Review Article Epigenetics and Epigenetic Alterations in Pancreatic Cancer
Noriyuki Omura and Michael Goggins
Departments of Pathology, Medicine and Oncology, The Sol Goldman Pancreatic Research Center, The Johns Hopkins Medical Institutions, Baltimore, MD
Received 21 October 2008; Accepted 28 October 2008; Available online 15 November 2008
Abstract: Pancreatic cancer remains a major therapeutic challenge. In 2008, there will be approximately 37,680 new cases and 34,290 deaths attributable to pancreatic cancer in the United States (U.S.), making it the fourth leading cause of cancer-related death. Recent comprehensive pancreatic cancer genome project found that pancreatic adenocarcinomas harbored 63 intragenic mutations or amplifications/homozygous deletions and these alterations clustered in 12 signaling pathways. In addition to widespread genetic alterations, it is now apparent that epigenetic mechanisms are also central to the evolution and progression of human cancers. Since epigenetic silencing processes are mitotically heritable, they can drive neoplastic progression and undergo the same selective pressure as genetic alterations. This review will describe recent developments in cancer epigenetics and their importance in our understanding of pancreatic adenocarcinoma. (IJCEP810007).
Address all correspondence to: Michael Goggins, MD, Professor of Pathology, Medicine and Oncology, Director of the Pancreatic Cancer Early Detection Laboratory, Cancer Research Building 2 Room 342, 1550 Orleans St., Baltimore, MD, 21231, Tel (410)-955-3511; Fax (410)-614-0671, E-mail: firstname.lastname@example.org