Backgrounds: Pancreatic carcinoma is one of the most serious forms of cancer, with a very high mortality rate, and is the fourth leading cause of cancer-related death in the Czech Republic. The etiology and molecular pathogenesis of the disease is still poorly understood. Gemcitabine is a cytotoxic nucleoside analog, which is widely used in the treatment of malignancies, and in particular in pancreatic carcinoma. Interindividual differences in gemcitabine pharmacokinetics and pharmacodynamics have been demonstrated, which can significantly influence the outcome of the therapy in thus treated patients. Resistance developed to nucleoside analogs limits their clinical use, just like in the case of any other cytostatics.
Aim: This review summarizes available data concerning the membrane proteins involved in the transport mechanism of gemcitabine through cellular membrane, and their role in the cellular resistance of pancreatic carcinoma to gemcitabine.