ライフサイエンスコーパス: antitumor drug

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

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

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

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

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

6 is potentially a highly selective target for antitumor drugs.

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

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

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

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

11 cent interest as potential antiprotozoal and antitumor drugs.

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

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

14 insights into the treatment efficacy of new antitumor drugs.

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

16 promising target for the development of new antitumor drugs.

17 g chemosensitivity of cancer cells to common antitumor drugs.

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

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

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

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

22 cells by ionizing radiation or radiomimetic antitumor drugs.

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

24 MMR also modulates sensitivity to other antitumor drugs.

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

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

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

28 The antitumor drug aclacinomycin A is a representative membe

29 The antitumor drug aclacinomycin A was previously shown to i

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

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

32 microenvironment, which can profoundly alter antitumor drug activity.

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

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

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

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

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

38 Many antitumor drugs and physiological stresses are known to

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

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

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

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

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

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

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

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

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

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

49 The antitumor drug bleomycin produces exclusively OAS in the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

95 The antitumor drug paclitaxel (Taxol) has been demonstrated

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

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

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

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

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

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

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

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

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

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

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

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

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

109 The antitumor drug Taxol stabilizes microtubules and reduces

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

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

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

113 Bortezomib is an antitumor drug that competitively inhibits proteasome be

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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