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Titolo:
Esophagogastric adenocarcinoma in an E1A/E1B transgenic model involves p53disruption
Autore:
Duncan, MD; Tihan, T; Donovan, DM; Phung, QH; Rowley, DL; Harmon, JW; Gearhart, PJ; Duncan, KLK;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Surg, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 t Surg, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Pathol, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 Pathol, Baltimore, MD 21205 USA NIA, Mol Genet Lab, NIH, Baltimore, MD 21224 USA NIA Baltimore MD USA 21224 A, Mol Genet Lab, NIH, Baltimore, MD 21224 USA NIA, Transgen & Knockout Facil, NIH, Baltimore, MD 21224 USA NIA Baltimore MD USA 21224 & Knockout Facil, NIH, Baltimore, MD 21224 USA
Titolo Testata:
JOURNAL OF GASTROINTESTINAL SURGERY
fascicolo: 3, volume: 4, anno: 2000,
pagine: 290 - 297
SICI:
1091-255X(200005/06)4:3<290:EAIAET>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
BARRETTS-ESOPHAGUS; CARCINOMA; PROTEIN; CANCER; EXPRESSION; EPITHELIUM; METAPLASIA; DYSPLASIA; JUNCTION;
Keywords:
esophageal cancer; transgenic; p53;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
27
Recensione:
Indirizzi per estratti:
Indirizzo: Duncan, MD John Hopkins Bayview Med Ctr, Sect Surg Sci, A-563,4940 EasternAve, Baltimore, MD 21224 USA John Hopkins Bayview Med Ctr A-563,4940 Eastern Ave Baltimore MD USA 21224
Citazione:
M.D. Duncan et al., "Esophagogastric adenocarcinoma in an E1A/E1B transgenic model involves p53disruption", J GASTRO S, 4(3), 2000, pp. 290-297

Abstract

We studied tumorigenesis and p53 immunostaining in a murine transgenic model introducing E1A/E1B under the control of the mouse mammary tumor virus-long terminal repeat (MMTV-LTR) promoter in which adenocarcinoma occurs at the squamocolumnar junction in the foregut, predominantly in males, and at no other site. Mutations of p53 are frequent in human esophageal adenocarcinoma and the E1B gene product interferes with p53-mediated apoptosis, inhibiting turner suppression at the G(1)/S checkpoint. Transgenic animals were generated utilizing a purified linear 6.7 kb fragment of plasmid DNA containing MMTV-LTR/E1A/E1B and were confirmed by dot blot hybridization of tail DNA to P-32-labeled E1A/E1B probe and polymerase chain reaction (PCR) amplification of E1A. Transgenic and control animals were observed for morbidity and weight changes. Eleven of 45 animals were transgenic (24% efficiency) with an estimated 5 to 57 copies of the gene per genome. Profound weight loss (>20%) led to sacrifice or death of one of five females (at 12 weeks) andfour of six males (at 16 to 17 weeks). Grossly visible tumors (2 to 10 mm)were noted in the forestomach at the visible margin between the: proximal (squamous-lined) stomach and the distal glandular stomach. Histologic sections confirmed adenocarcinoma arising in each case at the squamocolumnar junction with glandular formation, pleomorphism, and frequent mitotic figures. Immunostaining was positive for p53 indicating accumulation of mutated or altered p53 protein. E1A/E1B transgenic animals developed macroscopic and microscopic adenocarcinoma at the squamocolumnar junction, which correspondsto adenocarcinoma at the human esophagogastric junction. Disruption of p53was present in the transgenic model as in the human cancer.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 00:54:49