ライフサイエンスコーパス: ara-GTP

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1 ara-G, both dCK+ and dGK+ cells accumulated ara-GTP; however, the levels were significantly (P = 0.0

2 etween the peak fludarabine triphosphate and ara-GTP in each patient (r = 0.85).

3 Determination of tumor cell ara-GTP levels may provide a predictive test for respons

4 evaluate biochemical modulation of cellular ara-GTP metabolism by fludarabine triphosphate.

5 h the accumulation of the triphosphate form (ara-GTP).

6 These results demonstrate that high ara-GTP accumulation in T cells results in an S phase-de

7 contrast, at 100 microM ara-G, intracellular ara-GTP accumulated to similar levels (P = 0.5529) in th

8 presence of cytotoxic level of intracellular ara-GTP.

9 he G1-S boundary accumulated 75 +/- 7 microM ara-GTP with minimal incorporation into DNA (5 +/- 2 pmo

10 Intracellular accumulation of ara-GTP was neither cell cycle dependent nor affected by

11 cological differences in the accumulation of ara-GTP.

12 Blocking of ara-GTP incorporation into S-phase DNA abolished biochem

13 NA), although the cytosolic concentration of ara-GTP (85 +/- 7 microM) was similar to that in the G1-

14 Median peak concentrations of ara-GTP were 23, 42, 85, and 93 micromol/L at 20, 30, 40

15 median peak intracellular concentrations of ara-GTP were significantly different (P = .0003) between

16 median peak intracellular concentrations of ara-GTP were significantly different (P =.001) in respon

17 Determination of ara-GTP levels in the target tumor population may provid

18 groups of diagnoses, and the elimination of ara-GTP from leukemia cells was slow (median, > 24 hours

19 The cellular elimination of ara-GTP was slow (median, 35 hours; range, 18 to > 48 ho

20 e data demonstrate that the incorporation of ara-GTP into DNA is the critical event that mediates the

21 hological changes), and the incorporation of ara-GTP into DNA resulted in a >95% inhibition of DNA sy

22 ted significantly (P=.0005) higher levels of ara-GTP (median, 157 micromol/L) compared with patients

23 loid and B cells accumulated lower levels of ara-GTP and arrested in S phase, blocking any apoptotic

24 The pharmacokinetics of ara-GTP in leukemia cells are strongly correlated with c

25 The ratio of ara-GTP to its normal counterpart, deoxyguanosine tripho

26 The ara-GTP elimination was slow in all diagnoses (median, >

27 b-d-arabinofuranosylguanine, is converted to ara-GTP in T lymphoblasts.

28 higher peak arabinsylguanosine triphosphate (ara-GTP) (median, 140 micromol/L; n=7) compared with oth

29 onse and accumulation of ara-G triphosphate (ara-GTP) in circulating leukemia cells and to evaluate b

30 kemia, but how ara-G and ara-G triphosphate (ara-GTP) kill cells is not known.

31 (ara-G) and of cellular ara-G triphosphate (ara-GTP) were similar in the two groups of diagnoses, an

32 n leukemic cells to form ara-G triphosphate (ara-GTP), which acts to terminate DNA chain elongation,

33 ed the highest levels of ara-G triphosphate (ara-GTP).

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