Stomach – Genetic and epigenetic alterations of preneoplastic and neoplastic lesions

Issue title: Translational Pathology of Early Cancer

Guest editors: Sudhir Srivastavax and William E. Grizzley

Article type: Research Article

Authors: David, Stefan^{a; *} | Meltzer, Stephen J.^{a; b}

Affiliations: [a] Department of Medicine, Division of Gastroenterology, Johns Hopkins University, School of Medicine, Baltimore, MD, USA | [b] Department of Oncology, Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, School of Medicine, Baltimore, MD, USA | [x] Cancer Biomarkers Research Group, Division of Cancer Prevention, National Cancer Institute, Rockville, MD, USA | [y] Department of Pathology, Division of Anatomic Pathology, University of Alabama at Birmingham, Birmingham, AL, USA

Correspondence: [*] Corresponding author: Stefan David, Division of Gastroenterology, Department of Medicine, Johns Hopkins School of Medicine, Baltimore, MD, 1503 E Jefferson Street, Rm 106, Baltimore MD, 21231, USA. E-mail: [email protected].

Abstract: Gastric cancer is one of the most common neoplasias in the world and remains an important cause of cancer-related mortality. Vast resources have been invested in the study of the molecular events driving the development and progression of gastric tumors. Gastric cancer is known to result from an interaction between host and environmental factors. The present review will discuss the most how genetic and epigenetic changes contribute to gastric carcinogenesis and their potential for developing novel diagnostic and therapeutic tools.

Keywords: Gastric cancer, genetics, epigenetics, microsatellite instabilitychromosomal instability, mutation, deletion, translocation, methylation, oncogene, tumor suppressor gene

DOI: 10.3233/CBM-2011-0169

Journal: Cancer Biomarkers, vol. 9, no. 1-6, pp. 493-507, 2011