Molecular Mechanisms in Barrett's Metaplasia and Its Progression

Julie G. Izzo, Rajyalakshmi Luthra, Tseung Teh Wu, Arlene M. Correa, Madan Luthra, Sharmila Anandasabapathy, K. S.Clifford Chao, Mien Chie Hung, Bharat Aggarwal, Walter N. Hittelman, Jaffer A. Ajani

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


The dramatic increase in the incidence and poor overall survival rates of esophageal/gastroesophageal junction adenocarcinoma underscore the necessity to discover molecular markers that can be used for risk assessment, early diagnosis, and targeted therapeutic intervention. Barrett's esophagus (BE) is proposed to represent a precursor of esophageal/gastroesophageal junction adenocarcinoma. BE progression to invasive cancer is defined by a metaplasia-dysplasia-carcinoma progression characterized by an increasing accumulation of genetic changes associated with alterations in molecular gatekeepers of cell circuitries and tissue homeostasis. Using a combination of in situ tissue-based and high-throughput analyses, we investigated alterations of cell-cycle regulators and inflammation-associated molecular effectors. Our data suggest a potential synergistic effect of these alterations for the BE progression to cancer, and underscore the potential use of these markers: (1) in molecular panels assessing cancer risk in BE patients; and (2) as potential therapeutic targets for chemopreventive interventions and to enhance response to anti-neoplastic therapies.

Original languageEnglish
Pages (from-to)S2-S6
JournalSeminars in Oncology
Issue numberSUPPL. 1
StatePublished - Apr 2007
Externally publishedYes


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