コーパス検索結果 (1語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 was administered for conversion by CPG2 to a cytotoxic drug.
2 s while decreasing systemic exposure to this cytotoxic drug.
3 ly relevant hypersensitivity reaction to the cytotoxic drug.
4 oves the delivery and efficacy of a targeted cytotoxic drug.
5 n the therapeutic window of a nanoformulated cytotoxic drug.
6 icrometastatic disease using a low dose of a cytotoxic drug.
7 hypersensitivity if administered before the cytotoxic drug.
8 domimetics for site-directed delivery of the cytotoxic drug.
9 management of cancer beyond the conventional cytotoxic drugs.
10 is and therapeutic responses to DNA damaging cytotoxic drugs.
11 d antidotes for the active anti-osteosarcoma cytotoxic drugs.
12 sites following the treatment of cells with cytotoxic drugs.
13 t to recommend the routine third-line use of cytotoxic drugs.
14 nd reduce adverse systemic effects of potent cytotoxic drugs.
15 CV in patients treated with pyrimidine-based cytotoxic drugs.
16 on, and sensitized BCR/ABL-positive cells to cytotoxic drugs.
17 ufficient to improve sensitivity to TKIs and cytotoxic drugs.
18 ravenous immunoglobulin (IVIg), coupled with cytotoxic drugs.
19 or maximal apoptosis to occur in response to cytotoxic drugs.
20 can be difficult to treat with conventional cytotoxic drugs.
21 otic ceramide during treatment of cells with cytotoxic drugs.
22 erties of cancer cells and sensitize them to cytotoxic drugs.
23 ib are distinct from those with conventional cytotoxic drugs.
24 ating p53-independent cell death produced by cytotoxic drugs.
25 ppaB, or to sensitize them to treatment with cytotoxic drugs.
26 cular those on high-dose glucocorticoids and cytotoxic drugs.
27 explored to improve the therapeutic index of cytotoxic drugs.
28 to, for example, metastasize or to tolerate cytotoxic drugs.
29 to those looking at conventional anticancer cytotoxic drugs.
30 beta1 integrins causes resistance to certain cytotoxic drugs.
31 nd show the same sensitivity to a variety of cytotoxic drugs.
32 , thereby averting the risks associated with cytotoxic drugs.
33 s were reduced and cells became sensitive to cytotoxic drugs.
34 for sensitizing B-CLL cells to conventional cytotoxic drugs.
35 sed tissue, with the cell-killing ability of cytotoxic drugs.
36 rs that confer resistance to natural product cytotoxic drugs.
37 to the noted resistance of leukemia cells to cytotoxic drugs.
38 MRP3 is capable of conferring resistance to cytotoxic drugs.
39 o generate drug resistance than conventional cytotoxic drugs.
40 resistance or sensitivity) of these cells to cytotoxic drugs.
41 tients were treated with corticosteroids and cytotoxic drugs.
42 d in patients receiving etoposide plus other cytotoxic drugs.
43 nfers cellular resistance to natural product cytotoxic drugs.
44 s their roles in defending cancer cells from cytotoxic drugs.
45 s as a "safe house" to protect cells against cytotoxic drugs.
46 ic evolution in a cell population exposed to cytotoxic drugs.
47 giogenic agents rely upon a combination with cytotoxic drugs.
48 odify pharmacokinetic and safety profiles of cytotoxic drugs.
49 overexpression increased chemosensitivity to cytotoxic drugs.
50 xploited for the site-specific attachment of cytotoxic drugs.
51 sing LPP-targeting siRNA in combination with cytotoxic drugs.
52 ehavior of cancer cells under selection with cytotoxic drugs.
53 sensitized only Pgp-expressing cells to such cytotoxic drugs.
54 transition process, and chemosensitivity to cytotoxic drugs.
55 this nurturing milieu and sensitizes them to cytotoxic drugs.
56 utic index of Dox and potentially many other cytotoxic drugs.
57 e cancer cells, making them resistant to key cytotoxic drugs.
58 y of normal and tumor cells to radiation and cytotoxic drugs.
59 e the effect of various cell-cycle dependent cytotoxic drugs.
64 layed increased resistance to killing by the cytotoxic drug 6-thioguanine (6TG), indicating that the
66 ttracting CLL cells and protecting them from cytotoxic drugs, a mechanism that may account for residu
67 evaluated by enzymatic assay, resistance to cytotoxic drugs, ability to incorporate radiolabeled pur
68 doxorubicin may be used not only as a direct cytotoxic drug against tumor cells, but also as a potent
69 70-kDa P-glycoprotein that actively excludes cytotoxic drugs against their concentration gradient.
70 e marrow milieu may confer a protection from cytotoxic drugs, allowing the emergence of drug-resistan
73 h mildly cationic or neutral natural product cytotoxic drugs and anionic compounds such as DNP-SG, MK
76 that can bind, often structurally unrelated, cytotoxic drugs and control the expression of drug pumps
77 reviews data on the efficacy and toxicity of cytotoxic drugs and cyclosporine in selected autoimmune
78 lymphoblastic leukemic blasts cultured with cytotoxic drugs and dead epithelial cancer cells isolate
80 aditional cancer treatments have centered on cytotoxic drugs and general purpose chemotherapy that ma
81 tween cellular resistance to some classes of cytotoxic drugs and glutathione-mediated mechanisms of r
83 properties of melanoma cells by sequestering cytotoxic drugs and increasing melanosome-mediated drug
85 selected for long periods in the presence of cytotoxic drugs and may have other host alterations.
86 PTK, the cells were relatively resistant to cytotoxic drugs and MIP-1alpha treatment neither induced
92 e neutral or mildly cationic natural product cytotoxic drugs and the anionic products of glutathione
93 e neutral or mildly cationic natural product cytotoxic drugs and the anionic products of glutathione
94 als suggest that combination treatments with cytotoxic drugs and TRAIL receptor-targeted agents do no
95 , how best to minimise the time spent taking cytotoxic drugs and whether molecular selection can refi
96 lls either sensitive or resistant to Dex and cytotoxic drugs, and overcomes the growth and survival e
97 ablishes that MRP pumps unaltered lipophilic cytotoxic drugs, and suggests that this activity is an i
99 es high-dose corticosteroids, and additional cytotoxic drugs, antitumor necrosis factor monoclonal an
100 biodegradable polymeric nanogels loaded with cytotoxic drugs applied via the topical route, can be a
102 a disulfide linker between the antibody and cytotoxic drug are inspired by indirect evidence suggest
103 tive prostate cancer cells; therefore, other cytotoxic drugs are being used to induce apoptosis in an
104 These results indicate that the available cytotoxic drugs are better substrates for the rat enzyme
105 Both tumor metabolism and its response to cytotoxic drugs are intrinsic properties of tumor cells.
107 ionale to combine SS1P with Taxol or another cytotoxic drug as a strategy to increase immunotoxin upt
108 some of which were also modulated by IL-3 or cytotoxic drugs, as well as by specific sub-regions of t
109 eously to drug sensitivity in the absence of cytotoxic drugs at the high rates that are typical of ch
111 failure, blood pressure fluctuations, use of cytotoxic drugs, autoimmune disorders, or eclampsia.
112 py, neuroblastomas can acquire resistance to cytotoxic drugs because of the population expansion of t
113 ata implicate exogenous toxicants, including cytotoxic drugs, benzene, radiation, and cigarette smoki
114 rolongs life in comparison with conventional cytotoxic drugs but the optimal starting dosage, the def
115 state to trigger the catalytic release of a cytotoxic drug by promoting the association of a prodrug
117 Preventing melanosomal sequestration of cytotoxic drugs by inhibiting the functions of melanosom
118 hway induced by growth factor withdrawal and cytotoxic drugs by selectively activating the expression
120 etravalent M2pep, without conjugation of any cytotoxic drug cargo, exhibited M2 macrophage-selective
121 in their ability to reductively activate the cytotoxic drug CB 1954 (5-(aziridin-1-yl)-2,4-dinitroben
122 poptosis occurs in AML blasts in response to cytotoxic drugs, cells were incubated with daunorubicin
123 stic interaction between rhuMAb HER2 and the cytotoxic drug cisplatin in human breast and ovarian can
127 ggest modulation of ATP levels together with cytotoxic drugs could overcome drug-resistance in glycol
128 hibitors, alone or in combination with other cytotoxic drugs, could potentially be used to treat canc
129 e targeted anticancer agents consisting of a cytotoxic drug covalently linked to a monoclonal antibod
130 ugates (ADCs) are macromolecules composed of cytotoxic drugs covalently attached via a conditionally
133 -dependent transport for the natural product cytotoxic drugs daunorubicin and vincristine, as well as
134 mpetitively inhibited by the natural product cytotoxic drugs daunorubicin, vincristine, and etoposide
135 ibronectin coupled to one of a set of potent cytotoxic drugs (DM1 or one of two duocarmycin derivativ
139 targeted nanoparticle (NP) encapsulating the cytotoxic drug doxorubicin (Dox) for targeted drug deliv
140 imulate the transport of the clinically used cytotoxic drug doxorubicin across multicell layers (MCLs
145 hemotherapy of resistance to a wide range of cytotoxic drugs (either as a primary or acquired propert
147 1 and BRCA2 determine the sensitivity to the cytotoxic drug, etoposide, using genetic complementation
148 s in solid tumors with various molecular and cytotoxic drugs evaluated as single agents or as combina
150 d to the cellular response to irradiation or cytotoxic drug exposure in vitro and clinical outcome.
152 y showed that IL-4 induced resistance to the cytotoxic drugs fludarabine and chlorambucil and to the
153 d a number of other agents that compete with cytotoxic drugs for binding sites on P-glycoprotein can
156 evel of cell kill obtained by treatment with cytotoxic drugs for similar periods of time, indicating
160 s the diminished capacity of cells to remove cytotoxic drugs from the cytoplasm by sequestration of p
161 volume resulting from administration of the cytotoxic drug gemcitabine, reflecting the apoptotic vol
162 It has become increasingly apparent that cytotoxic drugs given systemically for non-CNS tumours m
164 ion of targeted treatments with conventional cytotoxic drugs has expanded the treatment of metastatic
165 ein pumps that confer cellular resistance to cytotoxic drugs has improved enormously with the recent
166 nergistic laboratory interactions with other cytotoxic drugs have been exploited to allow development
176 (FR) may be of use for targeted delivery of cytotoxic drugs in invasive urothelial carcinoma (iUC),
182 s with low REST score were more sensitive to cytotoxic drugs including Mitomycin, Camptothecin and Ci
183 death (ICD) is the process by which certain cytotoxic drugs induce apoptosis of tumor cells in a man
187 tep in programmed cell death (apoptosis) and cytotoxic drug-induced apoptosis is mediated by caspase
188 terference decreases IL-6-induced effects on cytotoxic drug-induced caspase activation and apoptosis.
190 tic function of MLK3 as a mechanism to limit cytotoxic drug-induced death of ER(+) breast cancer cell
192 ow being applied to clarify the mechanism of cytotoxic drug-induced fetal hemoglobin augmentation.
196 t resistance to chemosensitizing agents plus cytotoxic drugs is associated with a redistribution of P
200 the direct transport of unaltered lipophilic cytotoxic drugs is the predominant biochemical mechanism
204 est in the use of 17-AAG in combination with cytotoxic drugs led us to study both GA and 17-AAG with
205 lls susceptible to apoptosis by cytokines or cytotoxic drugs, likely due to its effects on NF-kappaB.
206 ng characteristics compared with traditional cytotoxic drugs, making it possible to estimate the stea
210 th a decrease in net production of bystander cytotoxic drug metabolites because of accelerated death
211 rolong localized, intratumoral production of cytotoxic drug metabolites without inducing tumor cell d
212 alkylating agents, such as the mutagenic and cytotoxic drug N-methyl-N'-nitro-N-nitrosoguanidine (MNN
214 ess toxic than the broadly antiproliferative cytotoxic drugs of the previous era, which still dominat
215 -toxicity antibiotic with a standard-of-care cytotoxic drug, offering immediate applications for clin
218 g variables such as concomitant use of other cytotoxic drugs, opportunistic infections, diffuse pulmo
221 improve outcome by intensifying conventional cytotoxic drugs or increasing the radiation dose have no
223 ning CDK inhibitors with either conventional cytotoxic drugs or novel signal transduction modulators
228 umber of regimens, and fail to fully capture cytotoxic drug pharmacodynamics and pharmacokinetic vari
229 eing investigated and include biological and cytotoxic drugs, phototherapy, and monoclonal antibodies
230 PSMA-producing cells can be used to deliver cytotoxic drugs, protein toxins, and viruses selectively
231 monoclonal antibodies with chemotherapeutic cytotoxic drugs provides clinical benefit to patients wi
235 sitivity of normal host tissue by delivering cytotoxic drug resistance genes to marrow precursor cell
236 ne, has an established role as a mediator of cytotoxic drug resistance in acute myeloid leukemia (AML
240 confer intrinsic resistance, and exposure to cytotoxic drugs select for the survival of these cells t
241 his panel of EBVs and challenge with various cytotoxic drugs showed that EBNA3A and EBNA3C cooperate
242 Antibody-drug conjugate (ADC) which delivers cytotoxic drugs specifically into targeted cells through
243 s subcellular sequestration of intracellular cytotoxic drugs such as cis-diaminedichloroplatinum II (
245 evidence suggests that one mechanism whereby cytotoxic drugs, such as doxorubicin, kill tumors is the
246 er genes and had a greater capacity to expel cytotoxic drugs, such as mitoxantrone, resulting in bett
249 nstrated in several tumor types treated with cytotoxic drugs, targeted agents, and radiotherapy.
251 Glioblastoma (GBM) is often treated with the cytotoxic drug temozolomide, but the disease inevitably
252 not only were more resistant to traditional cytotoxic drugs than were cells in 2D monolayer culture
256 resistance to a spectrum of natural product cytotoxic drugs, that expression of MRP is associated wi
257 RPGN benefits from high-dose steroids and cytotoxic drug therapy with the addition of plasma excha
258 s exhibit higher resistance to rituximab and cytotoxic drugs, these clones can be chemosensitized fol
259 treatment of recipients with irradiation or cytotoxic drugs to achieve lasting engraftment at levels
260 f PF-956980 in conjunction with conventional cytotoxic drugs to achieve more extensive killing of CLL
262 njugates (ADCs) allow selective targeting of cytotoxic drugs to cancer cells presenting tumor-associa
264 igned to facilitate the targeted delivery of cytotoxic drugs to improve their tumor fighting effects
265 was used to demonstrate that the ability of cytotoxic drugs to increase p53 expression level does no
266 tions that could be used in conjunction with cytotoxic drugs to inhibit the emergence of resistance.
268 ovides an opportunity to selectively deliver cytotoxic drugs to prostate cancer cells while sparing n
269 omising agents for the selective delivery of cytotoxic drugs to specific cells (for example, tumors).
270 se findings reveal that NP-based delivery of cytotoxic drugs to the alphanubeta3-positive tumor vascu
272 The ability of these liposomes to deliver cytotoxic drugs to the tumor and kill these cells was de
274 lopment in the field of targeted delivery of cytotoxic drugs to tumors was not successful because the
275 d autophagy associated with sensitization to cytotoxic drug treatment in a panel of highly malignant
279 allow for tumor-targeted in situ delivery of cytotoxic drugs, tumor resistance to apoptosis remains a
280 s used to establish whether PCFT can deliver cytotoxic drug under pH conditions that mimic the tumor
281 ation to other anti-cancer agents, including cytotoxic drugs, upregulation of immune processing and p
283 ion are the nonhematologic toxicities of the cytotoxic drugs used and the resistance of stem cells an
284 mimetic LBW242 alone or in combination with cytotoxic drugs used clinically to treat neuroblastoma.
287 ociated loss of MRP1 and accumulation of the cytotoxic drug vincristine, an MRP1 substrate, depleted
289 ion between rhuMAb HER2 and other classes of cytotoxic drugs, we applied multiple drug effect/combina
290 ted amifostine may potentiate the effects of cytotoxic drugs, we conducted a phase II trial of amifos
291 her with TEADs prevents apoptosis induced by cytotoxic drugs, whereas YAP knockdown sensitizes CC cel
292 The ligand-hapten conjugates are potential cytotoxic drugs which may (1) be specific for a given ta
293 This observation prompted us to choose a cytotoxic drug whose activity is potentiated by cellular
294 n regimens using angiogenesis inhibitors and cytotoxic drugs will be needed to determine how such com
295 imarily the malignant cells toward combining cytotoxic drugs with agents that interfere with the micr
296 ase I studies with single-agent molecular or cytotoxic drugs with favorable preclinical rationale and
WebLSDに未収録の専門用語(用法)は "新規対訳" から投稿できます。