Publication: From Barrett metaplasia to esophageal adenocarcinoma: the molecular background
Authors
Saraggi, Deborah ; Fassan, Matteo ; Bornschein, Jan ; Farinati, Fabio ; Realdon, Stefano ; Valeri, Nicola ; Rugge, Massimo
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Publisher
Universidad de Murcia. Departamento de Biología Celular e Histología
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DOI
10.14670/HH-11-659
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info:eu-repo/semantics/article
Description
Abstract
The molecular landscape of Barrett’s
esophagus and Barrett-related neoplastic lesions is still
far from being completely elucidated. Both in vitro and
in vivo studies pinpointed the pathogenetic role of
different morphogenic pathways (the para-homeobox,
the Notch and the Sonic Hedgehog families in particular)
implicated in the acquisition of the metaplastic
phenotype of the esophageal mucosa. On the other hand,
the most common genetic alterations observed during
Barrett's carcinogenesis include disorders of major
regulators of the cell cycle, as well as deregulation of the
TGF-β/Smad and receptor tyrosine kinases signalling
pathways. Recent comprehensive mutational profiling
studies identified that the inactivation of the TP53 and of
the SMAD4 tumour suppressor genes occurred in a
stage-specific manner, confined to (high grade)
dysplastic and neoplastic lesions, respectively. The next
step will be the correlation of these findings into
multidisciplinary diagnostic approaches integrating
endoscopy, histology, molecular profiling and liquid
biopsies. This will allow the introduction of innovative
strategies for secondary prevention of esophageal
adenocarcinoma based on biological rationales, and the
implementation of potential novel therapeutic targets.
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Citation
Histology and Histopathology, vol.31, nº 1, (2016)
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