The Effects Of Gemcitabine Resistance On Patients With Metastatic Pancreatic Cancer

1223 Words Jan 1st, 2015 5 Pages
Gemcitabine (2,2-difluoro 2-deoxycytidine, dFdC) is a deoxycytdine analog; a prodrug with activity against non-small cell lung cancer (NSCLC), small cell lung cancer (SCLC), ovarian and pancreatic cancers (Hertel et al., 1990; Braakhuis et al., 1995; Boven et al.,1993; Merriman et al., 1996; Jansen et al., 1995) Pancreatic cancer tumor [1 & 2 ref]. Nowadays gemcitabine is signified as a single agent in the treatment of patients with metastatic pancreatic cancer [2], (2,2-difluoro 2-deoxycytidine, dFdC) is an analogue of cytosine arabinoside (Ara-C) from which it vary structurally due to its fluorine substituents on position 29of the furanose ring [ref 1].

Gemcitabine has a gold drug standard and has very similar activation step as of ara-C but with more complicated mechanism and with more cellular targets. Gemcitabine resistance is the biggest problem in the chemotherapy of cancer patients, alterations in the cellular target of the gemcitabine results in decreased sensitivity of the drug. There many factors involved in the resistance of gemcitabine and thus, a thus a thorough study is required for better understanding of the mechanisms determining its activation and development of resistance. This paper / article / review deals with the mechanisms involving pharmacology of gemcitabine. [ref 2 & 3]
Gemcitabine Pharmacology:
Transport / Uptake of Gemcitabine :
Gemcitabine a nucleoside analogue is hydrophilic in nature and requires an active uptake through the cell…
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