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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...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Blackwell Publishing Ltd
1994
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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 |
format | Online Article Text |
id | pubmed-5919338 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1994 |
publisher | Blackwell Publishing Ltd |
record_format | MEDLINE/PubMed |
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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