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Int J Clin Exp Pathol 2(3),310-326;2009.

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).

Key Words: Epigenetics, pancreatic cancer

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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:
mgoggins@jhmi.edu