ライフサイエンスコーパス: FUdR

1 FUdR exposure caused elevation of RR activity at 10 and

2 By contrast, serine does not alter FUdR metabolism.

3 of sequential treatment with Adriamycin and FUdR (MCF-7 A/F) release the most IL-8 and express the g

4 lls treated sequentially with Adriamycin and FUdR expressed a metastatic phenotype.

5 ppress progeny, pop-1 RNAi was used to avoid FUdR use.

6 The effect of enhanced viral replication by FUdR was suppressed by hydroxyurea, a known inhibitor of

7 and serine enhance 5-fluoro 2'deoxyuridine (FUdR) toxicity in C. elegans through different microbial

8 Adriamycin and/or 5-fluoro-2'-deoxyuridine (FUdR), induced changes in the expressed phenotype.

9 orouridine (FUrd), 5-fluoro-2'-deoxyuridine (FUdR), trifluorothymidine (TFT); to the nonpyrimidine TS

10 dine nucleoside analog 5-fluorodeoxyuridine (FUdR) would inhibit growth, PhtC and PhtD conferred a gr

11 ynthetase (TS) inhibitor fluorodeoxyuridine (FUdR) can alter expression of cellular RR and GADD34, we

12 synthase (TS) inhibitor fluorodeoxyuridine (FUdR) in human cancer cell lines.

13 Treatment of H630-C6 cells with 5-FU, FUrd, FUdR, TFT, AG331, AG337, ZD1694, and methotrexate up-reg

14 rent hepatic arterial fluorodeoxyuridine (HA FUdR).

15 nstrate that the growth advantage of G207 in FUdR-treated cells is primarily based on an RR-dependent

16 HSV-1 was impaired in the presence of 10 nM FUdR, whereas G207 demonstrated increased replication un

17 The amino acid phosphoramidate diesters of FUdR (2) and Ara-C (6), 5-fluoro-2'-deoxy-5'-uridyl N-(1

18 etabolism of the phosphoramidate diesters of FUdR in proliferating tissue proceeds through two separa

19 lar RR and GADD34, we examined the effect of FUdR on G207 bioactivity with the hypothesis that FUdR-i

20 monophosphate and a lag in the generation of FUdR.

21 beled 5b resulted in the rapid production of FUdR 5'-monophosphate and a lag in the generation of FUd

22 Combined use of FUdR and G207 resulted in synergistic cytotoxicity.

23 osure of MCF-7 cells to either Adriamycin or FUdR rapidly increases, in a dose-dependent manner, the

24 promotes microbial conversion of the prodrug FUdR into toxic 5-fluorouridine-5'-monophosphate (FUMP),

25 inhibitors of deoxyribonucleotide synthesis FUdR, methotrexate and hydroxyurea than cells with wild-

26 on G207 bioactivity with the hypothesis that FUdR-induced cellular changes will alter viral prolifera

27 accompanied by a significant decrease in the FUdR IC(50)(72h) ( approximately 75-fold for SW620 cells

28 TS inhibition impairs viral replication, the FUdR-induced RR elevation may overcome this disadvantage

29 at a concentration of 100 microM, while the FUdR conjugates 5a,b exhibited IC50 values within a rang

30 te synthase inhibition that is comparable to FUdR in thymidine kinase deficient cells.

31 inhibition studies show that, in contrast to FUdR, the nitrofuran compound 2a is of comparable potenc