Immunohistochemical Analysis of Human Equilibrative Nucleoside Transporter-1 (hENT1) Predicts Survival in Resected Pancreatic Cancer Patients Treated with Adjuvant Gemcitabine Monotherapy

2011 ◽  
Vol 19 (S3) ◽  
pp. 558-564 ◽  
Author(s):  
Soichiro Morinaga ◽  
Yoshiyasu Nakamura ◽  
Takuo Watanabe ◽  
Hiroshi Mikayama ◽  
Hiroshi Tamagawa ◽  
...  
2013 ◽  
Vol 144 (5) ◽  
pp. S-1080
Author(s):  
Toshiyuki Moriya ◽  
Shigemi Fuyama ◽  
Yukinori Kamio ◽  
Koichiro Ozawa ◽  
Shigeo Hasegawa ◽  
...  

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

ISRN Oncology ◽  
2011 ◽  
Vol 2011 ◽  
pp. 1-5 ◽  
Author(s):  
Shuji Komori ◽  
Shinji Osada ◽  
Kazuhiro Yoshida

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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