Cellular and molecular mechanisms responsible for progression of Barrett's metaplasia to esophageal carcinoma

被引:25
作者
Beilstein, M
Silberg, D
机构
[1] Univ Penn, Dept Gastroenterol, Philadelphia, PA 19104 USA
[2] Hosp Univ Penn, Div Gastroenterol, Philadelphia, PA 19104 USA
关键词
D O I
10.1016/S0889-8553(02)00013-4
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Barrett's metaplasia is found in approximately 12% to 18% of patients undergoing upper endoscopy for symptoms of reflux. Barrett's metaplasia is a premalignant condition and remains the number one risk factor for developing esophageal adenocarcinoma. There has been an increase in the incidence of esophageal adenocarcinoma in the past two decades, making it the most rapidly rising cancer in the United States and Western Europe. This article describes the progression from Barrett's metaplasia to esophageal adenocarcinoma and predictors for the development of adenocarcinoma in Barrett's metaplasia. Barrett's metaplasia represents a histological mosaic, with dysplastic tissue adjacent to non-dysplastic tissue. The histologic changes leading to adenocarcinoma are accompanied by alterations at the molecular level, including the accumulation of gene mutations and changes in gene expression. The determination of the molecular events that occur in the transition from normal esophageal squamous mucosa to dysplasia and to esophageal adenocarcinoma have lead to a better understanding of the process of the transformation to adenocarcinoma. This knowledge will lead to better biomarkers to diagnose and assess cancer risk.
引用
收藏
页码:461 / +
页数:20
相关论文
共 129 条
[1]   AMPLIFICATION AND OVER-EXPRESSION OF THE EGFR AND ERBB-2 GENES IN HUMAN ESOPHAGEAL ADENOCARCINOMAS [J].
ALKASSPOOLES, M ;
MOORE, JH ;
ORRINGER, MB ;
BEER, DG .
INTERNATIONAL JOURNAL OF CANCER, 1993, 54 (02) :213-219
[2]   ROLE OF APOPTOSIS IN MODULATION OF THE GROWTH OF HUMAN COLORECTAL TUBULAR AND VILLOUS ADENOMAS [J].
ARAI, T ;
KINO, I .
JOURNAL OF PATHOLOGY, 1995, 176 (01) :37-44
[3]   Activation of c-K-ras mutations in human gastrointestinal tumors [J].
Arber, N ;
Shapira, I ;
Ratan, J ;
Stern, B ;
Hibshoosh, H ;
Moshkowitz, M ;
Gammon, M ;
Fabian, I ;
Halpern, Z .
GASTROENTEROLOGY, 2000, 118 (06) :1045-1050
[4]   Mucin gene expression in Barrett's oesophagus: an in situ hybridisation and immunohistochemical study [J].
Arul, GS ;
Moorghen, M ;
Myerscough, N ;
Alderson, DA ;
Spicer, RD ;
Corfield, AP .
GUT, 2000, 47 (06) :753-761
[5]  
Bailey T, 1998, AM J PATHOL, V152, P135
[6]   Evolution of neoplastic cell lineages in Barrett oesophagus [J].
Barrett, MT ;
Sanchez, CA ;
Prevo, LJ ;
Wong, DJ ;
Galipeau, PC ;
Paulson, TG ;
Rabinovitch, PS ;
Reid, BJ .
NATURE GENETICS, 1999, 22 (01) :106-109
[7]  
Barrett MT, 1996, ONCOGENE, V12, P1873
[8]  
Barrett MT, 1996, ONCOGENE, V13, P1867
[9]   Allelic loss involving the tumor suppressor genes APC and MCC and expression of the APC protein in the development of dysplasia and carcinoma in Barrett esophagus [J].
Bektas, N ;
Donner, A ;
Wirtz, C ;
Heep, H ;
Gabbert, HE ;
Sarbia, M .
AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 2000, 114 (06) :890-895
[10]   Nuclear accumulation of beta-catenin is a common and early event during neoplastic progression of Barrett esophagus [J].
Bian, YS ;
Osterheld, MC ;
Bosman, FT ;
Fontolliet, C ;
Benhattar, J .
AMERICAN JOURNAL OF CLINICAL PATHOLOGY, 2000, 114 (04) :583-590