ライフサイエンスコーパス: cytotoxic drug

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.

60 rocytosine (5-FC), thus converting it to the cytotoxic drug 5-fluorouracil (5-FU).

61 ic recovery in vivo after treatment with the cytotoxic drug 5-fluorouracil (5-FU).

62 However, after treatment with the cytotoxic drug 5-fluorouracil or with gamma-radiation, t

63 poietic recovery after administration of the cytotoxic drug, 5-fluorouracil.

64 layed increased resistance to killing by the cytotoxic drug 6-thioguanine (6TG), indicating that the

65 tumor cells is associated with resistance to cytotoxic drugs, a major obstacle in chemotherapy.

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

71 re unachievable using very high doses of the cytotoxic drug alone.

72 rmacokinetic interactions between the target cytotoxic drug and the modulating agent.

73 h mildly cationic or neutral natural product cytotoxic drugs and anionic compounds such as DNP-SG, MK

74 ly relied on genes that confer resistance to cytotoxic drugs and are encumbered by toxicity.

75 d by many extracellular stimulants including cytotoxic drugs and chemical carcinogens.

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

79 This peptide may be suitable for targeting cytotoxic drugs and gene therapy vectors into tumors.

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

82 it an attractive target for the delivery of cytotoxic drugs and imaging agents.

83 properties of melanoma cells by sequestering cytotoxic drugs and increasing melanosome-mediated drug

84 enders tumor cells resistant to treatment by cytotoxic drugs and irradiation.

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

87 Though a variety of cytotoxic drugs and radiation therapies are currently av

88 he underlying disease and its treatment with cytotoxic drugs and radiation therapy.

89 Better use of existing cytotoxic drugs and supportive care have made large cont

90 n rapidly evolving with the emergence of new cytotoxic drugs and targeted biologic agents.

91 ctal cancer is treated with a combination of cytotoxic drugs and targeted treatments.

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

98 oxic moieties, including recombinant toxins, cytotoxic drugs, and tubulin inhibitors.

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

101 The aglycone and sugar moieties of the cytotoxic drug are essential for inhibition.

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.

106 and drug-induced apoptosis occurs only when cytotoxic drugs are used as the selecting agent.

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

110 vel derivative of the microtubule-disrupting cytotoxic drug auristatin (FGFR2-ADC).

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

116 s then given, which is activated to a potent cytotoxic drug by the tumor-localized enzyme.

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

119 c lethality to the cell cycle phase-specific cytotoxic drugs, capecitabine and paclitaxel.

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

124 g cancer cells to the treatment of the chemo cytotoxic drug cisplatin.

125 interaction between tirapazamine and several cytotoxic drug classes, including cisplatin.

126 an SO-labile aminoacrylate linker (L), and a cytotoxic drug combretastatin A-4 (CA4).

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

131 Antibody-drug conjugates (ADC), potent cytotoxic drugs covalently linked to antibodies via chem

132 urine lymphoma models with the commonly used cytotoxic drug, cyclophosphamide.

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

136 Patients taking cytotoxic drugs do not often develop overt hypopituitari

137 embrane association, whereas that induced by cytotoxic drugs does not.

138 tients but, as expected, were not related to cytotoxic drug dosage.

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

141 t cells induce IRF-1 mRNA in response to the cytotoxic drug doxorubicin.

142 ILs were used to deliver cytotoxic drugs doxorubicin, vinorelbine, or methotrexat

143 (GBM) cells to subsequent treatment with the cytotoxic drug, doxorubicin (DOX).

144 aride, a fluorophore, and an analogue of the cytotoxic drug duocarmycin.

145 hemotherapy of resistance to a wide range of cytotoxic drugs (either as a primary or acquired propert

146 ered in murine NIH3T3 cells treated with the cytotoxic drug etoposide.

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

149 3A5 conjugated to cytotoxic drugs exhibited superior toxicity against tumo

150 d to the cellular response to irradiation or cytotoxic drug exposure in vitro and clinical outcome.

151 impaired cellular response to irradiation or cytotoxic drug exposure in vitro.

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

154 le formation are one of the major classes of cytotoxic drugs for cancer treatment.

155 tion from anoikis and relative resistance to cytotoxic drugs for cells within CTM.

156 evel of cell kill obtained by treatment with cytotoxic drugs for similar periods of time, indicating

157 Resistance to cytotoxic drugs frequently emerges during treatment of l

158 from ATP hydrolysis to transport pleiotropic cytotoxic drugs from inside to outside of cells.

159 ansporter, which hydrolyses ATP and extrudes cytotoxic drugs from mammalian cells.

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

163 Host conditioning with irradiation or cytotoxic drugs has been used in many protocols for chim

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

167 A second is that certain cytotoxic drugs have been reported to sensitize cancer c

168 Corticosteroids and cytotoxic drugs have been the mainstay of treatment for

169 Several cytotoxic drugs have shown activity in patients whose di

170 nd increased sensitivity of the cells to the cytotoxic drugs hydroxyurea and cytarabine.

171 These results suggest that adding a cytotoxic drug in combination antiviral chemotherapy may

172 mor cells are most sensitive to radiation or cytotoxic drug in this cell cycle phase.

173 bsequent administration of the corresponding cytotoxic drug in vivo.

174 roliferation, invasiveness, or resistance to cytotoxic drugs in A2780 cells.

175 nce to tyrosine kinase inhibitors (TKIs) and cytotoxic drugs in AML.

176 (FR) may be of use for targeted delivery of cytotoxic drugs in invasive urothelial carcinoma (iUC),

177 asion while affecting acquired resistance to cytotoxic drugs in the tumor microenvironment.

178 rtant role in resistance to chemotherapeutic cytotoxic drugs in treating multiple myeloma (MM).

179 locks GBM growth and sensitizes GBM cells to cytotoxic drugs in vivo.

180 genotoxic stress (UV, gamma-irradiation and cytotoxic drugs) in a p53-dependent manner.

181 encapsulate topotecan (TPT, 1), an important cytotoxic drug, in biodegradable nanoMOFs.

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

184 Because many cytotoxic drugs induce caspase-dependent apoptosis, fail

185 owth inhibition nor protected the cells from cytotoxic drug induced cell death.

186 DNA-damaging agents and cytotoxic drugs induced endogenous maspin expression in

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.

189 17beta-Estradiol (E(2)) hinders cytotoxic drug-induced cell death in estrogen receptor-p

190 tic function of MLK3 as a mechanism to limit cytotoxic drug-induced death of ER(+) breast cancer cell

191 However, despite cytotoxic drug-induced FasL expression, Fas-sensitive tu

192 ow being applied to clarify the mechanism of cytotoxic drug-induced fetal hemoglobin augmentation.

193 IX (CAIX), which can transport highly potent cytotoxic drugs into CAIX-expressing solid tumors.

194 ent mice, which were treated with either the cytotoxic drug, Irinotecan, or saline as control.

195 ients with performance status of 2, a single cytotoxic drug is sufficient.

196 t resistance to chemosensitizing agents plus cytotoxic drugs is associated with a redistribution of P

197 The performance of cytotoxic drugs is defined by their selectivity of uptak

198 Tumor resistance to cytotoxic drugs is one of the main obstacles to successf

199 1, a platinum-based two-drug combination of cytotoxic drugs is recommended.

200 the direct transport of unaltered lipophilic cytotoxic drugs is the predominant biochemical mechanism

201 cells and/or sensitize glioblastoma cells to cytotoxic drugs is therefore urgently needed.

202 valuation of enzastaurin in combination with cytotoxic drugs is warranted in NSCLC.

203 aluation of its activity in combination with cytotoxic drugs is warranted.

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

207 The active efflux of cytotoxic drugs mediated by multidrug transporters is th

208 ing VEGF-C or NRP-2 depletion contributes to cytotoxic drug-mediated cell death.

209 The findings demonstrate that cytotoxic drug-mediated sensitization primes both perfor

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

213 tigated the sensitivity of liver CAFs to the cytotoxic drug navitoclax, a BH3 mimetic.

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

216 The influences of cytotoxic drugs on endothelial cells remain incompletely

217 Furthermore, these effects of cytotoxic drugs on infiltrating immune phagocytes may ha

218 g variables such as concomitant use of other cytotoxic drugs, opportunistic infections, diffuse pulmo

219 motherapy regimen, generally the nonplatinum cytotoxic drug or a molecular targeted agent.

220 Upon exposure to standard-of-care cytotoxic drugs or epigenetic modifiers, NE and ML cell

221 improve outcome by intensifying conventional cytotoxic drugs or increasing the radiation dose have no

222 rapy inevitably develops upon treatment with cytotoxic drugs or molecularly targeted therapies.

223 ning CDK inhibitors with either conventional cytotoxic drugs or novel signal transduction modulators

224 limited oxygen availability, and exposure to cytotoxic drugs or radiation.

225 apy has yet to be superseded by either newer cytotoxic drugs or targeted agents.

226 transplantation, cancer, infection, certain cytotoxic drugs, or pregnancy.

227 Cytotoxic drug-- or irradiation-induced growth arrest an

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

232 toplasm, which in turn reduces the amount of cytotoxic drug reaching the nucleus.

233 Extensive research into mechanisms of cytotoxic drug resistance and subsequent clinical trials

234 the possibility that cMOAT may contribute to cytotoxic drug resistance as well.

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

237 link between mismatch repair deficiency and cytotoxic drug resistance.

238 ates many cellular processes contributing to cytotoxic drug resistance.

239 s FOXM1 activity and causes mitotic delay in cytotoxic drug response.

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 (

244 ention to enhance the therapeutic effects of cytotoxic drugs such as docetaxel.

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

247 accumulation and potency of ABCC10-exported cytotoxic drugs, such as paclitaxel.

248 ients, but suffer from higher constitutional cytotoxic drug susceptibility.

249 nstrated in several tumor types treated with cytotoxic drugs, targeted agents, and radiotherapy.

250 g drug class that uses antibodies to improve cytotoxic drug targeting for cancer treatment.

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

253 ted comparable sensitivity to vincristine, a cytotoxic drug that is not incorporated into DNA.

254 Cytotoxic drugs that cause CIPN exert their effects by i

255 This review focuses only on cytotoxic drugs that have been in clinical development f

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

261 Antibody-drug conjugates (ADC) target cytotoxic drugs to antigen-positive cells for treating c

262 njugates (ADCs) allow selective targeting of cytotoxic drugs to cancer cells presenting tumor-associa

263 Targeting cytotoxic drugs to cancer cells using antibody-drug conj

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.

267 labels, reporter groups, imaging agents, and cytotoxic drugs to peptides and proteins.

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

271 g these to deliver toxins, radioisotopes, or cytotoxic drugs to the cancer cells.

272 The ability of these liposomes to deliver cytotoxic drugs to the tumor and kill these cells was de

273 een developed to specifically deliver highly cytotoxic drugs to the tumor.

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

276 We also show that cytotoxic drug treatment produced a significant and sust

277 ic cancer cells that proliferate in spite of cytotoxic drug treatment.

278 tics vary dramatically between cell type and cytotoxic drug treatment.

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

282 Cisplatin is a cytotoxic drug used as a first-line therapy for a wide v

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.

285 Because many of the cytotoxic drugs used to treat ovarian cancer induce COX-

286 lls by extruding amphipathic natural product cytotoxic drugs using the energy of ATP.

287 ociated loss of MRP1 and accumulation of the cytotoxic drug vincristine, an MRP1 substrate, depleted

288 the tyrosine analog 4-tert-butylphenol, and cytotoxic drugs was examined.

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

297 desired cells typically relies on the use of cytotoxic drugs with long culture times.

298 The encapsulation of cytotoxic drugs within liposomes enhances pharmacokineti