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1 cture of human TS can confer resistance to 5-fluorodeoxyuridine.
2 the TS inhibitor and chemotherapeutic drug 5-fluorodeoxyuridine.
3         It also confers 8-fold resistance to fluorodeoxyuridine.
4 that mediates radiosensitization produced by fluorodeoxyuridine.
5 current continuous-infusion hepatic arterial fluorodeoxyuridine (0.2 mg/kg/d) during the first 4 week
6 hat in humans the dose-limiting toxicity for fluorodeoxyuridine [2-fluoro-5'-deoxyuridine (FdUrd)] wh
7  and obtain variants that are resistant to 5-fluorodeoxyuridine (5-FdUR).
8  other nucleoside analogs modified at C-5, 5-fluorodeoxyuridine and 5-fluorocytidine, did not induce
9              Trifluoromethyl thymidine and 5-fluorodeoxyuridine are good substrates for CpTK, and bot
10 tagens, including ultraviolet irradiation, 5-fluorodeoxyuridine, ethyl methanesulfonate, and methyl m
11  chromosomes that are induced by agents like fluorodeoxyuridine (FdU) that affect intracellular thymi
12 study shows that its deoxynucleoside form, 5-fluorodeoxyuridine (FdU), operates by a distinct DNA inc
13 ylase (hUNG) sensitizes some cell lines to 5-fluorodeoxyuridine (FdU).
14 s each containing either zero, one, or two 5-fluorodeoxyuridine (FdUrd) or 5-fluorouridine (FUrd) nuc
15 ines, in particular, fluorouracil (5-FU) and fluorodeoxyuridine (FdUrd), are active alone and in comb
16 amage and cytotoxicity caused by exposure to fluorodeoxyuridine (FdUrd).
17   5-Fluorouracil (5-FU) and its metabolite 5-fluorodeoxyuridine (FdUrd, floxuridine) are chemotherapy
18                  5-Fluorouracil (5-FU) and 5-fluorodeoxyuridine (FdUrd, floxuridine) have activity in
19                               Floxuridine (5-fluorodeoxyuridine, FdUrd), a U.S. Food and Drug Adminis
20 h the anticancer agents 5-fluorouracil and 5-fluorodeoxyuridine (floxuridine), a 5-fluorouracil metab
21          Treatment regimen included HAI with fluorodeoxyuridine (FUDR) 60 mg/m2/d and L 15 mg/m2/d co
22 se the thymidylate synthetase (TS) inhibitor fluorodeoxyuridine (FUdR) can alter expression of cellul
23 y to the thymidylate synthase (TS) inhibitor fluorodeoxyuridine (FUdR) in human cancer cell lines.
24 frequent pattern of disease progression when fluorodeoxyuridine (FUDR) is given by the intraarterial
25 nsport of the pyrimidine nucleoside analog 5-fluorodeoxyuridine (FUdR) would inhibit growth, PhtC and
26 s delivered with concurrent hepatic arterial fluorodeoxyuridine (HA FUdR).
27 DNA and then selected mutants resistant to 5-fluorodeoxyuridine in a bacterial complementation system
28  chemotherapy agents that are converted to 5-fluorodeoxyuridine monophosphate (FdUMP) and 5-fluorodeo
29 onophosphates (deoxyuridine monophosphate, 5-fluorodeoxyuridine monophosphate, 1-beta-D-arabinofurano
30                                     HAI with fluorodeoxyuridine plus dexamethasone was given on days
31 ransfected cells, respectively, also lead to fluorodeoxyuridine resistance (26- and 97-fold in IC50 v
32 etween UDG and duplex DNA containing 2'-beta-fluorodeoxyuridine shows similar increases in the level
33 3-Oxo-C12-(L)-HSL enhances the activity of 5-fluorodeoxyuridine, tomudex, and taxol but not the activ
34 uorodeoxyuridine monophosphate (FdUMP) and 5-fluorodeoxyuridine triphosphate (FdUTP).
35 five active metabolites, including Sch-B and fluorodeoxyuridine triphosphate, were found tumor-accumu
36 HT29 and SW620 human colon cancer cells with fluorodeoxyuridine under conditions that produced nearly
37  selected marker and cells grown in 0.5 mM 5-fluorodeoxyuridine, we have recovered up to 50 transform
38 S was established through the use of [6-3H]5-fluorodeoxyuridine, which forms a tight ternary complex