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1 ant after treatment with camptothecin, a DNA topoisomerase I inhibitor.
2 its nonthreading counterparts and was not a topoisomerase I inhibitor.
3 t after treatment with topotecan, a specific topoisomerase I inhibitor.
4 s from apoptosis mediated by camptothecin, a topoisomerase I inhibitor.
5 nsitivity to camptothecin, an antineoplastic topoisomerase I inhibitor.
6 the design of future clinical trials of this topoisomerase I inhibitor.
7 Moreover, they acted as topoisomerase I inhibitors.
8 myosin VI transcript were decreased only by topoisomerase I inhibitors.
9 as a strategy for enhancing the efficacy of topoisomerase I inhibitors.
10 AGT inhibitors or O6-alkylating agents with topoisomerase I inhibitors.
11 a novel class of cytotoxic non-camptothecin topoisomerase I inhibitors.
12 glucuronidation in de novo resistance to two topoisomerase I inhibitors.
13 checkpoint also enhanced the cytotoxicity of topoisomerase I inhibitors.
15 RC stress response was also activated by the topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin
16 ed prodrug irinotecan (CPT-11) to the potent topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin
19 he previously synthesized indenoisoquinoline topoisomerase I inhibitors, a series of compounds lackin
20 circadian toxicity patterns of irinotecan, a topoisomerase I inhibitor active against colorectal canc
21 ]isoquinoline hydrochloride (14) is a strong topoisomerase I inhibitor and also displays very high cy
22 53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest t
23 rtical neurons from mice, we identify twelve topoisomerase I inhibitors and four topoisomerase II inh
24 ibitor of topoisomerase II), camptothecin (a topoisomerase I inhibitor), and ultraviolet radiation in
27 s, which indicates that these two classes of topoisomerase I inhibitors are likely to target the canc
28 olar concentrations of camptothecin (CPT), a topoisomerase I inhibitor, arrest or delay cell cycle pr
29 hydrogen-bonding interactions in determining topoisomerase I inhibitor binding in the ternary cleavag
33 nd PRC2 exhibit synthetic sensitivity to the topoisomerase I inhibitor Camptothecin and accumulate ga
35 acilitate the cytotoxic effectiveness of the topoisomerase I inhibitor camptothecin in the killing of
36 HCT116 human carcinoma cells exposed to the topoisomerase I inhibitor camptothecin, the resulting ga
37 ries, Abbott Park, IL), and the DNA-damaging topoisomerase I inhibitor camptothecin-11 (CPT-11) or SN
40 , we identified DC-stimulatory potentials of topoisomerase I inhibitors (camptothecin derivatives) an
42 rylated within 1 h after addition of the DNA topoisomerase I inhibitor, camptothecin, and that lamin
47 l studies suggest that prolonged infusion of topoisomerase I inhibitors enhances cell toxicity due to
51 to determine the antitumor activity of this topoisomerase I inhibitor in 53 patients with metastatic
52 plays a predominant role in the response to topoisomerase I inhibitors in carcinoma cells and identi
53 optotic factors may increase the efficacy of topoisomerase I inhibitors in the clinical setting if gi
57 he biological activity of indenoisoquinoline topoisomerase I inhibitors is significantly enhanced by
58 a liposomal formulation of the water-soluble topoisomerase I inhibitor lurtotecan (GI147211), which d
60 eath or apoptosis, we studied campothecin (a topoisomerase I inhibitor)-mediated apoptosis in the hum
63 ne, camptothecin-derived and indolocarbazole topoisomerase I inhibitors, methotrexate, flavopiridol,
65 expression changes elicited by camptothecin (topoisomerase I inhibitor) or adriamycin (topoisomerase
67 In vitro data indicate that the addition of topoisomerase I inhibitors shortly after irradiation cau
69 ncer drug, and it is a prodrug of the potent topoisomerase I inhibitor, SN-38 (7-ethyl-10-hydroxycamp
73 t requires the p53 tumor suppressor, yet the topoisomerase I inhibitor SN38 induces p53 after the G(1
74 arrest and enhanced the cytotoxicity of the topoisomerase I inhibitor SN38 only in p53-defective cel
75 p synthesis of a series of clinically active topoisomerase I inhibitors such as NSC 314622, LMP-400,
76 ) mice are hypersensitive to camptothecin, a topoisomerase I inhibitor that causes DNA damage primari
77 anticancer agent camptothecin (CPT) is a DNA topoisomerase I inhibitor that causes fork collapse and
79 isoquinolines are a class of noncamptothecin topoisomerase I inhibitors that display significant cyto
80 indenoisoquinolines are a class of cytotoxic topoisomerase I inhibitors that offer certain advantages
82 reported that combining (131)I-MIBG with the topoisomerase I inhibitor topotecan induced long-term DN
83 A damage induced by gamma-irradiation or the topoisomerase I inhibitor topotecan was used to induce G
85 f bcl-2 family members on the ability of the topoisomerase I inhibitor, topotecan (TPT), to induce pr
86 raction of a PARP inhibitor, ABT-888, with a topoisomerase I inhibitor, topotecan, in PBMCs, tumor, a
87 n the present studies, an indenoisoquinoline topoisomerase I inhibitor was conjugated to DUPA via a p
90 ,2-c]isoquinolines are an important class of topoisomerase I inhibitors with anticancer activity.
91 an pegol (NKTR-102) is a unique, long-acting topoisomerase-I inhibitor with prolonged systemic exposu
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