ライフサイエンスコーパス: amsacrine

1 ant to the cytotoxic effects of etoposide or amsacrine.

2 itive to the topoisomerase II-targeting drug amsacrine.

3 agents, including etoposide, adriamycin, and amsacrine.

4 ntitatively unique pattern of sensitivity to amsacrine.

5 II isoforms, alpha and beta, are targeted by amsacrine.

6 randomized study compared the combination of amsacrine (100 mg/m2/d on days 1 to 5) and etoposide (20

7 plus cytarabine (12 g/m(2)) and one cycle of amsacrine (500 mg/m(2)) plus cytarabine (10 g/m(2); MAC/

8 itive top2 mutants resistant to etoposide or amsacrine also confer resistance to DMP-840.

9 atients given ara-C with either doxorubicin, amsacrine (AMSA), or daunorubicin without ATRA, using lo

10 toposide, and azatoxin and the intercalators amsacrine and mitoxantrone.

11 lamino)-3-methoxyphenyl]methane-sulfonamide (amsacrine) and single-stranded DNA showed that the two a

12 g topo II inhibitors, etoposide, teniposide, amsacrine, and doxorubicin, but not to other catalytic i

13 somerase II inhibitors, such as etoposide, m-amsacrine, and doxorubicin.

14 otherapeutic drugs (etoposide, mitoxantrone, amsacrine, and ellipticine).

15 ge sites in the presence of VP-16, azatoxin, amsacrine, and mitoxantrone.

16 e randomly assigned to a third course, MACE (amsacrine, Ara-C, and etoposide), plus a fourth course o

17 signed to GO in course 3 in combination with amsacrine, cytarabine, and etoposide or high-dose cytara

18 and idarubicin (FLAG-Ida; n = 1268), and to amsacrine, cytarabine, etoposide, and then mitoxantrone/

19 hat is, idarubicine-cytarabine (cycle I) and amsacrine-cytarabine (cycle II) without or with clofarab

20 a sequential transplant regimen, fludarabine/amsacrine/cytarabine-busulphan (FLAMSA-Bu), but the impa

21 the addition of azacitidine to etoposide and amsacrine did not improve response.

22 The intercalative drugs amsacrine, ellipticine, and daunorubicin inhibited NaeI-

23 conferred cellular resistance to CP-115,953, amsacrine, etoposide, and ellipticine.

24 rial quinolone) on the ability of etoposide, amsacrine, genistein, and the antineoplastic quinolone,

25 ateau-phase cells, aprt mutations induced by amsacrine in both log-phase and plateau-phase CHO cells

26 tiagent consolidation using mitoxantrone and amsacrine in combination with high-dose cytarabine does

27 7 x 10(-6) after treatment with 0.02 microM amsacrine in log phase and 27 x 10(-6) after treatment w

28 nd 27 x 10(-6) after treatment with 1 microM amsacrine in plateau phase, compared with a spontaneous

29 es in DNA treated with topoisomerase II plus amsacrine in vitro.

30 , presence of trisomy 21, and treatment with amsacrine increase the risk for anthracycline-associated

31 itivity of HL-60/S or HL-60/DOX0.05 cells to amsacrine may be due to the preferential interaction and

32 ce of trisomy 21 (RR = 3.4), and exposure to amsacrine (RR = 2.6).

33 n both parental sequences were hot spots for amsacrine-stimulated DNA cleavage in vitro, and the nove

34 more, anticancer drugs such as etoposide and amsacrine that strongly inhibit topoisomerase II-mediate

35 ry D422 cells by the topoisomerase II poison amsacrine, there was a reciprocal exchange between the a

36 th drug for 1 h revealed that mole-for-mole, amsacrine was 2-fold more effective than etoposide in ki