ライフサイエンスコーパス: cytotoxic drug

1 hypersensitivity if administered before the cytotoxic drug.

2 domimetics for site-directed delivery of the cytotoxic drug.

3 was administered for conversion by CPG2 to a cytotoxic drug.

4 s while decreasing systemic exposure to this cytotoxic drug.

5 nalyte and can respond with the release of a cytotoxic drug.

6 ly relevant hypersensitivity reaction to the cytotoxic drug.

7 n the therapeutic window of a nanoformulated cytotoxic drug.

8 oves the delivery and efficacy of a targeted cytotoxic drug.

9 icrometastatic disease using a low dose of a cytotoxic drug.

10 xploited for the site-specific attachment of cytotoxic drugs.

11 ehavior of cancer cells under selection with cytotoxic drugs.

12 sensitized only Pgp-expressing cells to such cytotoxic drugs.

13 transition process, and chemosensitivity to cytotoxic drugs.

14 this nurturing milieu and sensitizes them to cytotoxic drugs.

15 utic index of Dox and potentially many other cytotoxic drugs.

16 cted nanocarriers to improve the delivery of cytotoxic drugs.

17 e cancer cells, making them resistant to key cytotoxic drugs.

18 y of normal and tumor cells to radiation and cytotoxic drugs.

19 e the effect of various cell-cycle dependent cytotoxic drugs.

20 is and therapeutic responses to DNA damaging cytotoxic drugs.

21 PDA cells express Rgs16::GFP in response to cytotoxic drugs.

22 d antidotes for the active anti-osteosarcoma cytotoxic drugs.

23 sites following the treatment of cells with cytotoxic drugs.

24 t to recommend the routine third-line use of cytotoxic drugs.

25 nd reduce adverse systemic effects of potent cytotoxic drugs.

26 CV in patients treated with pyrimidine-based cytotoxic drugs.

27 on, and sensitized BCR/ABL-positive cells to cytotoxic drugs.

28 ravenous immunoglobulin (IVIg), coupled with cytotoxic drugs.

29 or maximal apoptosis to occur in response to cytotoxic drugs.

30 can be difficult to treat with conventional cytotoxic drugs.

31 otic ceramide during treatment of cells with cytotoxic drugs.

32 o tumors, which then allow the use of highly cytotoxic drugs.

33 r study the mechanisms of action of specific cytotoxic drugs.

34 erties of cancer cells and sensitize them to cytotoxic drugs.

35 ib are distinct from those with conventional cytotoxic drugs.

36 ating p53-independent cell death produced by cytotoxic drugs.

37 ppaB, or to sensitize them to treatment with cytotoxic drugs.

38 s equipped with functional compounds such as cytotoxic drugs.

39 cular those on high-dose glucocorticoids and cytotoxic drugs.

40 explored to improve the therapeutic index of cytotoxic drugs.

41 to those looking at conventional anticancer cytotoxic drugs.

42 beta1 integrins causes resistance to certain cytotoxic drugs.

43 nd show the same sensitivity to a variety of cytotoxic drugs.

44 , thereby averting the risks associated with cytotoxic drugs.

45 s were reduced and cells became sensitive to cytotoxic drugs.

46 for sensitizing B-CLL cells to conventional cytotoxic drugs.

47 rs that confer resistance to natural product cytotoxic drugs.

48 to the noted resistance of leukemia cells to cytotoxic drugs.

49 MRP3 is capable of conferring resistance to cytotoxic drugs.

50 o generate drug resistance than conventional cytotoxic drugs.

51 ity to potentiate the therapeutic effects of cytotoxic drugs.

52 resistance or sensitivity) of these cells to cytotoxic drugs.

53 management of cancer beyond the conventional cytotoxic drugs.

54 sing LPP-targeting siRNA in combination with cytotoxic drugs.

55 ufficient to improve sensitivity to TKIs and cytotoxic drugs.

56 to, for example, metastasize or to tolerate cytotoxic drugs.

57 sed tissue, with the cell-killing ability of cytotoxic drugs.

58 s their roles in defending cancer cells from cytotoxic drugs.

59 s as a "safe house" to protect cells against cytotoxic drugs.

60 ic evolution in a cell population exposed to cytotoxic drugs.

61 giogenic agents rely upon a combination with cytotoxic drugs.

62 odify pharmacokinetic and safety profiles of cytotoxic drugs.

63 overexpression increased chemosensitivity to cytotoxic drugs.

64 The major molecular mode of action of the cytotoxic drug 5-fluorouracil (5-FU) is generally consid

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

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

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

68 In cells, the protected analogues of cytotoxic drugs 5-fluorouracil (5-FU) and monomethyl aur

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

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

71 ttracting CLL cells and protecting them from cytotoxic drugs, a mechanism that may account for residu

72 evaluated by enzymatic assay, resistance to cytotoxic drugs, ability to incorporate radiolabeled pur

73 doxorubicin may be used not only as a direct cytotoxic drug against tumor cells, but also as a potent

74 70-kDa P-glycoprotein that actively excludes cytotoxic drugs against their concentration gradient.

75 e marrow milieu may confer a protection from cytotoxic drugs, allowing the emergence of drug-resistan

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

77 rs that are sensitive to other p53-dependent cytotoxic drugs, also display increased sensitivity to X

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

79 pies of (223)Ra with microtubule-stabilizing cytotoxic drugs and agents targeting the androgen recept

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

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

82 that can bind, often structurally unrelated, cytotoxic drugs and control the expression of drug pumps

83 reviews data on the efficacy and toxicity of cytotoxic drugs and cyclosporine in selected autoimmune

84 lymphoblastic leukemic blasts cultured with cytotoxic drugs and dead epithelial cancer cells isolate

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

86 aditional cancer treatments have centered on cytotoxic drugs and general purpose chemotherapy that ma

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

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

89 te to personalize combination therapies with cytotoxic drugs and inhibitors of signal transduction pa

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

91 ry vesicles to controllably release enclosed cytotoxic drugs and kill eukaryotic cells.

92 selected for long periods in the presence of cytotoxic drugs and may have other host alterations.

93 PTK, the cells were relatively resistant to cytotoxic drugs and MIP-1alpha treatment neither induced

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

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

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

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

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

99 als suggest that combination treatments with cytotoxic drugs and TRAIL receptor-targeted agents do no

100 , how best to minimise the time spent taking cytotoxic drugs and whether molecular selection can refi

101 lls either sensitive or resistant to Dex and cytotoxic drugs, and overcomes the growth and survival e

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

103 es high-dose corticosteroids, and additional cytotoxic drugs, antitumor necrosis factor monoclonal an

104 biodegradable polymeric nanogels loaded with cytotoxic drugs applied via the topical route, can be a

105 a disulfide linker between the antibody and cytotoxic drug are inspired by indirect evidence suggest

106 tive prostate cancer cells; therefore, other cytotoxic drugs are being used to induce apoptosis in an

107 Both tumor metabolism and its response to cytotoxic drugs are intrinsic properties of tumor cells.

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

109 ionale to combine SS1P with Taxol or another cytotoxic drug as a strategy to increase immunotoxin upt

110 some of which were also modulated by IL-3 or cytotoxic drugs, as well as by specific sub-regions of t

111 eously to drug sensitivity in the absence of cytotoxic drugs at the high rates that are typical of ch

112 ional ADCs have a stochastic distribution of cytotoxic drugs attached at several different sites on t

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

114 failure, blood pressure fluctuations, use of cytotoxic drugs, autoimmune disorders, or eclampsia.

115 py, neuroblastomas can acquire resistance to cytotoxic drugs because of the population expansion of t

116 ata implicate exogenous toxicants, including cytotoxic drugs, benzene, radiation, and cigarette smoki

117 Here we show that two classes of cytotoxic drugs broadly employed in pre-operative (neoad

118 rolongs life in comparison with conventional cytotoxic drugs but the optimal starting dosage, the def

119 state to trigger the catalytic release of a cytotoxic drug by promoting the association of a prodrug

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

121 Preventing melanosomal sequestration of cytotoxic drugs by inhibiting the functions of melanosom

122 hway induced by growth factor withdrawal and cytotoxic drugs by selectively activating the expression

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

124 etravalent M2pep, without conjugation of any cytotoxic drug cargo, exhibited M2 macrophage-selective

125 poptosis occurs in AML blasts in response to cytotoxic drugs, cells were incubated with daunorubicin

126 stic interaction between rhuMAb HER2 and the cytotoxic drug cisplatin in human breast and ovarian can

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

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

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

130 However, encapsulation of a strong cytotoxic drug completely shut off this unwanted immune

131 ggest modulation of ATP levels together with cytotoxic drugs could overcome drug-resistance in glycol

132 hibitors, alone or in combination with other cytotoxic drugs, could potentially be used to treat canc

133 e targeted anticancer agents consisting of a cytotoxic drug covalently linked to a monoclonal antibod

134 ugates (ADCs) are macromolecules composed of cytotoxic drugs covalently attached via a conditionally

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

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

137 ibronectin coupled to one of a set of potent cytotoxic drugs (DM1 or one of two duocarmycin derivativ

138 Patients taking cytotoxic drugs do not often develop overt hypopituitari

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

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

141 targeted nanoparticle (NP) encapsulating the cytotoxic drug doxorubicin (Dox) for targeted drug deliv

142 imulate the transport of the clinically used cytotoxic drug doxorubicin across multicell layers (MCLs

143 en conjugated one of these nanobodies to the cytotoxic drug doxorubicin, and we show that the conjuga

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

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

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

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

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

149 1 and BRCA2 determine the sensitivity to the cytotoxic drug, etoposide, using genetic complementation

150 s in solid tumors with various molecular and cytotoxic drugs evaluated as single agents or as combina

151 3A5 conjugated to cytotoxic drugs exhibited superior toxicity against tumo

152 ug-tolerant "persisters" (DTPs), can survive cytotoxic drug exposure despite lacking resistance-confe

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

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

155 y showed that IL-4 induced resistance to the cytotoxic drugs fludarabine and chlorambucil and to the

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

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

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

159 we have relied entirely on DNA-interactive, cytotoxic drugs for treating patients with leukemia.

160 Resistance to cytotoxic drugs frequently emerges during treatment of l

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

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

163 volume resulting from administration of the cytotoxic drug gemcitabine, reflecting the apoptotic vol

164 It has become increasingly apparent that cytotoxic drugs given systemically for non-CNS tumours m

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

166 ion of targeted treatments with conventional cytotoxic drugs has expanded the treatment of metastatic

167 ein pumps that confer cellular resistance to cytotoxic drugs has improved enormously with the recent

168 nergistic laboratory interactions with other cytotoxic drugs have been exploited to allow development

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

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

171 Several cytotoxic drugs have shown activity in patients whose di

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

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

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

175 bsequent administration of the corresponding cytotoxic drug in vivo.

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

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

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

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

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

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

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

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

184 s with low REST score were more sensitive to cytotoxic drugs including Mitomycin, Camptothecin and Ci

185 death (ICD) is the process by which certain cytotoxic drugs induce apoptosis of tumor cells in a man

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

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

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

189 tep in programmed cell death (apoptosis) and cytotoxic drug-induced apoptosis is mediated by caspase

190 terference decreases IL-6-induced effects on cytotoxic drug-induced caspase activation and apoptosis.

191 17beta-Estradiol (E(2)) hinders cytotoxic drug-induced cell death in estrogen receptor-p

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

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

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

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

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

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

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

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

200 1, a platinum-based two-drug combination of cytotoxic drugs is recommended.

201 kground Transarterial chemoembolization with cytotoxic drugs is standard treatment for unresectable i

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

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

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

205 rised of a monoclonal antibody tethered to a cytotoxic drug (known as the payload) via a chemical lin

206 est in the use of 17-AAG in combination with cytotoxic drugs led us to study both GA and 17-AAG with

207 lls susceptible to apoptosis by cytokines or cytotoxic drugs, likely due to its effects on NF-kappaB.

208 ng characteristics compared with traditional cytotoxic drugs, making it possible to estimate the stea

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

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

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

212 th a decrease in net production of bystander cytotoxic drug metabolites because of accelerated death

213 rolong localized, intratumoral production of cytotoxic drug metabolites without inducing tumor cell d

214 alkylating agents, such as the mutagenic and cytotoxic drug N-methyl-N'-nitro-N-nitrosoguanidine (MNN

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

216 ess toxic than the broadly antiproliferative cytotoxic drugs of the previous era, which still dominat

217 -toxicity antibiotic with a standard-of-care cytotoxic drug, offering immediate applications for clin

218 The influences of cytotoxic drugs on endothelial cells remain incompletely

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

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

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

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

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

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

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

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

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

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

229 umber of regimens, and fail to fully capture cytotoxic drug pharmacodynamics and pharmacokinetic vari

230 eing investigated and include biological and cytotoxic drugs, phototherapy, and monoclonal antibodies

231 PSMA-producing cells can be used to deliver cytotoxic drugs, protein toxins, and viruses selectively

232 monoclonal antibodies with chemotherapeutic cytotoxic drugs provides clinical benefit to patients wi

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

234 ne, has an established role as a mediator of cytotoxic drug resistance in acute myeloid leukemia (AML

235 link between mismatch repair deficiency and cytotoxic drug resistance.

236 ates many cellular processes contributing to cytotoxic drug resistance.

237 r DNA targeting chemotherapeutics and reduce cytotoxic drug resistance.New generation antibiotics suc

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

239 confer intrinsic resistance, and exposure to cytotoxic drugs select for the survival of these cells t

240 his panel of EBVs and challenge with various cytotoxic drugs showed that EBNA3A and EBNA3C cooperate

241 Antibody-drug conjugate (ADC) which delivers cytotoxic drugs specifically into targeted cells through

242 s subcellular sequestration of intracellular cytotoxic drugs such as cis-diaminedichloroplatinum II (

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

244 evidence suggests that one mechanism whereby cytotoxic drugs, such as doxorubicin, kill tumors is the

245 er genes and had a greater capacity to expel cytotoxic drugs, such as mitoxantrone, resulting in bett

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

247 ls as a tolerance response to routinely used cytotoxic drugs, such as taxanes, activated a metabolic

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 are mechanistically distinct from c

255 Cytotoxic drugs that cause CIPN exert their effects by i

256 RPGN benefits from high-dose steroids and cytotoxic drug therapy with the addition of plasma excha

257 s exhibit higher resistance to rituximab and cytotoxic drugs, these clones can be chemosensitized fol

258 ability of liposome particles containing the cytotoxic drug to cross the placenta.

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 based on the nonselective bioconjugation of cytotoxic drugs to lysine and cysteine residues.

268 rapy is currently shifting from broadly used cytotoxic drugs to patient-specific precision therapies.

269 ovides an opportunity to selectively deliver cytotoxic drugs to prostate cancer cells while sparing n

270 omising agents for the selective delivery of cytotoxic drugs to specific cells (for example, tumors).

271 se findings reveal that NP-based delivery of cytotoxic drugs to the alphanubeta3-positive tumor vascu

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

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

274 vercome these issues and efficiently deliver cytotoxic drugs to the tumor, we previously reported a s

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

276 lopment in the field of targeted delivery of cytotoxic drugs to tumors was not successful because the

277 d autophagy associated with sensitization to cytotoxic drug treatment in a panel of highly malignant

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

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

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

281 allow for tumor-targeted in situ delivery of cytotoxic drugs, tumor resistance to apoptosis remains a

282 s used to establish whether PCFT can deliver cytotoxic drug under pH conditions that mimic the tumor

283 ity of caged molecules, such as proteins and cytotoxic drugs, under biological conditions.

284 ation to other anti-cancer agents, including cytotoxic drugs, upregulation of immune processing and p

285 se membrane permeability, enhancing cellular cytotoxic drug uptake in tumors.

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

287 mimetic LBW242 alone or in combination with cytotoxic drugs used clinically to treat neuroblastoma.

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

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

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

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

292 ion between rhuMAb HER2 and other classes of cytotoxic drugs, we applied multiple drug effect/combina

293 ould be exploited for delivery of conjugated cytotoxic drugs, we generated an antibody-drug conjugate

294 her with TEADs prevents apoptosis induced by cytotoxic drugs, whereas YAP knockdown sensitizes CC cel

295 This observation prompted us to choose a cytotoxic drug whose activity is potentiated by cellular

296 imarily the malignant cells toward combining cytotoxic drugs with agents that interfere with the micr

297 ase I studies with single-agent molecular or cytotoxic drugs with favorable preclinical rationale and

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

299 The encapsulation of cytotoxic drugs within liposomes enhances pharmacokineti

300 ies) for the site-selective incorporation of cytotoxic drugs without loss of antigen-binding affinity