Open AccessInhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues
Author(s) -
Okayasu Takeshi,
Sugiyama Kazuhisa,
Miyauchi Shun
Publication year - 1994
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1994.tb02892.x
Subject(s) - fluorouracil , catabolism , phosphorylation , chemistry , cancer research , mechanism of action , lung cancer , moiety , pharmacology , biochemistry , biology , cancer , pathology , in vitro , metabolism , medicine , stereochemistry
Our studies of the degradation and the phosphorylation of S–fluorouracil (5–FU) in normal and tumor lung tissues from 10 cases of lung cancer have shown that the phosphorylation of 5–FU in the tumor tissues was about 2– to 3–fold higher than that in normal tissues, and that the degradation of 5–FU in tumor tissues was nearly 6–fold higher than that in normal tissues. BOF–A2 is an anti–neoplastic agent newly synthesized from l–ethoxymethyl–5–FU and 3–cyano–2,6–dihydroxypyridine (CNDP). The inhibitory effect of CNDP on the degradation of 5–FU in the tumor tissues was potent (IC 50 , 3.9 × 10 −9 M) , Thus, BOF–A2 exerts its anti–neoplastic effect on tumors by potentiating the action of 5–FU through inhibition of 5–FU degradation by the CNDP moiety