ライフサイエンスコーパス: cytotoxic agent

1 tibody conjugated to calicheamicin, a potent cytotoxic agent.

2 little activity as either an antitubulin or cytotoxic agent.

3 h inhibited when bexarotene was added to the cytotoxic agent.

4 by invading cancerous cells and releasing a cytotoxic agent.

5 oxide (UHP) is a stable form of H(2)O(2) and cytotoxic agent.

6 erapeutic potential as a tumor cell-specific cytotoxic agent.

7 n chromophore, was also found to be a potent cytotoxic agent.

8 is both glycoengineered and conjugated to a cytotoxic agent.

9 antigen with the delivery of a highly potent cytotoxic agent.

10 tibody conjugated to calicheamicin, a potent cytotoxic agent.

11 treatment with combinations of conventional cytotoxic agents.

12 ndrial priming might enhance the efficacy of cytotoxic agents.

13 gimen designed to decrease exposure to other cytotoxic agents.

14 een implicated in resistance to TRAIL and to cytotoxic agents.

15 t from the literature for several well-known cytotoxic agents.

16 tions of targeted therapies with traditional cytotoxic agents.

17 vation induced by growth factors and by some cytotoxic agents.

18 fer from those associated with cytokines and cytotoxic agents.

19 yeloma cell lines, enhancing the activity of cytotoxic agents.

20 her as a single agent or in combination with cytotoxic agents.

21 mitations associated with currently employed cytotoxic agents.

22 be involved in the resistance of BL cells to cytotoxic agents.

23 ciated with increased resistance of cells to cytotoxic agents.

24 ates are monoclonal antibodies conjugated to cytotoxic agents.

25 duce, not immunogenic, and easily coupled to cytotoxic agents.

26 ial for in vivo delivery of radioisotopes or cytotoxic agents.

27 atin and etoposide continue to be the chosen cytotoxic agents.

28 oids alone and a combination of steroids and cytotoxic agents.

29 provide a way to reduce systemic exposure to cytotoxic agents.

30 entarium has led to multiple combinations of cytotoxic agents.

31 nd conjugation of the monoclonal antibody to cytotoxic agents.

32 f which are different from those of standard cytotoxic agents.

33 the N-methylsansalvamide peptides are potent cytotoxic agents.

34 rogated by the presence of leukemia cells or cytotoxic agents.

35 hologic tissue damage through the release of cytotoxic agents.

36 nfirms that these VEGFR-2 inhibitors are not cytotoxic agents.

37 ce to structurally different antibiotics and cytotoxic agents.

38 utathione biosynthesis, is regulated by many cytotoxic agents.

39 he antiproliferative effects of conventional cytotoxic agents.

40 ng groups for intracellular cleavage of free cytotoxic agents.

41 activity of FTIs and their interactions with cytotoxic agents.

42 kely be in combination with more established cytotoxic agents.

43 s of growth factor deprivation or to various cytotoxic agents.

44 portant part of the defense of cells against cytotoxic agents.

45 se rapidly in hepatocytes exposed to broadly cytotoxic agents.

46 t affect the sensitivity of this organism to cytotoxic agents.

47 heir sensitivity to several non-DNA-damaging cytotoxic agents.

48 uman T98G glioblastoma cells to a variety of cytotoxic agents.

49 to ameliorate resistance of tumours against cytotoxic agents.

50 cts of hydrophobic bile acids and some other cytotoxic agents.

51 mination of the activity of many established cytotoxic agents.

52 R alpha/beta selective agonists with various cytotoxic agents.

53 e tumor growth and protect against damage by cytotoxic agents.

54 ducing intracellular accumulation of various cytotoxic agents.

55 r development despite wielding an arsenal of cytotoxic agents.

56 -renewal, differentiation, and resistance to cytotoxic agents.

57 ity of OVCAR8/ADR cells to Pgp-transportable cytotoxic agents.

58 r immune biomarkers of clinical responses to cytotoxic agents.

59 n combined with standard chemotherapeutic or cytotoxic agents.

60 elopment that could be applied to many other cytotoxic agents.

61 atural products that produce them are potent cytotoxic agents.

62 ed in the response of hematopoietic cells to cytotoxic agents.

63 m for SRC-3 and TRAF4-mediated resistance to cytotoxic agents.

64 (4a-g) as potential minor groove binders and cytotoxic agents.

65 on, with iron and reactive oxygen species as cytotoxic agents.

66 renders colon cancer cells more resistant to cytotoxic agents.

67 ytostatic influence of the CDK-inhibitor and cytotoxic agents.

68 s aimed at improving the efficacy of current cytotoxic agents.

69 sed for the targeted delivery and release of cytotoxic agents.

70 blocked these events in cells exposed to the cytotoxic agent 1-beta-d-arabinofuranosylcytosine (ara-C

71 own previously that the target of the potent cytotoxic agent 4-[(7-bromo-2-methyl-4-oxo-3H-quinazolin

72 role of p130(Cas) (Cas) in resistance to the cytotoxic agent Adriamycin.

73 Demonstration of long-lived cytotoxic agents after Pseudomonas infection may establi

74 l synthesis of demethyl calamenene, a potent cytotoxic agent against human adenocarcinoma A 549.

75 new compounds, BIHC was found to be the most cytotoxic agent against the HepG2 cell line while exhibi

76 (thiazol-5-yl)pyrimidin-2-amines were potent cytotoxic agents against cancer cell lines, suppressed m

77 e PARP-1 inhibitors to enhance the effect of cytotoxic agents against cancer cell lines.

78 found to be superior to the combination of a cytotoxic agent and corticosteroids.

79 ising strategy for the selective delivery of cytotoxic agents and fluorescent markers to hypoxic tiss

80 and nanomaterials have been investigated as cytotoxic agents and inhibitors, in photodynamic therapy

81 n cancer focus on novel drug combinations of cytotoxic agents and molecular targeted agents or novel

82 ovarian cancer based on drug combinations of cytotoxic agents and molecular targeted agents, delivere

83 Cancer chemotherapy has evolved from cytotoxic agents and now includes several new agents tha

84 y observed in patients with GPA treated with cytotoxic agents and should be avoided in these patients

85 ion of these agents differ from conventional cytotoxic agents and surrogate markers for inhibition of

86 n 30 months with the integration of multiple cytotoxic agents and targeted therapies.

87 ase to the use of varied hormonal analogues, cytotoxic agents and targeted therapy for the management

88 Antitumor activity of cytotoxic agents and the epidermal growth factor recepto

89 lta), or both (dph3Delta) for sensitivity to cytotoxic agents and thermal stress.

90 ly are differentially susceptible to various cytotoxic agents and treatments.

91 The tumor target, the cytotoxic agent, and the manner in which the agent is at

92 sistance, alterations in pharmacokinetics of cytotoxic agents, and clinical toxicities.

93 Corticosteroids, novel agents, conventional cytotoxic agents, and high-dose chemotherapy with autotr

94 air could affect the sensitivity of cells to cytotoxic agents, and would therefore be an important co

95 l death induced by only a selected subset of cytotoxic agents (antimicrotubule agents and a topoisome

96 ne-refractory prostate cancer, including new cytotoxic agents, antiproliferative agents, immune-based

97 The antibody and the cytotoxic agent are conjugated by means of a stable link

98 have been identified and the means by which cytotoxic agents are appended to antibodies has been gre

99 While potent cytotoxic agents are available to oncologists, the clini

100 Alternatives to cytotoxic agents are desirable for patients with HIV-ass

101 sts that the use of efaproxiral instead of a cytotoxic agent, as a radiation sensitizer, may be advan

102 w platinum compounds, new taxanes, and other cytotoxic agents, as well as non-cytotoxic compounds wit

103 produce high localized concentrations of the cytotoxic agent at the tumor site while limiting systemi

104 comparable with the most active conventional cytotoxic agents but with strikingly less toxicity.

105 loss of ovarian function due to exposure to cytotoxic agents, but GnRHa use for ovarian protection i

106 rs do not protect cancer cells from death by cytotoxic agents, but may switch drug-induced apoptosis

107 ed lavendustin A analogues, may be acting as cytotoxic agents by a mechanism involving the inhibition

108 OC144-093 had no effect on the response to cytotoxic agents by cells in vitro lacking P-gp expressi

109 16, HCT-116/VM46, resistant to many standard cytotoxic agents by means of a multiple drug resistance

110 trate that HDAC10 protects cancer cells from cytotoxic agents by mediating autophagy and identify thi

111 ans of a monoclonal antibody conjugated to a cytotoxic agent, calicheamicin.

112 cancers and consider how the use of existing cytotoxic agents can be optimised for this patient group

113 With this protocol, analogues of the cytotoxic agent chamaecypanone C have been synthesized v

114 t associated with general sensitivity to the cytotoxic agents cis-platin, placitaxel, and gemcitabine

115 ere examined in vivo after exposure to three cytotoxic agents (Cisplatin, Nitrogen Mustard and N-meth

116 molecular chaperone, induced by low doses of cytotoxic agents, clears cell debris.

117 Cisplatin is a potent cytotoxic agent commonly used for the treatment of solid

118 showed profound chemoresistance to multiple cytotoxic agents compared with adherent cultures, which

119 Distinct cytotoxic agents currently used in the oncological armam

120 b-PCL) micelles were loaded with paclitaxel (cytotoxic agent), cyclopamine (hedgehog inhibitor), and

121 rast, the putative end-point metabolite, the cytotoxic agent des-acetyl vinblastine (1b), was ineffec

122 Although 99% of trials with cytotoxic agents determined an MTD, only 64% of trials w

123 , an antibody-drug conjugate composed of the cytotoxic agent DM1 conjugated to trastuzumab via a stab

124 e, an antibody-drug conjugate comprising the cytotoxic agent DM1 linked to trastuzumab, with treatmen

125 ), an antibody-drug conjugate comprising the cytotoxic agent DM1, a stable linker, and trastuzumab, h

126 (cisplatin), targeted agents (imatinib), and cytotoxic agents (docetaxel).

127 ic amphipathic lytic peptides were chosen as cytotoxic agents due to their ability to depolarize mito

128 ading to the discovery of a number of potent cytotoxic agents (e.g., 27: GI50 = 51 nM against leukemi

129 cheduling strategies for anti-angiogenic and cytotoxic agents (either in monotherapy or in combinatio

130 improved pharmacokinetics, encapsulation of cytotoxic agents, enhanced accumulation of therapeutics

131 covery of a potent enantiospecific series of cytotoxic agents, exemplified by 4-methoxy-benzo[a]phena

132 e (6-MP) are effective immune modulators and cytotoxic agents extensively used in the treatment of au

133 vestigated, with some success, as a targeted cytotoxic agent for oncotherapy.

134 he introduction of the use of rapamycin as a cytotoxic agent for the treatment of DSRCT.

135 ld be tested in combination with traditional cytotoxic agents for recurrent and high-risk primary ped

136 optimal combinations of GSK3 inhibitors and cytotoxic agents for use in gliomas and other cancers.

137 quantities of a structurally dissimilar C30 cytotoxic agent, fredericamycin.

138 hocytes use to kill targets is exocytosis of cytotoxic agents from lytic granules, a process that req

139 ance of the availability of all three active cytotoxic agents, FU-LV, irinotecan, and oxaliplatin, on

140 4 could be enhanced by combining it with the cytotoxic agent gemcitabine.

141 The quest for markers of sensitivity to cytotoxic agents has been ongoing for decades.

142 y profile of bevacizumab in combination with cytotoxic agents has not changed significantly, there ma

143 urthin B, a potent and differentially active cytotoxic agent, has been accomplished.

144 For many years cytotoxic agents have been developed to target apoptotic

145 Recently, specific cytotoxic agents have been shown to extend survival time

146 inations of antiangiogenic agents (AAs) with cytotoxic agents have shown significant promise in cance

147 with phlebotomies (low-risk patients) and/or cytotoxic agents (high-risk patients) and antiplatelet t

148 If so, ACVP should be a cytotoxic agent if properly delivered to the cancer cell

149 Malignant cells may evade death from cytotoxic agents if they are in a dormant state.

150 istant prostate cancer (CRPC), including new cytotoxic agents, immune-based therapies, circulating tu

151 gher activity as a microtubule inhibitor and cytotoxic agent in comparison with the parent structure.

152 nitric oxide (NO), a signaling molecule and cytotoxic agent in higher organisms.

153 NO is an essential cytotoxic agent in host defense, yet can be autotoxic if

154 chemotherapy was manageable and typical of a cytotoxic agent in patients with acute leukemia.

155 ining a putative antiangiogenic agent with a cytotoxic agent in patients with primary brain tumors.

156 the surface of cancer cells, but release the cytotoxic agent in the cytoplasm.

157 e by producing a higher concentration of the cytotoxic agent in the tumors.

158 ance, anti-recombination, and sensitivity to cytotoxic agents in a dam mutant background.

159 NX1 was upregulated posttranscriptionally by cytotoxic agents in C57BL/6 mice in vivo and hematopoiet

160 roenvironment for enhancement of efficacy of cytotoxic agents in cancer therapy.

161 makes caspase-8/9 activities susceptible to cytotoxic agents in glioma cells and that PTP1B plays a

162 preferred end point for phase III trials of cytotoxic agents in HRPC.

163 agents might potentially replace traditional cytotoxic agents in lymphoma.

164 is induced by interferon-beta (IFN-beta) and cytotoxic agents in NIH-OVCAR-3 ovarian carcinoma cells.

165 sensitive test to assess the activity of new cytotoxic agents in phase II studies.

166 th while continually producing and releasing cytotoxic agents in situ.

167 demonstrating relative resistance to 70,000 cytotoxic agents in the NCI-ACDS being characterized by

168 e been used as gene delivery vehicles and as cytotoxic agents in their own right by selective replica

169 of novel angular benzophenazines were potent cytotoxic agents in these cell lines and may be able to

170 increased the sensitivity of B-ALL cells to cytotoxic agents in vitro by promoting apoptosis, and de

171 for CPT sensitivity, but not for many other cytotoxic agents, in non-S-phase cells.

172 Other active cytotoxic agents include doxorubicin, ifosfamide, and da

173 nses 6 h following treatment with a range of cytotoxic agents including gamma-irradiation, cisplatin,

174 Patients had been administered various cytotoxic agents, including alkylating agents (240 patie

175 t in LNCaP) cells led to their resistance to cytotoxic agents, including docetaxel, mitoxantrone, eto

176 CLU is upregulated after exposure to various cytotoxic agents, including ionizing radiation (IR), lea

177 (Pgp) is an ATPase efflux pump for multiple cytotoxic agents, including vinblastine and colchicine.

178 tance to reactive oxygen species-induced and cytotoxic agent-induced stress by attenuating activation

179 ising strategy for cancer therapy, as direct cytotoxic agents, inducers of antitumor immune responses

180 r functions, including resistance to several cytotoxic agents, iron homeostasis, and porphyrin transp

181 etylated lysine group to puromycin, a masked cytotoxic agent is created, which is serially activated

182 Resistance to cytotoxic agents is a major limitation for their clinica

183 ) the nonmyeloablative regimen together with cytotoxic agents is currently used especially for elderl

184 The usefulness of novel immunotherapies and cytotoxic agents is difficult to ascertain because of th

185 se of estramustine in combination with other cytotoxic agents is not recommended.

186 cells to this class of potent small molecule cytotoxic agents is presented.

187 reason, and cytoablation with irradiation or cytotoxic agents is routinely used with the belief that

188 f cryptophycin 52 (2), an exceedingly potent cytotoxic agent, is described.

189 lass of therapeutics, consisting of a potent cytotoxic agent linked covalently to an antibody or anti

190 ibitor that targets endothelial cells with a cytotoxic agent may be a useful therapeutic approach.

191 This gender difference in sensitivity to cytotoxic agents may be generalized to nonneuronal cells

192 gly, therefore, the toxicity of targeted and cytotoxic agents may differ in both clinical and radiolo

193 ways of combining antiangiogenic agents with cytotoxic agents may lead to more effective and tolerabl

194 -maytansine (DM1), a potent antimicrotubular cytotoxic agent, may provide targeted delivery of the dr

195 ked or conjugated to radioactive isotopes or cytotoxic agents, may prove useful in the therapy of inf

196 outcomes comparable with those that tested a cytotoxic agent (median RR, 5.1% [95% CI, 4.3%-6.0%] vs

197 We suggest criteria by which a cytotoxic agent might reasonably be considered to have m

198 cell is controlled by periodic addition of a cytotoxic agent, mitomycin C.

199 these activities by conjugating to cAC10 the cytotoxic agent monomethyl auristatin E (MMAE) to create

200 activity in vitro, were conjugated with the cytotoxic agents monomethyl auristatin E (MMAE) or monom

201 otein scaffold (Fcmu) and linked it with the cytotoxic agent monomethylauristatin F.

202 evelop frequently in relapsed neuroblastoma, cytotoxic agents more sensitive to mutant p53 might be m

203 DNA-based cytotoxic agents: Nanopores composed of folded DNA featu

204 among the top 0.1% most cell line selective cytotoxic agents of 37, 000 molecules tested against the

205 ould not be observed with a variety of other cytotoxic agents of diverse function.

206 ng 2-deoxyglucose (2DG), in combination with cytotoxic agents on the induction of immunogenic cell de

207 not provide additional benefit compared with cytotoxic agents on their own.

208 velopment of early tumors and the effects of cytotoxic agents on tumors in vitro.

209 In KB 3-1 or Jurkat cells treated with cytotoxic agents or C6-ceramide, TcapQ647 detected apopt

210 is effect was not seen in cells treated with cytotoxic agents or unrelated inhibitors.

211 Initiation of anti-TNFalpha therapy, cytotoxic agents other than methotrexate (MTX), noncytot

212 ed by 2, and it increased the potency of the cytotoxic agents paclitaxel and 5-fluorouracil when give

213 on of HDAC1 in cancer cells treated with the cytotoxic agent parthenolide.

214 response, where activated microglia and its cytotoxic agents play a crucial pathologic role.

215 litaxel and carboplatin, addition of a third cytotoxic agent provided no benefit in PFS or OS after o

216 s that can predict response to commonly used cytotoxic agents provides opportunities to better use th

217 The 2,4'- and 4,4'-linked variants of the cytotoxic agent secalonic acid A and their analogues hav

218 Local iontophoretic delivery of cytotoxic agents should be considered for the treatment

219 rapy is utilization of antibodies to deliver cytotoxic agents specifically to antigen-expressing tumo

220 neered peptidyl pro-drug will release active cytotoxic agent strictly within the microenvironment of

221 In comparison to a standard cytotoxic agent such as doxorubicin (GI50 = 45.3 nM), 3

222 ate that in contrast to certain conventional cytotoxic agents such as ara-C, overexpression of Bcl-2

223 vels may be modest surrogates of response to cytotoxic agents such as docetaxel, but have not been va

224 rostate cancer, alone or in combination with cytotoxic agents such as docetaxel, or in other combinat

225 is exocytosis of lytic granules that contain cytotoxic agents such as perforin and granzyme.

226 rgets is exocytosis of granules that contain cytotoxic agents such as perforin and granzymes.

227 es, but did not affect the response to other cytotoxic agents such as TRAIL, etoposide, and cyclohexi

228 l line is deficient for apoptosis induced by cytotoxic agents such as UV, staurosporine, and thapsiga

229 ich N-type cells die in response to specific cytotoxic agents (such as cisplatin and doxorubicin) com

230 MCF-7/DX1 cells when co-administered with a cytotoxic agent, such as doxorubicin.

231 d in pG1 and further in pG1-S in response to cytotoxic agents, such as the proteasome inhibitor borte

232 Poor delivery and systemic toxicity of many cytotoxic agents, such as the recent promising combinati

233 baseline conditions, i.e. in the absence of cytotoxic agent, suggesting that tryptase has a homeosta

234 tivity of certain resistant strains to other cytotoxic agents suggests that our findings may point to

235 doxorubicin and salinomycin (a CSC-selective cytotoxic agent) synergized to kill cells expressing LMW

236 nt oral in vivo efficacy in potentiating the cytotoxic agent temozolomide in a B16F10 murine melanoma

237 port of GSH likely makes it a more effective cytotoxic agent than an inhibitor with a single mode of

238 tubulin polymerization and less active as a cytotoxic agent than tasidotin, cemadotin, and dolastati

239 Calicheamicin is a potent cytotoxic agent that causes double-strand DNA breaks, re

240 initially identified as a melanoma-specific cytotoxic agent that exhibits low toxicity in animal mod

241 Cisplatin is a potent cytotoxic agent that functions as a bivalent electrophil

242 P3A7*1C allele, treatment of patients with a cytotoxic agent that is a CYP3A substrate, and clinical

243 Therefore, arming T cells with a cytotoxic agent that is capable of killing cancer cells

244 lated apoptosis-inducing ligand (TRAIL) is a cytotoxic agent that preferentially induces apoptosis in

245 ylase inhibitors may enhance the efficacy of cytotoxic agents that act by targeting DNA.

246 highly potent compounds could yield targeted cytotoxic agents that are effective treatments for many

247 recently, almost all cancer drugs were crude cytotoxic agents that discriminate poorly between cancer

248 hat the strategy of combining tumor-specific cytotoxic agents that function by differing mechanisms c

249 iviticin aglycon [aka: (-)-MK7-206, (3)] are cytotoxic agents that induce double-strand breaks (DSBs)

250 K-H deficient cells were hypersensitive to cytotoxic agents that induce DSBs, unable to reseal comp

251 capping components can be used to screen for cytotoxic agents that specifically target the fungal cap

252 baseline apoptosis, or sensitivity to other cytotoxic agents that target the mitochondria, cytoskele

253 If patients were receiving cytotoxic agents, the dosage was not increased.

254 r, the in vivo administration of the hypoxic cytotoxic agent tirapazamine exhibited selective toxicit

255 B-CLL) were resistant to the novel selective cytotoxic agent, TNF-related apoptosis-inducing ligand (

256 matory agents, disease-modifying agents, and cytotoxic agents to address the extraglandular manifesta

257 ribed among the top 0.1% most-cell-selective cytotoxic agents to be evaluated in the NCI 60 cell line

258 ly be used in synergy with more conventional cytotoxic agents to bring about more immediate responses

259 y-drug conjugates that deliver highly potent cytotoxic agents to cancer cells for cancer therapy, we

260 the benefit of antibody-targeted delivery of cytotoxic agents to cancer cells.

261 ll-molecule inhibitors of IDO cooperate with cytotoxic agents to elicit regression of established tum

262 apidly screen radiopharmaceuticals and other cytotoxic agents to formulate more effective cocktails f

263 tibodies (MAbs) for their ability to deliver cytotoxic agents to infected or Env-transfected cells, w

264 The precise targeting of cytotoxic agents to specific cell types or cellular comp

265 rexpression in GB tumors as a way to deliver cytotoxic agents to the glioma cells remaining after sur

266 e used for the selective pharmacodelivery of cytotoxic agents to the neoplastic mass.

267 to facilitate specific killing by confining cytotoxic agents to the synaptic cleft.

268 ternative approach is to selectively deliver cytotoxic agents to the tumor site.

269 Conjugation of cytotoxic agents to these nnAAs, yields homogeneous anti

270 Nanomedicines that preferentially deploy cytotoxic agents to tumors and molecular targeted therap

271 ssociated antigens have been used to deliver cytotoxic agents to tumour cells.

272 Targeted delivery of cytotoxic agents to tumours is believed to improve both

273 (NPC) expressing a secretable variant of the cytotoxic agent tumor necrosis factor-related apoptosis

274 thylating agent, and cytarabine, a frontline cytotoxic agent used in the treatment of AML, either alo

275 Genomic mutations caused by cytotoxic agents used in cancer chemotherapy may cause s

276 Traditional cytotoxic agents used in cancer therapy were initially d

277 he impact of RB depletion on the response to cytotoxic agents used to treat advanced disease.

278 o not confer resistance to several important cytotoxic agents used to treat neuroblastoma, we explore

279 cells by extruding a variety of amphipathic cytotoxic agents using energy from ATP hydrolysis.

280 ty of EGFR x c-MET bsAbs with the potency of cytotoxic agents via bispecific antibody-toxin conjugati

281 e development of peptidyl conjugate 5 of the cytotoxic agent vinblastine (1), along with the results

282 able but insignificant case cohort use among cytotoxic agents was found for exposure to cyclophospham

283 Using X-irradiation as a model cytotoxic agent we investigated whether keratinocyte gro

284 when antiangiogenic agents are combined with cytotoxic agents, we explored the clinical activity of t

285 tion strains are cross-resistant to selected cytotoxic agents whereas hypersensitive to others.

286 inhibition of PKCzeta converted TCDC into a cytotoxic agent, whereas overexpression of wild-type PKC

287 itional phase I, II, and III trials used for cytotoxic agents (which typically shrink tumors and in a

288 Thus, 9 may represent a promising cytotoxic agent, which is worthy of being further develo

289 eavage reaction intermediate is exploited by cytotoxic agents, which have important applications as a

290 ated with significantly poorer outcomes than cytotoxic agents, which in turn were worse than personal

291 ifferent mechanism of action than do classic cytotoxic agents, which predominantly attack rapidly pro

292 sensitivity of the deletion strains to other cytotoxic agents, which resulted in different drug-speci

293 er chemotherapy heavily relies on the use of cytotoxic agents, which typically do not preferentially

294 sphenazine anticancer drug MLN944 is a novel cytotoxic agent with exceptional anti-tumor activity aga

295 Bendamustine is a unique cytotoxic agent with structural similarities to alkylati

296 potent tubulin polymerization promoters and cytotoxic agents with (12R,13S,15S)-cyclopropyl 5-methyl

297 These compounds were potent cytotoxic agents with IC(50) values in the low micromola

298 compounds resulted in the identification of cytotoxic agents with potent activity toward both the Y7

299 ined tirapazamine (TPZ), a hypoxia-activated cytotoxic agent, with hepatic artery ligation (HAL), whi

300 play a unique role in general resistance to cytotoxic agents, with the cell lines demonstrating rela