Review
Copyright ©2007 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Sep 7, 2007; 13(33): 4423-4430
Published online Sep 7, 2007. doi: 10.3748/wjg.v13.i33.4423
Genetic alterations in pancreatic cancer
Muhammad Wasif Saif, Lena Karapanagiotou, Kostas Syrigos
Muhammad Wasif Saif, Kostas Syrigos, Yale University School of Medicine, Section of Medical Oncology, 333 Cedar Street, New Haven, CT 06520-8032, United States
Lena Karapanagiotou, Oncology Unit, Third Department of Medicine, Athens Medical School, Sotiria General Hospital, Mesogion 152, 11526 Athens, Greece
Author contributions: All authors contributed equally to the work.
Correspondence to: Muhammad Wasif Saif, MD, MBBS, Associate Professor, Yale University School of Medicine, Section of Medical Oncology, 333 Cedar Street; FMP 116, New Haven, CT 06520, United States. wasif.saif@yale.edu
Telephone: +1-203-7371569 Fax: +1-203-7853788
Received: May 3, 2007
Revised: May 23, 2007
Accepted: May 28, 2007
Published online: September 7, 2007
Abstract

The diagnosis of pancreatic cancer is devastating for patients and their relatives as the incidence rate is approximately the same as mortality rate. Only a small percentage, which ranges from 0.4% to 4% of patients who have been given this diagnosis, will be alive at five years. At the time of diagnosis, 80% of pancreatic cancer patients have unresectable or metastatic disease. Moreover, the therapeutic alternatives offered by chemotherapy or radiotherapy are few, if not zero. For all these reasons, there is an imperative need of analyzing and understanding the primitive lesions that lead to invasive pancreatic adenocarcinoma. Molecular pathology of these lesions is the key of our understanding of the mechanisms underlying the development of this cancer and will probably help us in earlier diagnosis and better therapeutic results. This review focuses on medical research on pancreatic cancer models and the underlying genetic alterations.

Keywords: Carcinogenesis; Telomerase; p21; p16; Oncogenes; Epidermal growth factor