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1 totoxic agents (antimicrotubule agents and a topoisomerase inhibitor).
2 poside and, unlike podophyllotoxin, a potent topoisomerase inhibitor.
3  hypersensitivity of USP37 knockout cells to topoisomerase inhibitors.
4 n opportunity to identify additional natural topoisomerase inhibitors.
5 othetically potentiate the cytotoxicities of topoisomerase inhibitors.
6 tigated toxicological issues often seen with topoisomerase inhibitors.
7 sitivity to alkylating anticancer agents and topoisomerase inhibitors.
8 esses, including ionizing radiation (IR) and topoisomerase inhibitors.
9 ed RAMS11 expression increases resistance to topoisomerase inhibitors.
10 d SLFN11 expression predicted sensitivity to topoisomerase inhibitors.
11 vation in response to ionizing radiation and topoisomerase inhibitors.
12 e of further expanding the chemical space of topoisomerase inhibitors.
13 ic stress through a different mechanism than topoisomerase inhibitors.
14  paves the way for future studies of various topoisomerase inhibitors.
15  high susceptibility to DNA damage caused by topoisomerase inhibitors.
16 ukemogenesis of thiopurines, with or without topoisomerase inhibitors.
17 nsensitive to five other previously reported topoisomerase inhibitors.
18 ffect DNA metabolism, such as irradiation or topoisomerase inhibitors.
19  of triple-negative breast cancer cells with topoisomerase inhibitors activates DNA damage response p
20 etables, which sensitizes leukaemia cells to topoisomerase inhibitor agents (e.g., etoposide), and al
21 th potent biological activity, including the topoisomerase inhibitor and chemotherapeutic etoposide.
22 s that can repair damaged DNA resulting from topoisomerase inhibitors and a variety of other DNA-dama
23 of DNA-damaging agents such as temozolomide, topoisomerase inhibitors and radiation in both in vitro
24 ity of several predicted compounds including topoisomerase inhibitors and resveratrol towards breast
25 or maximal induction of apoptosis, including topoisomerase inhibitors and TRAIL.
26 lung cancer cells are largely insensitive to topoisomerase inhibitors, and depletion of PKCdelta can
27 -Ras-independent cells are more sensitive to topoisomerase inhibitors, and depletion of PKCdelta in t
28 mulin, a pleuromutilin, and new nonquinolone topoisomerase inhibitors are attractive possibilities th
29         A number of therapeutically relevant topoisomerase inhibitors are bacterial natural products.
30                                              Topoisomerase inhibitors are important and clinically ef
31                                              Topoisomerase inhibitors are in common use as chemothera
32                                      Type II topoisomerase inhibitors are used to treat both tumors a
33 a modified anthraquinone that functions as a topoisomerase inhibitor as well as an alkylating agent.
34  of small-molecule inhibitors, we identified topoisomerase inhibitors as a class of drugs that enhanc
35 alpha]anthracene (mutagen) and camptothecin (topoisomerase inhibitor), as well as to agents targeting
36 maging agents such as ionizing radiation and topoisomerase inhibitors, but also enhances the toxicity
37 t (HT) analysis is desirable to identify new topoisomerase inhibitors, but standard in vitro assays f
38 cle profiles observed in the potentiation of topoisomerase inhibitors by Chk1 siRNA, which showed mit
39 cent transcription in cells treated with the topoisomerase inhibitor camptothecin (CPT).
40 quitinating FANCD2 and were sensitive to the topoisomerase inhibitor camptothecin, a feature shared o
41              In human cells treated with the topoisomerase inhibitors camptothecin or etoposide (VP-1
42  histiocytic lymphoma cell line U937 and the topoisomerase inhibitors camptothecin, etoposide, and do
43                         We previously showed topoisomerase inhibitors can reactivate paternal UBE3A,
44 such as fluoroquinolones and novel bacterial topoisomerase inhibitors, can trap DNA cleavage complexe
45 antly, we demonstrate that DNA damage drugs, topoisomerase inhibitors, can trigger CKI activation to
46                        One, sensitive to the topoisomerase inhibitor ciprofloxacin, appears to initia
47 utants to ETX0914 cross-resistant with other topoisomerase inhibitor classes, including the widely us
48 amptothecin and doxorubicin, two widely used topoisomerase inhibitors conferring S and G2 arrest, res
49                                    Bacterial topoisomerase inhibitors continue to be actively develop
50        Overall, recent clinical trials using topoisomerase inhibitors coupled with our findings of RA
51                     We find that S-phase and topoisomerase inhibitors delay both the initiation and t
52 ation of myosin VI in various tumor cells by topoisomerase inhibitors dictates whether knockdown of m
53           A novel class of bacterial type-II topoisomerase inhibitor displaying a spiropyrimidinetrio
54 rate and are significantly more sensitive to topoisomerase inhibitors (especially camptothecin) than
55 ing agents, e.g., cisplatin, and also to DNA topoisomerase inhibitor etoposide (ETO) than A2780.
56                  Although treatment with the topoisomerase inhibitor etoposide dramatically enhanced
57 te in mouse liver by up to 900-fold, and the topoisomerase inhibitor etoposide increased transduction
58 e G(2) arrest that occurs in response to the topoisomerase inhibitors etoposide and merbarone.
59  human breast carcinoma cells exposed to the topoisomerase inhibitor, etoposide.
60 ic semiconductors from deoxyribonucleic acid topoisomerase inhibitors, featuring conjugated backbone
61                   Screens for new classes of topoisomerase inhibitors generally employ methods, such
62               Clinically, a large arsenal of topoisomerase inhibitors has been used to suppress DNA r
63                                     However, topoisomerase inhibitors have little or no antineoplasti
64                              Combinations of topoisomerase inhibitors I and II have been found to syn
65      GSK2140944 is a novel bacterial type II topoisomerase inhibitor in development for the treatment
66 ls more susceptible to cell death induced by topoisomerase inhibitors in an oncology drug screening a
67 , two combinations using a DNA alkylating or topoisomerase inhibitors in combination with an ataxia t
68 crosslinker) and camptothecin (CPT, a type 1 topoisomerase inhibitor) in FANCB-defective cells.
69         We report that DNA damage induced by topoisomerase inhibitors, including etoposide (ETO), res
70                               Interestingly, topoisomerase inhibitors, including topotecan, were rece
71 frequency and sensitivity to UV radiation or topoisomerase inhibitors is unaltered.
72 eutic efficacy of irinotecan (CPT-11), a DNA topoisomerase inhibitor, is often limited by the inducti
73  the toxicity of a parenterally administered topoisomerase inhibitor, it enhanced the activity of dox
74                                 Topotecan, a topoisomerase inhibitor, killed both hair cells and prol
75      Thus, the cytotoxicity of this class of topoisomerase inhibitors likely results from a two-step
76 eing well-characterized DNA-damaging agents, topoisomerase inhibitors may evoke a biological response
77 enetically engineered oncolytic reovirus and topoisomerase inhibitors may provide a potent therapeuti
78 326A mutant cells were modestly sensitive to topoisomerase inhibitors, mice expressing Ctip-S326A pol
79 or low KRT18-expressing HNSCC cases, and the topoisomerase inhibitor mitoxantrone, for IL6R-activated
80 ated by forward genetics in combination with topoisomerase inhibitors more efficiently infect and kil
81                   BWC0977, a Novel Bacterial Topoisomerase Inhibitor (NBTI) selectively inhibits bact
82                              Novel bacterial topoisomerase inhibitors (NBTIs) are among the most prom
83                              Novel bacterial topoisomerase inhibitors (NBTIs) provide a new strategy
84                          The novel bacterial topoisomerase inhibitors (NBTIs) represent one of the ne
85                      Novel bacterial type II topoisomerase inhibitors (NBTIs) stabilize single-strand
86 type II inhibitors known as "novel bacterial topoisomerase inhibitors", NBTIs.
87 nd, DeltatopB cells treated with the type II topoisomerase inhibitor novobiocin displayed aberrant ch
88 protein family, we studied the effect of the topoisomerase inhibitors on NaeI-L43K activity.
89  cells to be more sensitive to type I and II topoisomerase inhibitors, Raf inhibitors, and other drug
90                                   Therefore, topoisomerase inhibitors regulate SAMHD1 and HIV permiss
91 h its dual action as an alkylating agent and topoisomerase inhibitor, represents a novel anti-cancer
92 p-2) antibody-drug conjugate linked with the topoisomerase-inhibitor SN-38, over single-agent chemoth
93  and light were required to release a potent topoisomerase inhibitor, SN38.
94 inhibition of Chk1 sensitizes tumor cells to topoisomerase inhibitors such as camptothecin and doxoru
95                                     Although topoisomerase inhibitors, such as camptothecin and topot
96                           Bacterial type IIA topoisomerase inhibitors, such as fluoroquinolones and n
97 , and chemical synthesis to produce the dual topoisomerase inhibitor tapcin.
98 , we show that Mitoxantrone, an FDA-approved topoisomerase inhibitor, targets a heparan sulfate-spike
99 res of an antiprotozoal agent and the potent topoisomerase inhibitor Tas-103.
100 ncer cells to treatment with camptothecin, a topoisomerase inhibitor that induces DNA double-strand b
101 not hypersensitive to camptothecin, a type-1 topoisomerase inhibitor that induces DSBs at replication
102                                    Bacterial topoisomerase inhibitors that are built on a tetrahydrop
103  Because WRN syndrome cells are sensitive to topoisomerase inhibitors, these observations suggest tha
104                                     By using topoisomerase inhibitors to alter the balance between su
105 e and temporally limited use of etoposide, a topoisomerase inhibitor, to eliminate encephalitogenic T
106 tization of cancer cells to the FDA-approved topoisomerase inhibitors topotecan and irinotecan.
107                                         Some topoisomerase inhibitors trap covalent topoisomerase-DNA
108 loss of BAK1 exhibit an inferior response to topoisomerase inhibitor treatment in the clinic.
109 , DNA damage caused by ionizing radiation or topoisomerase inhibitors triggered DNA-PK-dependent phos
110 ce 7-ethyl-10-hydroxycamptothecin (SN-38), a topoisomerase inhibitor used in cancer therapy.
111 optosis induced by imatinib mesylate and the topoisomerase inhibitor VP-16 in LAMA-R cells.
112                 Organisms resistant to other topoisomerase inhibitors were not cross-resistant with E
113 response to the perturbations of topology by topoisomerase inhibitors, whereas human cells do not.
114     One of them is microcin B17, a bacterial topoisomerase inhibitor whose activity depends on the co
115    The peptide antibiotic albicidin is a DNA topoisomerase inhibitor with low-nanomolar bactericidal
116                 This defines novel bacterial topoisomerase inhibitors with promising antibacterial ac

 
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