Genetic and Epigenetic Alterations in Barrett's Esophagus and Esophageal Adenocarcinoma

被引：43

作者：

Kaz, Andrew M. ^{[1
,2
,3
]}

Grady, William M. ^{[2
,3
]}

Stachler, Matthew D. ^{[4
]}

Bass, Adam J. ^{[5
]}

机构：

[1] VA Puget Sound Hlth Care Syst, R&D Dept, Seattle, WA 98109 USA

[2] Fred Hutchinson Canc Res Ctr, Div Clin Res, Seattle, WA 98109 USA

[3] Univ Washington, Sch Med, Dept Internal Med, Seattle, WA 98195 USA

[4] Harvard Univ, Sch Med, Dept Pathol, Brigham & Womens Hosp, Boston, MA 02115 USA

[5] Dana Farber Canc Inst, Dept Med Oncol, Boston, MA 02215 USA

来源：

GASTROENTEROLOGY CLINICS OF NORTH AMERICA | 2015年 / 44卷 / 02期

基金：

美国国家卫生研究院;

关键词：

Barrett's esophagus; Esophageal adenocarcinoma; Cancer genomics; LOH; Aneuploidy; Genomic instability; DNA methylation; METHYLATION INHIBITS BINDING; CPG ISLAND SHORES; DNA METHYLATION; NEOPLASTIC PROGRESSION; PROMOTER HYPERMETHYLATION; EARLY EVENT; POTENTIAL BIOMARKER; CLONAL EXPANSION; POOR-PROGNOSIS; E-CADHERIN;

D O I：

10.1016/j.gtc.2015.02.015

中图分类号：

R57 [消化系及腹部疾病];

学科分类号：

摘要：

Esophageal adenocarcinoma (EAC) develops from Barrett's esophagus (BE), wherein normal squamous epithelia is replaced by specialized intestinal metaplasia in response to chronic gastroesophageal acid reflux. BE can progress to low- and high-grade dysplasia, intramucosal, and invasive carcinoma. Both BE and EAC are characterized by loss of heterozygosity, aneuploidy, specific genetic mutations, and clonal diversity. Given the limitations of histopathology, genomic and epigenomic analyses may improve the precision of risk stratification. Assays to detect molecular alterations associated with neoplastic progression could be used to improve the pathologic assessment of BE/EAC and to select high-risk patients for more intensive surveillance.

引用

页码：473 / +

页数：18

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