ライフサイエンスコーパス: antitumor drug

1 ovaquone (ATO) recently was repurposed as an antitumor drug.

2 ke activity was the only one affected by the antitumor drug.

3 ctive recognition of 6-thioguanine (6TG), an antitumor drug.

4 c, and this feature prevents its usage as an antitumor drug.

5 ery of 5-fluorouracil, an important systemic antitumor drug.

6 alkaloid (MIA) used to produce semisynthetic antitumor drugs.

7 is potentially a highly selective target for antitumor drugs.

8 including 2-chloroethyl-N-nitrosourea-based antitumor drugs.

9 ivity and the effectiveness of this class of antitumor drugs.

10 lar model for the study of the action of new antitumor drugs.

11 the design of a new generation of potential antitumor drugs.

12 f DNA are in clinical use as antibiotics and antitumor drugs.

13 ungal, antiparasitic, immunosuppressive, and antitumor drugs.

14 ecrease the uptake and, thus, the effects of antitumor drugs.

15 ients and hence may increase the delivery of antitumor drugs.

16 cent interest as potential antiprotozoal and antitumor drugs.

17 ll-division molecules for the development of antitumor drugs.

18 athway and is a target for antimalarials and antitumor drugs.

19 insights into the treatment efficacy of new antitumor drugs.

20 tribute to the cell-wide effects of platinum antitumor drugs.

21 promising target for the development of new antitumor drugs.

22 g chemosensitivity of cancer cells to common antitumor drugs.

23 anism of DNA damage within this new class of antitumor drugs.

24 bility that ADAM9 might be a good target for antitumor drugs.

25 t have a mode of action different from known antitumor drugs.

26 cells by ionizing radiation or radiomimetic antitumor drugs.

27 MMR also modulates sensitivity to other antitumor drugs.

28 selectivity, and to identify new targets for antitumor drugs.

29 Unlike conventional antitumor drugs, 3 micro M DCB-3503 did not cause DNA br

30 The antitumor drug 5-fluoro-2'-deoxyuridine (FdUrd) also sen

31 ut also as a stimulus to activate release of antitumor drugs, achieving enhanced efficacy through the

32 The antitumor drug aclacinomycin A is a representative membe

33 The antitumor drug aclacinomycin A was previously shown to i

34 Many currently used antitumor drugs act by damaging DNA, and DNA repair ofte

35 ther, these data elucidate a novel basis for antitumor drug action: induction in sensitive cells of a

36 sis-inducing ligand (TRAIL) is a mediator of antitumor drug activity and in itself is a promising age

37 microenvironment, which can profoundly alter antitumor drug activity.

38 The antitumor drug adozelesin is a potent cytotoxic DNA-dama

39 Reaction of the anthracycline, antitumor drugs adriamycin and daunomycin with the self-

40 e as a promising new type of mechanism-based antitumor drug, also for the treatment of hyperprolifera

41 Etoposide, a widely used antitumor drug and a topoisomerase II inhibitor, is a pr

42 acids have been among the first targets for antitumor drugs and antibiotics.

43 s a suitable target for specific delivery of antitumor drugs and diagnostic agents due to its overexp

44 nificant obstacle for the biodistribution of antitumor drugs and immune cells.

45 air system in the cytotoxic effects of these antitumor drugs and may have ramifications for their cli

46 Many antitumor drugs and physiological stresses are known to

47 als combining autophagy-blocking agents with antitumor drugs and radiation.

48 o may respond favorably, selecting effective antitumor drugs, and balancing drug efficacy and toxicit

49 tant drugs, including anti-HIV therapeutics, antitumor drugs, antibiotics, antihypertensives, and ant

50 tant drugs, including anti-HIV therapeutics, antitumor drugs, antibiotics, antihypertensives, and ant

51 tant drugs, including anti-HIV therapeutics, antitumor drugs, antibiotics, antihypertensives, and ant

52 nt anionic drugs, including antiviral drugs, antitumor drugs, antibiotics, antihypertensives, and ant

53 mpounds that offer potential applications as antitumor drugs, based on the ability of some members of

54 ls revealed limitations of aphidicolin as an antitumor drug because of its low solubility and fast cl

55 rs are currently in human clinical trials as antitumor drugs because of their ability to induce cell

56 vious well-defined dendrimers to deliver the antitumor drug betulinic acid (BA) and paclitaxel (PDCM@

57 ion chemistry of the iron(II) complex of the antitumor drug bleomycin has been extensively investigat

58 The antitumor drug bleomycin produces exclusively OAS in the

59 es in the repair of DNA damage caused by the antitumor drug bleomycin, but the lesion(s) recognized b

60 Doxorubicin (DOX) is a widely used antitumor drug, but its application is limited because o

61 The antitumor drug camptothecin (CPT) and its analogs inhibi

62 topoisomerase I (top I) is the target of the antitumor drug camptothecin (CPT) and its analogs.

63 A topology and is the cellular target of the antitumor drug camptothecin (Cpt).

64 complex that is reversibly stabilized by the antitumor drug, camptothecin (CPT).

65 Herein, to identify new potent G4 binders as antitumor drug candidates, we have targeted a 24-nt G4-f

66 the DNA-cleaving properties of this class of antitumor drug candidates.

67 t a promising class of natural product-based antitumor drug candidates.

68 Interstrand cross-linking studies with the antitumor drug cis-diamminedichloroplatinum(II) and its

69 The broadly prescribed antitumor drug cisplatin coordinates to DNA, altering th

70 netics for the monofunctional binding of the antitumor drug cisplatin, cis-diamminedichloroplatinum(I

71 ds specifically to DNA adducts formed by the antitumor drug cisplatin.

72 e treated with a combination of antibody and antitumor drugs, cisplatin or doxorubicin.

73 ared favorably with those of the established antitumor drugs, cyclophosphamide, mitomycin C, and the

74 the biosynthesis of the clinically valuable antitumor drugs daunorubicin (DNR) and doxorubicin (DXR)

75 This report provides the first evidence that antitumor drugs delivered by sterically stabilized lipos

76 HU nanodrugs are a promising multifunctional antitumor drug delivery system.

77 The cytotoxicity of several important antitumor drugs depends on formation of the covalent top

78 D2-selective agents are valid candidates for antitumor drug design for pediatric malignancies driven

79 athway and, as such, has been the target for antitumor drug design.

80 n-protein interactions involving PKCiota for antitumor drug development and provide proof of concept

81 of HIF-1 is one of the molecular targets for antitumor drug discovery.

82 The antitumor drug ditercalinium is a rare example of a nonc

83 The anthracycline antitumor drug doxorubicin (DOX) has been utilized for d

84 A172R exhibited cross-resistance to the antitumor drug doxorubicin and heavy metal sodium arsena

85 cent discovery that the clinically important antitumor drugs doxorubicin and daunorubicin alkylate DN

86 The anthracycline antitumor drug, doxorubicin (DOX), has long been used as

87 oocytes exposed to therapeutic levels of the antitumor drug, doxorubicin (DXR), undergo apoptosis; ho

88 olved in breast tumor progression as well as antitumor drug effects as a function of tumor progressio

89 e, holding forth the possibility of improved antitumor drug efficacy.

90 terologous production of the semisynthesized antitumor drug epidoxorubicin.

91 EPR signal of phenoxyl radical of a phenolic antitumor drug, etoposide, in the absence of the OR.

92 d compounds provides considerable promise as antitumor drugs for the treatment of advanced prostate c

93 e, may decrease the effectiveness of 5-FU an antitumor drug in carriers.

94 trials to determine its potential use as an antitumor drug in humans.

95 eration, tumor growth and chemoresistance to antitumor drugs including the EGFR-targeting monoclonal

96 ptosis by sublethal-dose single and combined antitumor drugs, including geldanamycin, PS-341, Trichos

97 model system, we have previously shown that antitumor drug-induced cleavage complexes block replicat

98 -acetic acid (FAA; [Flavonoid]), an adjuvant antitumor drug, inhibits ristocetin-induced aggregation

99 Poor penetration of antitumor drugs into the extravascular tumor tissue is o

100 process, and effective targeted delivery of antitumor drugs is demonstrated.

101 g ligand (TRAIL) receptor-targeted agents as antitumor drugs is the evolution of resistance, a common

102 group in hydroxymethylacylfulvene, a potent antitumor drug, is readily replaced by thiols including

103 Cancer cells exposed to antitumor drugs may be directly induced to express a sub

104 s microorganism from its own antibiotic, the antitumor drug mitomycin C.

105 Further analysis finds the antitumor drug pacilitaxel (TaxotereR) to reduce flexibi

106 The antitumor drug paclitaxel (Taxol) has been demonstrated

107 t of ovarian carcinomas with the antimitotic antitumor drug paclitaxel is highly efficacious.

108 To understand how antitumor drugs prevent neurodegeneration, here we use s

109 Primary end points were the number of antitumor drug-related problems (ie, side effects and un

110 Antitumor drug-related problems were significantly lower

111 icate that the cascade of ROS generation and antitumor-drug release can effectively inhibit tumor gro

112 , GGTIs could be valuable agents to overcome antitumor drug resistance.

113 erapeutic response of xenografts and measure antitumor drug responses in human tumor-derived organoid

114 (iii) strengths and weaknesses of the NCI's antitumor drug screen data for assigning compounds to th

115 the complete set of NCI's publicly available antitumor drug-screening data.

116 ause cleavage of DNA exposed to the enediyne antitumor drugs, should allow tuning of the reactivity o

117 First, we review experiments involving antitumor drug-stabilized topoisomerase cleavage complex

118 exposure to alkylnitrosamines and alkylating antitumor drugs such as 2-chloroethyl-N-nitrosourea (CNU

119 Of particular importance is the fact that antitumor drugs such as Actinomycin D can selectively bi

120 nificantly enhance the tumoricidaleffects of antitumor drugs such as paclitaxel (Taxol) in patients w

121 ucturally diverse topoisomerase II-targeting antitumor drugs such as VM-26, doxorubicin, m-AMSA, and

122 hypoxic solid tumors resist treatment using antitumor drugs (such as doxorubicin, DOX), owing to the

123 development of a new generation of selective antitumor drugs suppressing efficiently the proliferatio

124 The antitumor drug Taxol stabilizes microtubules and reduces

125 Taxol 2'-acetate, an analog of the antitumor drug taxol, displays no significant in vitro m

126 Three new pathways to the antitumor drug temozolomide (4) have been explored via i

127 th triggered by doxorubicin (DOX, 1 mum), an antitumor drug that can cause heart failure.

128 Bortezomib is an antitumor drug that competitively inhibits proteasome be

129 Thus, an antitumor drug that damages DNA can induce an abnormal r

130 d or third) therapy was defined as use of an antitumor drug that was not part of the previous regimen

131 Bizelesin and adozelesin are DNA-reactive antitumor drugs that alkylate adenines at the 3' ends of

132 Geldanamycins (GA) are antitumor drugs that bind and inhibit HSP90 chaperone ac

133 erase inhibitors (FTIs) are a novel class of antitumor drugs that block the oncogenic activity of Ras

134 itinated and destroyed in cells treated with antitumor drugs that block the religation step of the TO

135 and its role in determining the efficacy of antitumor drugs that damage DNA, we examined the effects

136 prominent member of a series of platinum(II) antitumor drugs that demonstrate activity based on bindi

137 cleavage contributes to the cytotoxicity of antitumor drugs that target DNA topoisomerases.

138 potential of the new compounds as prototype antitumor drugs that would downregulate HSP90 and AR in

139 esence of a topoisomerase cleavage site, the antitumor drug, the type II topoisomerase, and a T4 repl

140 to increase tumorigenicity and resistance to antitumor drugs, this activity of E2 protein may be invo

141 m derivative of the active metabolite of the antitumor drug tiazofurin.

142 d in MDA-MB-231 human cells treated with the antitumor drug tirapazamine (TPZ; much more Polbeta-DPC

143 t that the administration of hydroxyurea, an antitumor drug, to rats at pharmacological doses formed

144 lision of an active replication fork with an antitumor drug-trapped cleavage complex.

145 The anthracycline class of antitumor drugs undergoes redox cycling in living cells

146 The cellular targets for estramustine, an antitumor drug used in the treatment of hormone-refracto

147 the antimitotic mechanisms of action of the antitumor drugs vinblastine and taxol, the antimitotic m

148 t autophagy may also mediate the toxicity of antitumor drugs while evidence also exists for a nonprot

149 at ARC-111 is a promising new TOP1-targeting antitumor drug with a different drug resistance profile

150 alent lead ZD-4, which was developed from an antitumor drug ZD6474 (Vandetanib) with combined hybrid