From Barrett metaplasia to esophageal adenocarcinoma: The molecular background

Deborah Saraggi, Matteo Fassan, Jan Bornschein, Fabio Farinati, Stefano Realdon, Nicola Valeri, Massimo Rugge

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)25-32
Number of pages8
JournalHistology and Histopathology
Volume31
Issue number1
DOIs
Publication statusPublished - Jan 1 2016

Keywords

  • Barrett’s esophagus
  • Biomarker
  • MicroRNA
  • Molecular pathology

ASJC Scopus subject areas

  • Histology
  • Pathology and Forensic Medicine

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    Saraggi, D., Fassan, M., Bornschein, J., Farinati, F., Realdon, S., Valeri, N., & Rugge, M. (2016). From Barrett metaplasia to esophageal adenocarcinoma: The molecular background. Histology and Histopathology, 31(1), 25-32. https://doi.org/10.14670/HH-11-659