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. © 2009 Informa UK Ltd All rights reserved.
CITATION STYLE
Andersson, R., Aho, U., Nilsson, B. I., Peters, G. J., Pastor-Anglada, M., Rasch, W., & Sandvold, M. L. (2009). Gemcitabine chemoresistance in pancreatic cancer: Molecular mechanisms and potential solutions. Scandinavian Journal of Gastroenterology. https://doi.org/10.1080/00365520902745039
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