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1 ecan, irinotecan, etoposide and dexrazoxane (ICRF-187).
2 ic CEM cells were selected for resistance to ICRF-187.
3 cities appear to be unaffected by the use of ICRF-187.
4 ven as an intravenous bolus) with or without ICRF-187.
5 ne and complexed with the bisdioxopiperazine ICRF-187.
6 tingly, resveratrol is chemically similar to ICRF-187, a clinically approved chemotherapeutic that st
8 The ternary drug-bound complex reveals that ICRF-187 acts by an unusual mechanism of inhibition in w
10 I alpha was essential for rapid dynamics, as ICRF-187, an inhibitor of topoII alpha, blocked recovery
12 alpha in yeast cells sensitizes them to both ICRF-187 and ICRF-193, compared with cells expressing ye
14 analysis of the biochemical effects of both ICRF-187 and resveratrol on the human isoforms of topo I
15 e approximately 40- and 69-fold resistant to ICRF-187, and 12- and 67-fold cross-resistant to ICRF-19
16 ind that resveratrol indeed acts through the ICRF-187 binding locus, but that it inhibits topo II by
18 marked contrast, when treated with equitoxic ICRF-187 doses, the drug-resistant clones exhibit either
22 However, the killing caused by ICRF-193 and ICRF-187 is not enhanced by mutations in the RAD52 pathw
24 topoIIalpha transcriptional up-regulation in ICRF-187-resistant cells is mediated in part by altered
26 ptional regulation in ICRF-187-sensitive and ICRF-187-resistant human leukemic cell lines that expres
27 ed topoIIalpha transcriptional regulation in ICRF-187-sensitive and ICRF-187-resistant human leukemic
32 the short-term cardioprotection afforded by ICRF-187 will reduce the incidence of late cardiac compl
33 label, randomized trial to determine whether ICRF-187 would reduce doxorubicin-induced cardiotoxicity
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