ASSOCIATED DESMOID TUMORS AND CUTANEOUS CYSTS", Gastroenterology, 114(2), 1998, pp. 275-283

Abstract

Background & Aims: Germline mutations in the adenomatous polyposis coli (APC) gene are responsible for familiar adenomatous polyposis (FAP), an autosomal dominant predisposition to the formation of multiple colorectal adenomas. Moreover, patients with FAP are at high risk of developing several extracolonic manifestations, including desmoids, cutaneous cysts, and tumors of the upper gastrointestinal tract. Although by definition desmoids are nonmalignant, because of their aggressive invasion of local structures, they represent one of the major causes of morbidity and mortality among patients with FAP. Methods:This study describes the histopathologic and molecular characterization of Apc1638N, a mouse model for the broad spectrum of extracolonic manifestations characteristic of FAP. Results: Heterozygous Apc(+)/Apc1638N animals develop fully penetrant and multifocal cutaneous follicular cysts and desmoid tumors in addition to attenuated polyposis of the upper gastrointestinal tract. Moreover, breeding of Apc(+)/Apc1638N mice in a p53-deficient background results in a dramatic sevenfold increase of the desmoid multiplicity. Conclusions: Because of the attenuated nature of their intestinal phenotype, these mice survive longer than other murinemodels for Ape-driven tumorigenesis. Therefore, Apc1638N represents an ideal laboratory tool to test various therapeutic intervention strategies for the management of intestinal as well as extraintestinal tumors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 06:50:35