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1 ted apoptosis by etoposide, a representative antineoplastic agent.
2 to improve the therapeutic efficacy of this antineoplastic agent.
3 oing Phase I clinical testing as a potential antineoplastic agent.
4 ed to sensitize these cancer cells toward an antineoplastic agent.
5 as significant data supporting its use as an antineoplastic agent.
6 e II diabetes that has gained interest as an antineoplastic agent.
7 )F-FLT) in assessing its effectiveness as an antineoplastic agent.
8 rent clinical assessment of clioquinol as an antineoplastic agent.
9 n attractive candidate for development as an antineoplastic agent.
10 hibitor developed specifically for use as an antineoplastic agent.
11 door for clinical trials evaluating it as an antineoplastic agent.
12 linical information on gallium nitrate as an antineoplastic agent.
13 the tumor-specific activity of DNA-damaging antineoplastic agents.
14 of IAP proteins can modulate the efficacy of antineoplastic agents.
15 ificantly increases the efficacy of existing antineoplastic agents.
16 ts that can be mitigated by encapsulation of antineoplastic agents.
17 plausible pharmacological strategy for novel antineoplastic agents.
18 e viable resources in the development of new antineoplastic agents.
19 ases as novel targets for the development of antineoplastic agents.
20 iatric patients who receive high-emetic-risk antineoplastic agents.
21 ramifications for the use of these drugs as antineoplastic agents.
22 ications of these findings for resistance to antineoplastic agents.
23 nts may have applicability as biotherapeutic antineoplastic agents.
24 signal transduction modulators as potential antineoplastic agents.
25 tients who are treated with high emetic risk antineoplastic agents.
26 the development of new immunosuppressive and antineoplastic agents.
27 proach for the development of new classes of antineoplastic agents.
28 e for the development of cdk2 antagonists as antineoplastic agents.
29 n cancer patients who receive these drugs as antineoplastic agents.
30 ellular targets of many structurally diverse antineoplastic agents.
31 ramide in the lethal actions of conventional antineoplastic agents.
32 on may contribute to NF-kappaB activation by antineoplastic agents.
33 l sensitivity to this promising new class of antineoplastic agents.
34 form the basis for the development of novel antineoplastic agents.
35 timal combinations of these drugs with other antineoplastic agents.
36 as mapped with respect to several classes of antineoplastic agents.
37 nique intracellular and selective target for antineoplastic agents.
38 asing their susceptibility to cycle-specific antineoplastic agents.
39 er or cancer survivors treated with systemic antineoplastic agents.
40 olecules targeting translation initiation as antineoplastic agents.
41 outinely, alone or in combination with other antineoplastic agents.
42 rotoxicity profiles of an important class of antineoplastic agents.
43 multiple oncoproteins may lead to effective antineoplastic agents.
44 ifaceted approach for the development of new antineoplastic agents.
45 to improve performance and safety of current antineoplastic agents.
46 ng beta-lactam antibiotics and antiviral and antineoplastic agents.
47 for designing biocompatible target specific antineoplastic agents.
48 described possible activity of quinolones as antineoplastic agents.
49 lation to cytotoxic chemotherapy or targeted antineoplastic agents.
50 resistance to paclitaxel and possibly other antineoplastic agents.
51 entify complex III as a potential target for antineoplastic agents.
52 e proposal that these ligands may be used as antineoplastic agents.
53 reast cancer cells to cytoskeletal targeting antineoplastic agents.
54 logic utility as angiogenesis inhibitors and antineoplastic agents.
55 by current or previous treatment with other antineoplastic agents.
56 hione conjugates and several natural product antineoplastic agents.
57 ed for cancer cell apoptosis induced by many antineoplastic agents.
58 metabolism and may be a suitable target for antineoplastic agents.
59 a group, are unresponsive to treatment with antineoplastic agents.
60 l scaffold to improve the design of specific antineoplastic agents.
61 logic-based therapies are being developed as antineoplastic agents.
64 n of cellular apoptotic responses to various antineoplastic agents, a laser-based technology, Optopho
65 tide or FK228) is a member of a new class of antineoplastic agents active in T-cell lymphoma, the his
66 bacterial, fungal, and parasitic infections, antineoplastic agents against cancer cells, and perturba
67 ts with a pregnancy-related condition and an antineoplastic agent (Anatomical Therapeutic Chemical cl
68 tioning a pregnancy-related condition and an antineoplastic agent (Anatomical Therapeutic Chemical cl
69 n continue to be treated with this important antineoplastic agent and how such retreatment might be u
70 e transport of many amphiphilic antibiotics, antineoplastic agents and cytotoxic compounds that are d
71 city that are reported to be associated with antineoplastic agents and discuss their putative mechani
72 ic investigation of PPARdelta antagonists as antineoplastic agents and implicate altered PPARdelta-cy
75 , for a 1-year period, suffered reactions to antineoplastic agents and were referred to the Desensiti
76 kers has revealed many potential targets for antineoplastic agents, and a particularly important aber
77 argeting of these immunosuppressive cells by antineoplastic agents, and consider current challenges a
78 ncer cell proliferation by aurones and known antineoplastic agents, and in vitro inhibition of tubuli
79 in C given before mechanistically dissimilar antineoplastic agents antagonizes therapeutic efficacy i
80 new low molecular weight, protein-targeted, antineoplastic agents approved by the US FDA 2019-2023.
81 tional chemotherapy, many molecular targeted antineoplastic agents are available in oral formulation,
87 o asparaginyl residues and that DNA-damaging antineoplastic agents as well as other stimuli can incre
89 f advanced-stage NSCLC and were treated with antineoplastic agents between 2000 and 2011 (N = 22,163)
90 otic enzyme that inactivates the widely used antineoplastic agent bleomycin (BLM) and is a primary ca
92 was combined with seven of the eight tested antineoplastic agents but was highly dependent upon admi
94 pathy is a dose-limiting side effect of many antineoplastic agents, but the mechanisms underlying the
95 ate the response of an individual's tumor to antineoplastic agents, but these tumor fragments are cul
96 ion can affect the sensitivity of cancers to antineoplastic agents by altering expression of genes cr
97 ADCs is to improve the therapeutic index of antineoplastic agents by restricting their systemic deli
100 e induction of a senescent-like phenotype by antineoplastic agents can contribute therapeutic efficac
101 ce or its displacement from the chromatin by antineoplastic agents caused an increase in the levels o
102 sis included young age and chemotherapy with antineoplastic agents, cefotaxime, vancomycin, and cefta
108 , CREB, SP-1, or TFIID were not activated by antineoplastic agents demonstrating specificity of NF-ka
109 ast, docetaxel (Taxotere), a closely related antineoplastic agent, did not activate SXR and displayed
110 novel procedure to couple enzymatically the antineoplastic agent doxorubicin (Dox) on the galactose
114 xel (Taxol) is a potent and highly effective antineoplastic agent for the treatment of advanced, drug
116 port the clinical development of CV890 as an antineoplastic agent for the treatment of localized or m
119 structurally diverse hydrophobic amphipathic antineoplastic agents from cells, with different mechani
122 activity of multiple widely used classes of antineoplastic agents, human cancer cell lines were trea
123 , a PP2A inhibitor which has been used as an antineoplastic agent in clinical trials, is also able to
124 th RXR-selective ligand may thus be a useful antineoplastic agent in differentiation induction therap
125 275) has been identified recently as a novel antineoplastic agent in the primary screen conducted by
127 e inhibitor to undergo clinical trials as an antineoplastic agent in the United States, has attracted
129 notherapy and in co-administation with other antineoplastic agents in clinical trials as a strategy f
130 from combining flavopiridol with eight other antineoplastic agents in four different administration s
131 d consider how to combine antiretroviral and antineoplastic agents in patients with HIV who are recei
133 ggest that As(2)O(3) and AA may be effective antineoplastic agents in refractory MM and that AA might
135 d in B cell lymphomas by anti-Fas or various antineoplastic agents in the presence and absence of FDC
136 ng term antiproliferative effects of diverse antineoplastic agents including paclitaxel, etoposide, 7
137 d resistant (MCF-7/Adr-, T47D, and SKBr3) to antineoplastic agents, incubation with the sigma-2 subty
139 paullones, a dual property observed in other antineoplastic agents influencing phosphoester transfer.
144 inical use of doxorubicin, widely used as an antineoplastic agent, is markedly hampered by severe car
145 ed the sensitivity of these cells to several antineoplastic agents known to be cell cycle-dependent o
146 though some of the mechanisms by which these antineoplastic agents lead to hypertension have been cha
147 tial for increased exposure of the tumour to antineoplastic agents leading to improved cytotoxicity.
149 the side effects of cisplatin, a widely used antineoplastic agent, major efforts have been made to de
150 storically, it has been well recognized that antineoplastic agents may have adverse effects on multip
151 idoreductase 1 (NQO1) on the activity of the antineoplastic agent mitomycin C (MC) under aerobic and
152 List price increases were lowest (59%) for antineoplastic agents (n = 44), but discounts only offse
153 as osteosarcoma, for preclinical testing of antineoplastic agents offers significant advantages over
154 xic effect of ET-743 combined with six other antineoplastic agents on human breast cancer cell lines,
155 ated the effect of bryostatin-1 (Bryo-1), an antineoplastic agent, on dendritic cell (DC) maturation,
156 antiemetic regimens that are appropriate for antineoplastic agents or radiotherapy being administered
157 mens for adults who receive high-emetic-risk antineoplastic agents or who experience breakthrough nau
158 apeutic tool for hypersensitivity to several antineoplastic agents (oxaliplatin, carboplatin, paclita
160 consist of topo I-targeting agents and other antineoplastic agents, particularly DNA-damaging agents.
162 ne compound previously used clinically as an antineoplastic agent potentiates the presynaptic functio
163 edules and combining temozolomide with other antineoplastic agents, radiation therapy, or drug resist
165 omplex subunits confer resistance to several antineoplastic agents routinely used for the treatment o
167 menting the transvascular delivery of larger antineoplastic agents such as gene targeting vectors and
168 F ablation augments the delivery of systemic antineoplastic agents such as liposomal doxorubicin.
175 o Targeted HSV-1 editing results in a unique antineoplastic agent that enables inflammation without m
178 Bryostatin-1, a macrocyclic lactone, is an antineoplastic agent that potently activates protein kin
180 tment with paclitaxel (trade name Taxol), an antineoplastic agent that stabilizes cellular microtubul
182 raf-1 kinase may be of considerable value as antineoplastic agents that display activity against a wi
186 thesis that flavopiridol, like several other antineoplastic agents that kill noncycling cells, might
187 at can enhance the efficacy of biguanides as antineoplastic agents that target cancer cell energy met
188 rease in apoptosis in cells treated with the antineoplastic agents that was not due to up-regulation
189 n deazapurines as antibiotic, antiviral, and antineoplastic agents, the biosynthetic route toward dea
190 of development and availability of new oral antineoplastic agents, the purpose of this review is to
191 ew the development of successful preclinical antineoplastic agents, their associated limitations, and
192 ficant advancements in nanotechnology-driven antineoplastic agents, there remains a conspicuous gap i
193 zymatically mediated, glycosidic coupling of antineoplastic agents to antibodies specific for tumor-a
195 om our own laboratory, exploring how various antineoplastic agents trigger different forms of autopha
197 of the interaction between ET-743 and other antineoplastic agents using the combination index method
199 a desensitization to cell cycle-independent antineoplastic agents was found in the cells arrested by
200 increased resistance to cell cycle-dependent antineoplastic agents was found in the cells when the ex
201 apy, 51 candidate genes from the pathways of antineoplastic agents were resequenced to identify commo
204 is likely that interest in CDK inhibitors as antineoplastic agents will continue for the foreseeable