Ann. N.Y. Acad. Sci. ISSN 0077-8923 ANNALS OF THE NEW YORK ACADEMY OF SCIENCES Issue: The 12th OESO World Conference: Cancers of the Esophagus Strategy for prevention of cancers of the esophagus Junichi Akiyama, 1 Leo Alexandre, 2,3 Anushka Baruah, 4 Navtej Buttar, 4 Raghav Chandra, 4 Allan B. Clark, 2 Andrew R. Hart, 2,3 Ernest Hawk, 5 Daniela Kandioler, 6 Sonja Kappel, 6 Sheila K. Krishnadath, 7 Anamay Sharma, 4 Ishtpreet Singh, 4 Danielle Straub, 7 George Triadafilopoulos, 8 Asad Umar, 1 and Brigitte Wolf 6 1 National Center for Global Health and Medicine, Tokyo, Japan. 2 Norwich Medical School, University of East Anglia, Norwich, United Kingdom. 3 Department of Gastroenterology, Norfolk & Norwich University Hospital NHS Foundation Trust, Norwich, United Kingdom. 4 Division of Gastroenterology & Hepatology, Mayo Clinic College of Medicine, Rochester, Minnesota. 5 Division of Cancer Prevention & Population Sciences, MD Anderson Cancer Center, Houston, Texas. 6 Department of Surgery and Surgical Research, Medical University of Vienna, Vienna, Austria. 7 Oncology Group, Academisch Medisch Centrum, Universiteit van Amsterdam, Amsterdam, the Netherlands. 8 Division of Gastroenterology and Hepatology, Stanford University, Stanford, California Address for correspondence: annals@nyas.org The following, from the 12th OESO World Conference: Cancers of the Esophagus, includes commentaries on the animal reflux–inflammation models for Barrett’s esophagus and esophageal adenocarcinoma; genomic/epigenomic analyses; eflornithine-based combinations; the molecular derangements that promote neoplastic transformation; the role of COX-2 inhibitors, proton pump inhibitors, and phase II trials in Barrett’s adenocarcinoma; statins in chemo- prevention and treatment of esophageal cancer; and biomarkers as potential targets in Barrett’s adenocarcinoma. Keywords: animal reflux–inflammation models; Barrett’s adenocarcinoma; elofrnithine; COXIBs, PPIs; statins; biomarkers; OESO Concise summary An animal model of Barrett’s esophagus (BE) and esophageal adenocarcinoma (EAC) could provide better understanding of the pathogenesis and could be used for investigating new prevention and treat- ment strategies. The Levrat in vivo model is widely accepted and adapted since it mimics the stepwise event of esophagitis, BE, and EAC, showing im- munohistochemical characteristics resembling hu- man BE. The use of rat models for mechanistic stud- ies is limited owing to a lack of genetically modified rat strains. On the other hand, the mouse has a well- characterized genome, and transgenic or knockout mice can be used to investigate the functional role of specific genes. Although none of the models of- fers an ideal system for the complex study of en- vironmental exposure, genetic risk, and prevention strategies, the rodent models are the best options that we have to improve our understanding of the pathogenesis of BE. The science of genomics and epigenomics seems to have successfully identified promising targets for the prevention and treatment of esophageal can- cers. It is critical to identify not only the common and diverse categories but also to distinguish the drivers from the passenger mutations at the early stages of carcinogenesis. The Cancer Genome Atlas has revealed copy number abnormalities and gene amplification events at distinct loci in the two broad esophageal cancer types. There are some copy num- ber abnormalities with similar frequencies in both histologies and there are some genes with copy num- ber abnormalities with different frequencies in the two histologies. Some are amplified and interven- tions are available, and a number of genes are deleted with similar frequencies in both histologies: hence, possible targeted interventions for amplified genes in esophageal cancer. Beyond these targets, addi- tional efforts are underway in the form of a pan- cancer initiative comparing genomic data across doi: 10.1111/nyas.12529 108 Ann. N.Y. Acad. Sci. 1325 (2014) 108–126 C  2014 New York Academy of Sciences.