Editorial
Copyright ©2011 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastrointest Oncol. Nov 15, 2011; 3(11): 153-164
Published online Nov 15, 2011. doi: 10.4251/wjgo.v3.i11.153
Molecular predictors of gemcitabine response in pancreatic cancer
Ioannis A Voutsadakis
Ioannis A Voutsadakis, Centre Pluridisciplinaire d’Oncologie, Centre Hospitalier Universitaire Vaudois, Lausanne 1011, Switzerland
Author contributions: Voutsadakis IA solely contributed to this paper.
Correspondence to: Ioannis A Voutsadakis, MD, PhD, Centre Pluridisciplinaire d’Oncologie, BH06, Centre Hospitalier Universitaire Vaudois, Bugnon 46, Lausanne 1011, Switzerland. ivoutsadakis@yahoo.com
Telephone: +41-21-3145122 Fax: +41-21-2140188
Received: April 20, 2011
Revised: September 30, 2011
Accepted: October 7, 2011
Published online: November 15, 2011
Abstract

Gemcitabine is one of the most used anti-neoplastic drugs with documented activity in almost all major localizations of cancer. In pancreatic cancer treatment, gemcitabine occupies a prominent place as a first line chemotherapy, partly because of the paucity of other efficacious chemotherapy options. In fact, only a minority of pancreatic cancer patients display a response or even stability of disease with the drug. There are currently no clinically applicable means of predicting which patient will derive a clinical benefit from gemcitabine although several proposed markers have been studied. These markers are proteins involved in drug up-take, activation and catabolism or proteins that define the ability of the cell to undergo apoptosis in response to the drug. Several of these markers are reviewed in this paper. We also briefly discuss the possible role of stem cells in drug resistance to gemcitabine.

Keywords: Pancreatic cancer; Gemcitabine; Chemotherapy; Drug resistance; Metabolism; Akt kinase; Nuclear factor-κB