Publication: The molecular pathology of Barrett's esophagus
Authors
Werner, M. ; Mueller, J. ; Walch, A. ; Hofler, H.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The incidence of adenocarcinoma of the
distal esophagus is rapidly increasing in the Western
world. The histopathological sequence of (Barrett's)
metaplasia, which develops as a consequence of chronic
reflux, to dysplasia and then to carcinoma is well
established for these tumors. In Barrett's esophagus a
variety of molecular changes have been characterized
and correlated with tumor initiation and progression.
Among the early changes in premalignant stages of
metaplasia are alterations of the transcripts of FHIT, a
presumptive tumor suppressor gene which spans the
common fragile site FRA3B. Mutations of p53 seem to
accumulate mainly in the transition from low to high
grade dysplasia. Inactivation of other tumor suppressor
genes by mutation (APC, p16) or hypermethylation
(p16) as well as amplification of oncogenes such as cerbB2
are relatively late events in the development of
adenocarcinoma. Among the phenotypic changes in
Barrett's esophagus are an expansion of the Ki67
proliferation compartment which correlates with the
degree of dysplasia. Moreover, accumulation of rabll
molecules which are involved in membrane trafficking
has been reported to be specific for the loss of polarity
seen in low grade dysplasia. Reduced expression of the
cadherinlcatenin complex as well as increased
expression of various proteases develop chiefly in
invasive carcinomas. Despite the progress that has been
made in the identification of molecular markers in
Barrett's carcinoma, to date the histopathogical
diagnosis of high grade dysplasia in endoscopic biopsies
remains the best predictor of invasive cancer. Immunohistochemistry
applying a panel of antibodies including
p53, Mib-l or rabll can be helpful to diagnose
regenerative metaplastic epithelium or low and high
grade dysplasia.
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