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Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues

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 i...

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Detalles Bibliográficos
Autores principales: Okayasu, Takeshi, Sugiyama, Kazuhisa, Miyauchi, Shun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 1994
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5919338/
https://www.ncbi.nlm.nih.gov/pubmed/8106287
http://dx.doi.org/10.1111/j.1349-7006.1994.tb02892.x
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author Okayasu, Takeshi
Sugiyama, Kazuhisa
Miyauchi, Shun
author_facet Okayasu, Takeshi
Sugiyama, Kazuhisa
Miyauchi, Shun
author_sort Okayasu, Takeshi
collection PubMed
description 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
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spelling pubmed-59193382018-05-11 Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues Okayasu, Takeshi Sugiyama, Kazuhisa Miyauchi, Shun Jpn J Cancer Res Article 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 Blackwell Publishing Ltd 1994-01 /pmc/articles/PMC5919338/ /pubmed/8106287 http://dx.doi.org/10.1111/j.1349-7006.1994.tb02892.x Text en
spellingShingle Article
Okayasu, Takeshi
Sugiyama, Kazuhisa
Miyauchi, Shun
Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues
title Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues
title_full Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues
title_fullStr Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues
title_full_unstemmed Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues
title_short Inhibition of Catabolic Pathway of 5‐Fluorouracil by 3‐Cyano‐2,6‐dihydroxypyridine in Human Lung Cancer Tissues
title_sort inhibition of catabolic pathway of 5‐fluorouracil by 3‐cyano‐2,6‐dihydroxypyridine in human lung cancer tissues
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5919338/
https://www.ncbi.nlm.nih.gov/pubmed/8106287
http://dx.doi.org/10.1111/j.1349-7006.1994.tb02892.x
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