Gemcitabine chemoresistance in pancreatic cancer: Molecular mechanisms and potential solutions.

Research output: Contribution to journalArticle

Abstract

Ductal pancreatic adenocarcinoma is associated with a very poor prognosis and most patients are given palliative care. Chemotherapy in the form of gemcitabine has been found to reduce disease-related pain, and the otherwise frequently occurring weight changes, to increase Karnofsky performance status and quality of life and has also resulted in a modest improvement in survival time. The intracellular uptake of gemcitabine is dependent on nucleoside transporters, predominantly human equilibrative nucleoside transporter-1 (hENT-1), which is over-expressed in human pancreatic adenocarcinoma cells. Cellular resistance to gemcitabine can be intrinsic or acquired during gemcitabine treatment. One of the mechanisms is a decrease in hENT-1 expression. Modifications of gemcitabine not rendering it dependent on the nucleoside transporter may be a successful future mode of chemotherapy treatment, and determination of the nucleoside receptor status at the time of diagnosis could potentially also contribute to a more targeted therapy in the future.

Details

Authors
  • Roland Andersson
  • Ursula Aho
  • Bo Nilsson
  • Godefridus Peters
  • Marcal Pastor-Anglada
  • Wenche Rasch
  • Marit Sandvold
Organisations
Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Gastroenterology and Hepatology
Original languageEnglish
Pages (from-to)782-786
JournalScandinavian Journal of Gastroenterology
Volume44
Publication statusPublished - 2009
Publication categoryResearch
Peer-reviewedYes