| Literature DB >> 26021206 |
Andrew M Kaz1, William M Grady2, Matthew D Stachler3, Adam J Bass4.
Abstract
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.Entities:
Keywords: Aneuploidy; Barrett’s esophagus; Cancer genomics; DNA methylation; Esophageal adenocarcinoma; Genomic instability; LOH
Mesh:
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Year: 2015 PMID: 26021206 PMCID: PMC4449457 DOI: 10.1016/j.gtc.2015.02.015
Source DB: PubMed Journal: Gastroenterol Clin North Am ISSN: 0889-8553 Impact factor: 3.806