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1 al one-pot synthesis of indenoisoquinolines (topoisomerase I inhibitors).
2 ant after treatment with camptothecin, a DNA topoisomerase I inhibitor.
3 its nonthreading counterparts and was not a topoisomerase I inhibitor.
4 t after treatment with topotecan, a specific topoisomerase I inhibitor.
5 s from apoptosis mediated by camptothecin, a topoisomerase I inhibitor.
6 nsitivity to camptothecin, an antineoplastic topoisomerase I inhibitor.
7 the design of future clinical trials of this topoisomerase I inhibitor.
8 Moreover, they acted as topoisomerase I inhibitors.
9 myosin VI transcript were decreased only by topoisomerase I inhibitors.
10 as a strategy for enhancing the efficacy of topoisomerase I inhibitors.
11 AGT inhibitors or O6-alkylating agents with topoisomerase I inhibitors.
12 a novel class of cytotoxic non-camptothecin topoisomerase I inhibitors.
13 glucuronidation in de novo resistance to two topoisomerase I inhibitors.
14 checkpoint also enhanced the cytotoxicity of topoisomerase I inhibitors.
15 1-dihydro-6H-indolo[3,2-c]quinolin-6-ones as topoisomerase-I inhibitors.
17 RC stress response was also activated by the topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin
18 ed prodrug irinotecan (CPT-11) to the potent topoisomerase I inhibitor 7-ethyl-10-hydroxycamptothecin
19 latform, the effect of an apoptotic inducer, topoisomerase I inhibitor, 7-ethyl-10-hydrocamptothecin
22 he previously synthesized indenoisoquinoline topoisomerase I inhibitors, a series of compounds lackin
23 circadian toxicity patterns of irinotecan, a topoisomerase I inhibitor active against colorectal canc
24 ]isoquinoline hydrochloride (14) is a strong topoisomerase I inhibitor and also displays very high cy
26 applied to the total synthesis of a reported topoisomerase I inhibitor and to the formal synthesis of
27 53-independent channel of cross-talk between topoisomerase I inhibitors and Apo2L/TRAIL and suggest t
28 rtical neurons from mice, we identify twelve topoisomerase I inhibitors and four topoisomerase II inh
29 ibitor of topoisomerase II), camptothecin (a topoisomerase I inhibitor), and ultraviolet radiation in
32 s, which indicates that these two classes of topoisomerase I inhibitors are likely to target the canc
33 olar concentrations of camptothecin (CPT), a topoisomerase I inhibitor, arrest or delay cell cycle pr
34 hydrogen-bonding interactions in determining topoisomerase I inhibitor binding in the ternary cleavag
38 nd PRC2 exhibit synthetic sensitivity to the topoisomerase I inhibitor Camptothecin and accumulate ga
40 acilitate the cytotoxic effectiveness of the topoisomerase I inhibitor camptothecin in the killing of
41 h clinically-relevant nanomolar doses of the Topoisomerase I inhibitor camptothecin, loss of WRN exon
42 HCT116 human carcinoma cells exposed to the topoisomerase I inhibitor camptothecin, the resulting ga
43 ries, Abbott Park, IL), and the DNA-damaging topoisomerase I inhibitor camptothecin-11 (CPT-11) or SN
46 , we identified DC-stimulatory potentials of topoisomerase I inhibitors (camptothecin derivatives) an
48 rylated within 1 h after addition of the DNA topoisomerase I inhibitor, camptothecin, and that lamin
51 rationale for combining PARP inhibitors with topoisomerase I inhibitors, clinical use has been hinder
52 erent mass spectrometers: an example using a topoisomerase I inhibitor-conjugated ADC (SCIEX ZenoTOF
55 hypothesized that integrating tumor-targeted topoisomerase I inhibitor delivery with optimized PARP i
56 l studies suggest that prolonged infusion of topoisomerase I inhibitors enhances cell toxicity due to
60 to determine the antitumor activity of this topoisomerase I inhibitor in 53 patients with metastatic
61 plays a predominant role in the response to topoisomerase I inhibitors in carcinoma cells and identi
63 rgistic with low picomolar concentrations of topoisomerase I inhibitors in improving survival in vivo
64 optotic factors may increase the efficacy of topoisomerase I inhibitors in the clinical setting if gi
66 storation of RAD51 foci in mutant cells when Topoisomerase I inhibitor-induced single strand breaks a
70 he biological activity of indenoisoquinoline topoisomerase I inhibitors is significantly enhanced by
71 a liposomal formulation of the water-soluble topoisomerase I inhibitor lurtotecan (GI147211), which d
73 eath or apoptosis, we studied campothecin (a topoisomerase I inhibitor)-mediated apoptosis in the hum
76 ne, camptothecin-derived and indolocarbazole topoisomerase I inhibitors, methotrexate, flavopiridol,
78 expression changes elicited by camptothecin (topoisomerase I inhibitor) or adriamycin (topoisomerase
79 antibody (patritumab) covalently linked to a topoisomerase I inhibitor payload via a stable, tumor-se
80 consisting of a HER3 antibody attached to a topoisomerase I inhibitor payload via a tetrapeptide-bas
81 cted cysteine-conjugated ADC bearing a novel topoisomerase I inhibitor payload, with durable DAR, cur
85 njugate of humanised anti-HER2 antibody with topoisomerase I inhibitor payloads) in patients with HER
87 iated with POLE mutations and corresponds to topoisomerase I inhibitor resistance, which can be overc
88 amage induced by chemotherapy drugs, such as topoisomerase I inhibitors, results in S and G2 phase ar
89 In vitro data indicate that the addition of topoisomerase I inhibitors shortly after irradiation cau
90 assembly induced by the clinically relevant topoisomerase I inhibitor SN-38, thereby inhibiting the
92 ncer drug, and it is a prodrug of the potent topoisomerase I inhibitor, SN-38 (7-ethyl-10-hydroxycamp
96 t requires the p53 tumor suppressor, yet the topoisomerase I inhibitor SN38 induces p53 after the G(1
97 arrest and enhanced the cytotoxicity of the topoisomerase I inhibitor SN38 only in p53-defective cel
98 efficacy of DNA-damaging agents, such as the topoisomerase I inhibitor SN38, is often compromised by
99 p synthesis of a series of clinically active topoisomerase I inhibitors such as NSC 314622, LMP-400,
101 ) mice are hypersensitive to camptothecin, a topoisomerase I inhibitor that causes DNA damage primari
102 anticancer agent camptothecin (CPT) is a DNA topoisomerase I inhibitor that causes fork collapse and
104 isoquinolines are a class of noncamptothecin topoisomerase I inhibitors that display significant cyto
105 indenoisoquinolines are a class of cytotoxic topoisomerase I inhibitors that offer certain advantages
107 ajority of breast cancers, coupled to SN-38 (topoisomerase I inhibitor) through a proprietary hydroly
108 s synthesized by conjugating camptothecin, a topoisomerase I inhibitor, to our proprietary, 'clickabl
109 egumain-cleavable ADCs that release a potent topoisomerase-I inhibitor (TOP1i) without the need for a
110 reported that combining (131)I-MIBG with the topoisomerase I inhibitor topotecan induced long-term DN
111 A damage induced by gamma-irradiation or the topoisomerase I inhibitor topotecan was used to induce G
114 f bcl-2 family members on the ability of the topoisomerase I inhibitor, topotecan (TPT), to induce pr
115 raction of a PARP inhibitor, ABT-888, with a topoisomerase I inhibitor, topotecan, in PBMCs, tumor, a
117 n the present studies, an indenoisoquinoline topoisomerase I inhibitor was conjugated to DUPA via a p
120 ,2-c]isoquinolines are an important class of topoisomerase I inhibitors with anticancer activity.
121 an pegol (NKTR-102) is a unique, long-acting topoisomerase-I inhibitor with prolonged systemic exposu
122 769962), we combined CRLX101, a nanoparticle topoisomerase I inhibitor, with olaparib using a gapped