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1 ted apoptosis by etoposide, a representative antineoplastic agent.
2 e II diabetes that has gained interest as an antineoplastic agent.
3 to improve the therapeutic efficacy of this antineoplastic agent.
4 oing Phase I clinical testing as a potential antineoplastic agent.
5 )F-FLT) in assessing its effectiveness as an antineoplastic agent.
6 rent clinical assessment of clioquinol as an antineoplastic agent.
7 n attractive candidate for development as an antineoplastic agent.
8 hibitor developed specifically for use as an antineoplastic agent.
9 door for clinical trials evaluating it as an antineoplastic agent.
10 linical information on gallium nitrate as an antineoplastic agent.
11 of IAP proteins can modulate the efficacy of antineoplastic agents.
12 ificantly increases the efficacy of existing antineoplastic agents.
13 ts that can be mitigated by encapsulation of antineoplastic agents.
14 plausible pharmacological strategy for novel antineoplastic agents.
15 e viable resources in the development of new antineoplastic agents.
16 ases as novel targets for the development of antineoplastic agents.
17 olecules targeting translation initiation as antineoplastic agents.
18 ramifications for the use of these drugs as antineoplastic agents.
19 ications of these findings for resistance to antineoplastic agents.
20 nts may have applicability as biotherapeutic antineoplastic agents.
21 signal transduction modulators as potential antineoplastic agents.
22 the development of new immunosuppressive and antineoplastic agents.
23 multiple oncoproteins may lead to effective antineoplastic agents.
24 proach for the development of new classes of antineoplastic agents.
25 e for the development of cdk2 antagonists as antineoplastic agents.
26 n cancer patients who receive these drugs as antineoplastic agents.
27 ellular targets of many structurally diverse antineoplastic agents.
28 ramide in the lethal actions of conventional antineoplastic agents.
29 on may contribute to NF-kappaB activation by antineoplastic agents.
30 ifaceted approach for the development of new antineoplastic agents.
31 l sensitivity to this promising new class of antineoplastic agents.
32 form the basis for the development of novel antineoplastic agents.
33 timal combinations of these drugs with other antineoplastic agents.
34 as mapped with respect to several classes of antineoplastic agents.
35 nique intracellular and selective target for antineoplastic agents.
36 asing their susceptibility to cycle-specific antineoplastic agents.
37 to improve performance and safety of current antineoplastic agents.
38 for designing biocompatible target specific antineoplastic agents.
39 described possible activity of quinolones as antineoplastic agents.
40 lation to cytotoxic chemotherapy or targeted antineoplastic agents.
41 iatric patients who receive high-emetic-risk antineoplastic agents.
42 resistance to paclitaxel and possibly other antineoplastic agents.
43 entify complex III as a potential target for antineoplastic agents.
44 e proposal that these ligands may be used as antineoplastic agents.
45 reast cancer cells to cytoskeletal targeting antineoplastic agents.
46 tients who are treated with high emetic risk antineoplastic agents.
47 logic utility as angiogenesis inhibitors and antineoplastic agents.
48 by current or previous treatment with other antineoplastic agents.
49 hione conjugates and several natural product antineoplastic agents.
50 ed for cancer cell apoptosis induced by many antineoplastic agents.
51 metabolism and may be a suitable target for antineoplastic agents.
52 a group, are unresponsive to treatment with antineoplastic agents.
53 l scaffold to improve the design of specific antineoplastic agents.
54 logic-based therapies are being developed as antineoplastic agents.
55 the tumor-specific activity of DNA-damaging antineoplastic agents.
58 n of cellular apoptotic responses to various antineoplastic agents, a laser-based technology, Optopho
59 tide or FK228) is a member of a new class of antineoplastic agents active in T-cell lymphoma, the his
60 bacterial, fungal, and parasitic infections, antineoplastic agents against cancer cells, and perturba
61 n continue to be treated with this important antineoplastic agent and how such retreatment might be u
62 city that are reported to be associated with antineoplastic agents and discuss their putative mechani
63 ic investigation of PPARdelta antagonists as antineoplastic agents and implicate altered PPARdelta-cy
66 , for a 1-year period, suffered reactions to antineoplastic agents and were referred to the Desensiti
67 kers has revealed many potential targets for antineoplastic agents, and a particularly important aber
68 argeting of these immunosuppressive cells by antineoplastic agents, and consider current challenges a
69 in C given before mechanistically dissimilar antineoplastic agents antagonizes therapeutic efficacy i
74 o asparaginyl residues and that DNA-damaging antineoplastic agents as well as other stimuli can incre
76 f advanced-stage NSCLC and were treated with antineoplastic agents between 2000 and 2011 (N = 22,163)
77 otic enzyme that inactivates the widely used antineoplastic agent bleomycin (BLM) and is a primary ca
79 was combined with seven of the eight tested antineoplastic agents but was highly dependent upon admi
81 pathy is a dose-limiting side effect of many antineoplastic agents, but the mechanisms underlying the
82 ate the response of an individual's tumor to antineoplastic agents, but these tumor fragments are cul
83 ion can affect the sensitivity of cancers to antineoplastic agents by altering expression of genes cr
86 e induction of a senescent-like phenotype by antineoplastic agents can contribute therapeutic efficac
87 ce or its displacement from the chromatin by antineoplastic agents caused an increase in the levels o
88 sis included young age and chemotherapy with antineoplastic agents, cefotaxime, vancomycin, and cefta
94 , CREB, SP-1, or TFIID were not activated by antineoplastic agents demonstrating specificity of NF-ka
95 ast, docetaxel (Taxotere), a closely related antineoplastic agent, did not activate SXR and displayed
96 novel procedure to couple enzymatically the antineoplastic agent doxorubicin (Dox) on the galactose
99 xel (Taxol) is a potent and highly effective antineoplastic agent for the treatment of advanced, drug
101 port the clinical development of CV890 as an antineoplastic agent for the treatment of localized or m
103 structurally diverse hydrophobic amphipathic antineoplastic agents from cells, with different mechani
106 activity of multiple widely used classes of antineoplastic agents, human cancer cell lines were trea
107 , a PP2A inhibitor which has been used as an antineoplastic agent in clinical trials, is also able to
108 th RXR-selective ligand may thus be a useful antineoplastic agent in differentiation induction therap
109 275) has been identified recently as a novel antineoplastic agent in the primary screen conducted by
111 e inhibitor to undergo clinical trials as an antineoplastic agent in the United States, has attracted
113 from combining flavopiridol with eight other antineoplastic agents in four different administration s
114 d consider how to combine antiretroviral and antineoplastic agents in patients with HIV who are recei
116 ggest that As(2)O(3) and AA may be effective antineoplastic agents in refractory MM and that AA might
118 d in B cell lymphomas by anti-Fas or various antineoplastic agents in the presence and absence of FDC
119 ng term antiproliferative effects of diverse antineoplastic agents including paclitaxel, etoposide, 7
120 d resistant (MCF-7/Adr-, T47D, and SKBr3) to antineoplastic agents, incubation with the sigma-2 subty
122 paullones, a dual property observed in other antineoplastic agents influencing phosphoester transfer.
127 inical use of doxorubicin, widely used as an antineoplastic agent, is markedly hampered by severe car
128 ed the sensitivity of these cells to several antineoplastic agents known to be cell cycle-dependent o
129 tial for increased exposure of the tumour to antineoplastic agents leading to improved cytotoxicity.
131 the side effects of cisplatin, a widely used antineoplastic agent, major efforts have been made to de
132 storically, it has been well recognized that antineoplastic agents may have adverse effects on multip
133 idoreductase 1 (NQO1) on the activity of the antineoplastic agent mitomycin C (MC) under aerobic and
134 as osteosarcoma, for preclinical testing of antineoplastic agents offers significant advantages over
135 xic effect of ET-743 combined with six other antineoplastic agents on human breast cancer cell lines,
136 ated the effect of bryostatin-1 (Bryo-1), an antineoplastic agent, on dendritic cell (DC) maturation,
137 antiemetic regimens that are appropriate for antineoplastic agents or radiotherapy being administered
138 mens for adults who receive high-emetic-risk antineoplastic agents or who experience breakthrough nau
139 apeutic tool for hypersensitivity to several antineoplastic agents (oxaliplatin, carboplatin, paclita
141 consist of topo I-targeting agents and other antineoplastic agents, particularly DNA-damaging agents.
143 ne compound previously used clinically as an antineoplastic agent potentiates the presynaptic functio
144 edules and combining temozolomide with other antineoplastic agents, radiation therapy, or drug resist
146 menting the transvascular delivery of larger antineoplastic agents such as gene targeting vectors and
147 F ablation augments the delivery of systemic antineoplastic agents such as liposomal doxorubicin.
155 Bryostatin-1, a macrocyclic lactone, is an antineoplastic agent that potently activates protein kin
157 tment with paclitaxel (trade name Taxol), an antineoplastic agent that stabilizes cellular microtubul
159 raf-1 kinase may be of considerable value as antineoplastic agents that display activity against a wi
162 thesis that flavopiridol, like several other antineoplastic agents that kill noncycling cells, might
163 at can enhance the efficacy of biguanides as antineoplastic agents that target cancer cell energy met
164 rease in apoptosis in cells treated with the antineoplastic agents that was not due to up-regulation
165 n deazapurines as antibiotic, antiviral, and antineoplastic agents, the biosynthetic route toward dea
166 ew the development of successful preclinical antineoplastic agents, their associated limitations, and
167 zymatically mediated, glycosidic coupling of antineoplastic agents to antibodies specific for tumor-a
170 of the interaction between ET-743 and other antineoplastic agents using the combination index method
172 a desensitization to cell cycle-independent antineoplastic agents was found in the cells arrested by
173 increased resistance to cell cycle-dependent antineoplastic agents was found in the cells when the ex
174 apy, 51 candidate genes from the pathways of antineoplastic agents were resequenced to identify commo
177 is likely that interest in CDK inhibitors as antineoplastic agents will continue for the foreseeable
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