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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
7                                      Second, ICRF-187, a Top2 catalytic inhibitor known to deplete To
8  The ternary drug-bound complex reveals that ICRF-187 acts by an unusual mechanism of inhibition in w
9                 Dexrazoxane [(DZR), ADR 529, ICRF-187] ameliorates doxorubicin (DOX)-induced cardioto
10 I alpha was essential for rapid dynamics, as ICRF-187, an inhibitor of topoII alpha, blocked recovery
11                  We examined cell killing by ICRF-187 and ICRF-193 in yeast cells expressing human to
12 alpha in yeast cells sensitizes them to both ICRF-187 and ICRF-193, compared with cells expressing ye
13 amaging catalytic Topo II inhibitors such as ICRF-187 and merbarone do not do this.
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
17               The topo II-specific inhibitor ICRF-187 blocks this effect, indicating that it is cause
18 marked contrast, when treated with equitoxic ICRF-187 doses, the drug-resistant clones exhibit either
19         Dexrazoxane (Zinecard, also known as ICRF-187) has been used in the clinic as a cardioprotect
20                    In summary, resistance to ICRF-187 in CEM cells is associated with increased level
21                                              ICRF-187 is a bisdioxopiperazine anticancer drug that in
22  However, the killing caused by ICRF-193 and ICRF-187 is not enhanced by mutations in the RAD52 pathw
23                                              ICRF-187 reduces the risk of developing short-term subcl
24 topoIIalpha transcriptional up-regulation in ICRF-187-resistant cells is mediated in part by altered
25                                          The ICRF-187-resistant clones contain approximately 5-fold i
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
28     Finally, the catalytic Topo II inhibitor ICRF-187 suppressed VM-26-induced-FasL expression.
29                                     Eighteen ICRF-187-treated and 15 control patients were assessable
30                                              ICRF-187-treated patients had a significantly higher inc
31                                              ICRF-187-treated patients were less likely to develop su
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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