ライフサイエンスコーパス: ara-G

1 te lymphoblastic leukemia, but how ara-G and ara-G triphosphate (ara-GTP) kill cells is not known.

2 Peak plasma concentrations of GW506U78 and ara-G were dose-dependent.

3 r the determination of plasma nelarabine and ara-G concentrations.

4 ro-drug of 9-beta-D-arabinofuranosylguanine (ara-G), a deoxyguanosine derivative.

5 of plasma nelarabine and arabinosylguanine (ara-G) and of cellular ara-G triphosphate (ara-GTP) were

6 9-Beta-D-Arabinosylguanine (ara-G) is a recently introduced and effective treatment

7 The prodrug of 9-beta-D-arabinosylguanine (ara-G), nelarabine, demonstrated efficacy against T-cell

8 Nelarabine, prodrug of arabinosylguanine (ara-G), has demonstrated T-lymphoblastic antileukemic ac

9 vitro investigations with arabinosylguanine (ara-G) demonstrated potent cytotoxicity to T-lymphoblast

10 elarabine (the prodrug of arabinosylguanine [ara-G]) in patients with hematologic malignancies.

11 in an S phase-dependent apoptosis induced by ara-G incorporation into DNA, which may lead to a T cell

12 zed that, in cycling T-lymphoblastoid cells, ara-G may act directly by incorporation into DNA, which

13 nd arabinosylguanine (ara-G) and of cellular ara-G triphosphate (ara-GTP) were similar in the two gro

14 age cell lines, CEM cells incorporated fewer ara-G molecules-which were at internucleotide positions

15 phosphorylated within leukemic cells to form ara-G triphosphate (ara-GTP), which acts to terminate DN

16 dGK seems to predominate, whereas at higher ara-G concentrations, dCK seems to be the preferred enzy

17 T-cell acute lymphoblastic leukemia, but how ara-G and ara-G triphosphate (ara-GTP) kill cells is not

18 dCK-) to assess the role of these kinases in ara-G phosphorylation.

19 s with a Fas antagonistic antibody inhibited ara-G-mediated cell death.

20 and dGK can phosphorylate ara-G, but at low ara-G concentrations, dGK seems to predominate, whereas

21 product was observed in dGK+ extracts at low ara-G levels (10 microM) and in dCK+ extracts at high co

22 ystems after a 3-h incubation with 10 microM ara-G, both dCK+ and dGK+ cells accumulated ara-GTP; how

23 In contrast, at 100 microM ara-G, intracellular ara-GTP accumulated to similar leve

24 ast, cells in S phase had significantly more ara-G incorporated into DNA (24 +/- 4 pmol ara-GMP/mg DN

25 The t1/2 of ara-G was shorter in pediatric patients as compared with

26 ionship between response and accumulation of ara-G triphosphate (ara-GTP) in circulating leukemia cel

27 However, the clearance of ara-G was higher in pediatric patients (0.312 L.h(-1).kg

28 d in dCK+ extracts at high concentrations of ara-G (100 microM).

29 f ara-G, allowing systemic concentrations of ara-G that result in clinical activity.

30 d the steady-state volume of distribution of ara-G were similar.

31 or lineage-specific toxicity, the effects of ara-G were compared in CEM (T-lymphoblast), Raji (B-lymp

32 minutes) was faster than the elimination of ara-G (t1/2=3.7 hours).

33 r the pharmacokinetic parameter estimates of ara-G between adult male and female patients.

34 Within 3 hours of ara-G treatment, the levels of soluble Fas ligand (sFasL

35 Hence, blocking the incorporation of ara-G monophosphate (ara-GMP) into DNA may prevent apopt

36 ptosis and accumulated the highest levels of ara-G triphosphate (ara-GTP).

37 The C(max) of ara-G ranged from 11.6 micromol/L to 308.7 micromol/L at

38 The maximum concentrations (C(max)) of ara-G occurred at or near the end of the nelarabine infu

39 tudy were to evaluate GW506U78, a prodrug of ara-G, against human hematologic malignancies and to det

40 Nelarabine is an effective prodrug of ara-G, allowing systemic concentrations of ara-G that re

41 The pharmacokinetics of nelarabine and/or ara-G were evaluated in 71 patients (25 pediatric and 46

42 Thus, both dCK and dGK can phosphorylate ara-G, but at low ara-G concentrations, dGK seems to pre

43 e cell-free system and strongly suggest that ara-G is phosphorylated by both kinases, and at low subs

44 r deoxyguanosine kinase (dGK) suggested that ara-G is a substrate for both enzymes, controversy exist

45 CEM cells were the most sensitive to ara-G-induced apoptosis and accumulated the highest leve

46 When ara-G was used as a substrate in a cell-free system, the