Human equilibrative nucleoside transporter 1 (hENT1): Do we really have a new predictive biomarker of chemotherapy outcome in pancreatic cancer patients?

Pancreatology ◽  
2013 ◽  
Vol 13 (6) ◽  
pp. 558-563 ◽  
Author(s):  
Beatrice Mohelnikova-Duchonova ◽  
Bohuslav Melichar
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Patients ◽  
Predictive Biomarker ◽  
Nucleoside Transporter ◽  
Equilibrative Nucleoside Transporter

Su1644 Human Equilibrate Nucleoside Transporter 1 Expression Predicts Survival of Pancreatic Cancer Patients Trated With Gemcitabine-Based Adjuvant Chemotherapy After Resection

2013 ◽  
Vol 144 (5) ◽  
pp. S-1080
Author(s):  
Toshiyuki Moriya ◽  
Shigemi Fuyama ◽  
Yukinori Kamio ◽  
Koichiro Ozawa ◽  
Shigeo Hasegawa ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Adjuvant Chemotherapy ◽  
Cancer Patients ◽  
Nucleoside Transporter

Human Equilibrative Nucleoside Transporter 1 Levels Predict Response to Gemcitabine in Patients With Pancreatic Cancer

2009 ◽  
Vol 136 (1) ◽  
pp. 187-195 ◽  
Author(s):  
James J. Farrell ◽  
Hany Elsaleh ◽  
Miguel Garcia ◽  
Raymond Lai ◽  
Ali Ammar ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Nucleoside Transporter ◽  
Equilibrative Nucleoside Transporter

scholarly journals Novel Strategy with Gemcitabine for Advanced Pancreatic Cancer

ISRN Oncology ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Shuji Komori ◽  
Shinji Osada ◽  
Kazuhiro Yoshida
Keyword(s):  
Pancreatic Cancer ◽  
Advanced Pancreatic Cancer ◽  
Metabolic Enzymes ◽  
Interindividual Variation ◽  
Nucleoside Transporter ◽  
Standard Drug ◽  
Equilibrative Nucleoside Transporter ◽  
Nucleotide Pools ◽  
Novel Strategy

5-fluorouracil (5-FU) is widely used in chemotherapy for gastric and colorectal cancer, but gemcitabine (GEM), and not 5-FU, is approved as a standard drug for use in pancreatic cancer. Interindividual variation in the enzyme activity of the GEM metabolic pathway can affect the extent of GEM metabolism and the efficacy of GEM chemotherapy. Human equilibrative nucleoside transporter 1 (hENT1) is recognized as a major transporter of GEM into cells. In addition, a factor that activates hENT1 is the inhibition of thymidylate synthase (TS), one of the 5-FU metabolic enzymes; TS inhibition mediates depleting intracellular nucleotide pools, resulting in the activation of the salvage pathway mediated through hENT1. In this paper, the role of 5-FU in GEM-based chemotherapy for pancreatic cancer is discussed with special emphasis on enzymes involved in the 5-FU and GEM metabolic pathways and in the correlation between GEM responsiveness and the expression of 5-FU and GEM metabolic enzymes.

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