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

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Gemcitabine chemoresistance in pancreatic cancer: Molecular mechanisms and potential solutions. / Andersson, Roland; Aho, Ursula; Nilsson, Bo; Peters, Godefridus; Pastor-Anglada, Marcal; Rasch, Wenche; Sandvold, Marit.

I: Scandinavian Journal of Gastroenterology, Vol. 44, 2009, s. 782-786.

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Andersson, Roland ; Aho, Ursula ; Nilsson, Bo ; Peters, Godefridus ; Pastor-Anglada, Marcal ; Rasch, Wenche ; Sandvold, Marit. / Gemcitabine chemoresistance in pancreatic cancer: Molecular mechanisms and potential solutions. I: Scandinavian Journal of Gastroenterology. 2009 ; Vol. 44. s. 782-786.

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TY - JOUR

T1 - Gemcitabine chemoresistance in pancreatic cancer: Molecular mechanisms and potential solutions.

AU - Andersson, Roland

AU - Aho, Ursula

AU - Nilsson, Bo

AU - Peters, Godefridus

AU - Pastor-Anglada, Marcal

AU - Rasch, Wenche

AU - Sandvold, Marit

PY - 2009

Y1 - 2009

N2 - 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.

AB - 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.

U2 - 10.1080/00365520902745039

DO - 10.1080/00365520902745039

M3 - Article

VL - 44

SP - 782

EP - 786

JO - Scandinavian Journal of Gastroenterology

JF - Scandinavian Journal of Gastroenterology

SN - 1502-7708

ER -