Copyright
©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Dec 28, 2007; 13(48): 6465-6469
Published online Dec 28, 2007. doi: 10.3748/wjg.v13.i48.6465
Published online Dec 28, 2007. doi: 10.3748/wjg.v13.i48.6465
Genetic and epigenetic changes associated with cholangiocarcinoma: From DNA methylation to microRNAs
Monique Stutes, Sharon DeMorrow, Division of Research and Education Scott and White Hospital, Temple, Texas 76504, United States
Steven Tran, Sharon DeMorrow, Department of Medicine, Texas A&M Health Science Center, College of Medicine, Temple, Texas 76504, United States
Supported by a NIH mentored award (KO1 DK078532) as well as a grant award from Scott & White Hospital
Correspondence to: Sharon DeMorrow, PhD, Division of Research and Education, Scott & White Hospital, Department of Internal Medicine, Texas A&M Health Science Center, Medical Research Building, 702 SW H.K Dodgen Loop, Temple, TX 76504, United States. demorrow@medicine.tamhsc.edu
Telephone: +1-254-7246240 Fax: +1-254-7248070
Received: August 18, 2007
Revised: September 3, 2007
Accepted: September 26, 2007
Published online: December 28, 2007
Revised: September 3, 2007
Accepted: September 26, 2007
Published online: December 28, 2007
Abstract
Cholangiocarcinomas are malignant epithelial liver tumors arising from the intra- and extra-hepatic bile ducts. Little is known about the molecular development of this disease, and very few effective treatment options are available. Thus, prognosis is poor. Genetic and epigenetic changes play an integral role in the neoplastic transformation of human cells to their malignant counterparts. This review summarizes some of the more prevalent genetic alterations (by microRNA expression) and epigenetic changes (hypermethylation of specific gene promoters) that are thought to contribute to the carcinogenic process in cholangiocarcinoma.
Keywords: Promoter regions, CpG islands, Tumor suppressor, Oncogene, Inflammation