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Titolo:
Relationship between dysplasia, p53 protein accumulation, DNA ploidy, and Glut1 overexpression in Barrett metaplasia
Autore:
Younes, M; Lechago, J; Chakraborty, S; Ostrowski, M; Bridges, M; Meriano, F; Solcher, D; Barroso, A; Whitman, D; Schwartz, J; Johnson, C; Schmulen, AC; Verm, R; Balsaver, A; Carlson, N; Ertant, A;
Indirizzi:
Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 , Dept Pathol, Houston, TX 77030 USA Baylor Coll Med, Dept Med, Div Gastroenterol, Houston, TX 77030 USA BaylorColl Med Houston TX USA 77030 Gastroenterol, Houston, TX 77030 USA Methodist Hosp, Houston, TX 77030 USA Methodist Hosp Houston TX USA 77030Methodist Hosp, Houston, TX 77030 USA Diagnost Clin Houston, Dept Gastroenterol, Houston, TX USA Diagnost Clin Houston Houston TX USA Dept Gastroenterol, Houston, TX USA Diagnost Clin Houston, Dept Pathol, Houston, TX USA Diagnost Clin HoustonHouston TX USA uston, Dept Pathol, Houston, TX USA
Titolo Testata:
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY
fascicolo: 2, volume: 35, anno: 2000,
pagine: 131 - 137
SICI:
0036-5521(200002)35:2<131:RBDPPA>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUCOSE-TRANSPORTER GLUT1; HIGH-GRADE DYSPLASIA; ENDOSCOPIC SURVEILLANCE; FLOW-CYTOMETRY; GROWTH-FACTORS; BREAST-CANCER; MESSENGER-RNA; LATE EVENT; ESOPHAGUS; ADENOCARCINOMA;
Keywords:
adenocarcinoma; Barrett esophagus; cancer; dysplasia; esophagus; image analysis; immunohistochemistry; progression;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Younes, M Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 hol, Houston, TX 77030 USA
Citazione:
M. Younes et al., "Relationship between dysplasia, p53 protein accumulation, DNA ploidy, and Glut1 overexpression in Barrett metaplasia", SC J GASTR, 35(2), 2000, pp. 131-137

Abstract

Background: There is a need for molecular markers of malignant progressionin Barrett metaplasia (BM). The aim of this study is to determine the relationship between dysplasia, p53 protein accumulation, DNA ploidy, and Glut1in BM. Methods: Sections of esophageal biopsy specimens from 120 patients with BM were evaluated for dysplasia, p53 protein, and Glut1 expression by immunohistochemistry, and DNA ploidy by Feulgen stain and image analysis. In cases with diploid DNA histograms, the percentage cells in the G0G1 and G2M phases of the cell cycle were determined. Results: Of 108 diploid cases 19 (28%) of 69 cases with G0G1 greater than or equal to 90% or G2M greater than or equal to 8.33% were p53-positive: in contrast to only 1 (3%) of 39 cases with lower G0G1 or G2M (P = 0.0008). Of 32 p53-positive: cases 11 (32%) were aneuploid, in contrast to none (0%) of 88 p53-negative cases (P < 0.0001). Ten (91%) of Ii aneuploid cases were high-grade dysplasia/ adenocarcinoma (HGD/CA), compared with only 1 (1%) of 109 diploid casts (P < 0.0001). Five (45%) Of 11 cases with HGD/CA were Glut1-positive, in; contrast to none (0%) Of 109 cases without HGD/CA (P < 0.0001). Conclusions: Our data strongly suggest that in BM, after oxidative DNA damage, as a result of gastroesophageal reflux, there is an increase in the percentage of cells in theG0G1 or G2M phases of the cell cycle to enable repair of damaged DNA; in some of these cases this is followed sequentially by p53 gene mutation and protein accumulation, DNA aneuploidy, HGD, and CA with or without Glut1 overexpression. These events can be detected in routinely processed biopsy samples.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/11/20 alle ore 06:54:24