alexa Genomics, Epigenetics and Molecular Considerations in E
ISSN: 1747-0862

Journal of Molecular and Genetic Medicine
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Genomics, Epigenetics and Molecular Considerations in Esophageal Adenocarcinoma: What You Need to Know?

Schizas D1,2, Mylonas KS2,3, Patelis N1*, Sioulas A4 and Liakakos T1

1First Department of Surgery, Laiko General Hospital, National and Kapodistrian University of Athens, Athens, Greece

2Surgery Working Group, Society of Junior Doctors, Athens, Greece

3Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

4Department of Gastroenterology, Hygeia Hospital, Athens, Greece

*Corresponding Author:
Dr. Nikolaos Patelis
First Department of Surgery
Laiko General Hospital
National and Kapodistrian University
of Athens, Athens, Greece
Tel: 302132060800
E-mail: [email protected]

Received date: February 16, 2017; Accepted date: March 03, 2017; Published date: March 07, 2017

Citation: Schizas D, Mylonas KS, Patelis N, Sioulas A, Liakakos T (2017) Genomics, Epigenetics and Molecular Considerations in Esophageal Adenocarcinoma: What You Need to Know? J Mol Genet Med 11:252 doi:10.4172/1747-0862.1000252

Copyright: © 2017 Schizas D, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

 

Abstract

Esophageal malignancies are usually encountered in patients over 50 years old and are associated with significant morbidity and mortality. Efforts to improve patient outcomes are slowly shifted towards unravelling the molecular basis of esophageal cancer as this approach could lead to designing individualized treatment protocols and implementing precision medicine paradigms. Our aim was to present recent advances in esophageal adenocarcinoma genomics, epigenetics and molecular biology with regards to their role on disease pathophysiology, patient outcomes and applications to clinical care. Disease progression is correlated with missense mutations and in-frame deletions of EGFR, as well as with upregulation of a variety of genes (CXCL1 CXCL3, GATA6 and DMBT1), microsatellite instability and telomerase overexpression. On the other hand, p53 loss of heterozygosity as well as HER2 and c-MYC amplifications tend to develop in later stages of the disease and are associated with poor prognosis. Downregulation of CDKN2A, e-cadherin, SMAD4, RUNX3 and aneuploidy/tetraploidy are also correlated with unfavorable outcomes. Lastly, p53 immunohistochemistry and methylation panels are already being applied in clinical practice.

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