ライフサイエンスコーパス: VP-16

1 nts such as doxorubicin (Dox) and etoposide (VP-16).

2 h chemotherapeutic agents (i.e. cisplatin or VP-16).

3 A-topoII complex-stabilizing drug etoposide (VP-16).

4 5 (doxorubicin), 10 (topotecan), and 150 nM (VP-16).

5 s and confers hypersensitivity to etoposide (VP-16).

6 compared with the prototype drug etoposide (VP-16).

7 sence of the clinical Topo IIalpha inhibitor VP-16.

8 le clones from parental cells by exposure to VP-16.

9 tration of repeated courses of low-dose oral VP-16.

10 to the Topo IIalpha inhibitors ICRF-193 and VP-16.

11 c agents and schedules, including parenteral VP-16.

12 s of the DNA-damaging agents mitomycin C and Vp-16.

13 main of human beta-catenin was stronger than VP-16.

14 ere observed in resistant cells treated with VP-16.

15 mediastinal yolk sac tumor, followed by oral VP-16.

16 ected in resistant Jurkat cells treated with VP-16.

17 emic cell apoptosis when exposed to Ara-C or VP-16.

18 ross-resistant to doxorubicin, topotecan, or VP-16.

19 ptose by anti-Fas antibody, staurosporin, or VP-16.

20 nd mIkappaBalpha cells treated with SN-38 or VP-16.

21 Bcl-2 abrogated the cleavage in response to VP-16.

22 tosis but not DNA damage induced by SN-38 or VP-16.

23 of vincristine, doxorubicin, bleomycin, and VP-16 (2 g/m2 total) over 4 months, followed by 25.5 Gy

24 ek doses of cyclophosphamide (CY, 84 mg/kg), VP-16 (24 mg/kg) + cisplatinum (2.4 mg/kg), carboplatinu

25 tan in combination with high-dose etoposide (VP-16) 40 to 60 mg/kg (day -4) and cyclophosphamide 100

26 All anticancer drugs tested including VP-16 (a TOP2-directed drug), camptothecin (a topoisomer

27 ing resistance, MRP expression increased and VP-16 accumulation decreased.

28 on the transactivation functions of p53 and VP-16 activation domain.

29 patients age 4 to 16 years were treated with VP-16 after neuroradiographic and clinical evidence of t

30 JNK activation, Adriamycin, vinblastine, and VP-16 all induced MDR1 mRNA expression in KB-3 cells.

31 Treatment with vinblastine or etoposide (VP-16) also activated JNK, with maximum increases of 6.5

32 Camptothecin (CPT) and etoposide (VP-16) also markedly enhanced PKCalpha activity during a

33 latively low levels of H2O2 (75-100 microM), VP-16 and A23187 were unable to induce apoptosis in thes

34 erase II-targeting anticancer drugs, such as VP-16 and Adriamycin, but not cisplatin.

35 osis rate and enhancing their sensitivity to VP-16 and ADRIAMYCIN:

36 VP-16 and Ara-C were omitted in the face of acute myelog

37 However, the cytotoxicity of VP-16 and cisplatin was similar in both the transfected

38 ity of Bcl-XL against cell death mediated by VP-16 and cisplatin.

39 in animals treated with cyclophosphamide or VP-16 and cisplatinum.

40 to ultraviolet radiation chemotherapy (UVC), VP-16 and daunorubicin (DNR)-induced apoptosis compared

41 Of these, three responded to oral VP-16 and underwent resection of residual mediastinal, r

42 marked sensitivity to X-rays, bleomycin, and VP-16 and were more x-ray-sensitive in G(1) than late S

43 Therefore, Bax can antagonize Bcl-XL during VP-16 and, in a lesser degree, during cisplatin-induced

44 Initially, etoposide (VP-16) and cytarabine (Ara-C) pulses were included.

45 nes, increased in the presence of etoposide (VP-16) and sodium arsenite, accompanied by equivalent de

46 ent PBPC mobilization with cyclophosphamide, VP-16, and G-CSF.

47 eas the nonintercalating drugs camptothecin, VP-16, and oxolinic acid did not.

48 onse of B-lineage leukemic cells to Ara-C or VP-16, and they indicate specific molecular interactions

49 following exposure to the DNA-damaging agent VP-16, and we monitored the changes in gene expression u

50 novel DNA cleavage sites in the presence of VP-16, azatoxin, amsacrine, and mitoxantrone.

51 nt to apoptosis induced by UV, staurosporin, VP-16, bleomycin, or cisplatin.

52 tivity to conventional agents (eg, Taxol and VP-16) but significantly increased susceptibility to Chk

53 ve G2/M arrest following exposure to UVC and VP-16, but not to DNR, indicating the existence of diffe

54 The use of low-dose or oral VP-16 can be associated with the development of sAML.

55 nd was much more cytotoxic against the MCF-7/VP-16 cell line than was doxorubicin.

56 activity of a constitutively active RARgamma-VP-16 chimeric receptor by the inverse agonist AGN193109

57 ed by doxorubicin, topotecan, and etoposide (VP-16) could elicit a similar cytotoxic response in TS-

58 VP-16 cytotoxicity in transformed cells expressing both

59 pH, like the topoisomerase II (TOP2) poison VP-16 (demethylepipodophyllotoxin ethylidene-beta-D-gluc

60 One cluster (Cluster A) revealed a VP-16-dependent but Myc-independent induction of a set o

61 DQ3.2 molecule regulated binding of an HSV-2 VP-16-derived peptide.

62 Cells killed with H(2)O(2) (with or without VP-16) do ultimately undergo phagocytosis, but this occu

63 opoisomerase II (Top2), including etoposide (VP-16), doxorubicin, and mitoxantrone, are among the mos

64 e ability of 4 different chemotherapy drugs (VP-16, doxorubicin, cisplatin, and AraC) to induce apopt

65 ment of cells with the chemotherapeutic drug VP-16 dramatically reduced E6 and increased p53 levels.

66 ulation of cytarabine (Ara-C) and etoposide (VP-16) efficacy by bone marrow stromal cells in vitro wa

67 ase inhibitors, before exposing the cells to VP-16, ellipticine, camptothecin, doxorubicin, cisplatin

68 or SAHA increased the killing efficiency of VP-16, ellipticine, doxorubicin, and cisplatin.

69 x-stabilizing DNA-topo II inhibitors such as VP-16 (etoposide) has been partially elucidated, the cyt

70 VP-16 (etoposide) has recently been shown to induce topo

71 ese cells, the sensitivity of these cells to VP-16 (etoposide) was enhanced 18-fold and to Adriamycin

72 o test this hypothesis, the anticancer drug, VP-16 (etoposide), was employed to induce TopII-DNA cova

73 xic damage induced by ionizing radiation and VP-16/etoposide.

74 ore, the Myc level dropped sharply following VP-16 exposure, which varied inversely with the inductio

75 viability of leukemic cells during Ara-C and VP-16 exposure.

76 AML, especially those receiving priming with VP-16 for peripheral stem cell collection.

77 However, patients who had been primed with VP-16 for stem cell mobilization were at a 12.3-fold inc

78 studies of the antitumor compound etoposide (VP-16) have suggested that replacement of the glycoside

79 Indiana University, we recommend etoposide (VP-16), ifosfamide and cisplatin (VIPx4) instead of bleo

80 ectively, with a 24-hr exposure to 30 microM VP-16 in attached cell populations.

81 s displayed greater or comparable potency to VP-16 in cell growth-inhibition studies and were less af

82 Z-VAD-FMK did not rescue cells treated with VP-16 in contrast to treatment with CH-11 or thymineless

83 on is cell type specific and is >10-fold for VP-16 in D54, a brain tumor cell line intrinsically resi

84 nib mesylate and the topoisomerase inhibitor VP-16 in LAMA-R cells.

85 Clinicians should be cautious in the use of VP-16 in low-risk diseases.

86 s a coactivator of AP-1 and acidic activator VP-16 in mammalian cells, had no effect on the transacti

87 his report demonstrates the activity of oral VP-16 in the treatment of a small cohort of pretreated p

88 In the present report, 10 analogues of VP-16 in which the glycosidyl moiety was replaced with a

89 -chlorodeoxyadenosine (2-CDA) and etoposide (VP-16) in patients who did not respond to mitoxantrone a

90 For etoposide (VP-16), increased expression of MDR-1 or MRP and alterat

91 ppaBalpha (mIkappaBalpha) inhibited SN-38 or VP-16 induced transcription and DNA binding activity of

92 We found that etoposide (VP-16) induced apoptosis in human DU-145 prostatic carci

93 enhanced doxorubicin- (Dox) and etoposide- (VP-16) induced cytotoxicity in a subset of NB cell lines

94 Both the number of VP-16- induced DNA-topoII complexes formed and the amoun

95 Its depletion prevents UV- and VP-16-induced apoptosis and G1/S arrest in HCT116 and U2

96 reover, pretreatment with TSA also increased VP-16-induced apoptosis in a p53-dependent and -independ

97 gene clusters, however, were associated with VP-16-induced apoptosis.

98 We show here that VP-16-induced carcinogenesis involves mainly the beta ra

99 which TopIIalpha was absent, we showed that VP-16-induced DNA damage signals were attenuated upon pr

100 Furthermore, VP-16-induced DNA sequence rearrangements and double-str

101 on of the Top2beta-DNA cleavage complexes in VP-16-induced DNA sequence rearrangements.

102 Consistent with the hypothesis, VP-16-induced DSBs as monitored by neutral comet assay,

103 skin carcinogenesis model, the incidence of VP-16-induced melanomas in the skin of 7,12-dimethylbenz

104 The VP-16-induced top2(S740W) cleavage complexes were also m

105 ethyl ester produced a > 2-fold reduction in VP-16-induced TOPO II-mediated DNA cleavable complex for

106 In vitro, purified Metnase prevents VP-16 inhibition of Topo IIalpha decatenation of tangled

107 He was treated with VP-16 intravenously (IV) and orally (0.3 g and 2.8 g/m2,

108 sensitivity to staurosporine and etoposide (VP-16; intrinsic pathway agonists).

109 Etoposide (VP-16) is extensively used to treat cancer, yet its effi

110 oison SN-38 or the topo II poison etoposide (VP-16) leads to activation of NF-kappaB before induction

111 eavage-inducing inhibitors including m-AMSA, VP-16, mitoxantrone, ellipticine, and oxolinic acid.

112 doxorubicin using MCF-7-sensitive and MCF-7/VP-16 MRP-mediated multidrug-resistant cell lines.

113 cis-dichlorodiammineplatinum(II) but not to VP-16 or ionizing radiation.

114 c/mitochondrial pathways of death induced by VP-16 or staurosporin.

115 as-induced apoptosis were cross-resistant to VP-16 or staurosporin.

116 was established using the chemotherapy drug VP-16 or the calcium ionophore A23187 to induce apoptosi

117 itized TuBECs to the chemotherapeutic agents VP-16, paclitaxel, thapsigargin, and temozolomide.

118 ific cis-regulatory specificities: the HSV-1 VP-16 protein activates transcription from the HSV-1 VP1

119 VP-16 redox-cycling by purified myeloperoxidase (in the

120 Further, the selection of VP-16-resistant mitochondria via elimination of Fas-susc

121 nd > 20-fold resistant to DOX and etoposide (VP-16), respectively.

122 ntire cohort revealed stem cell priming with VP-16 (RR = 7.7, P = 0.002) to be independently associat

123 Analysis of the VP-16 sites indicated that the changes in the cleavage p

124 The reduced formation of VP-16-stabilized DNA cleavable complex in the HL-60/DOX

125 To further understand resistance to VP-16, three sublines, designated MCF-7-VP17, ZR-75B-VP1

126 required > 20-fold higher concentrations of VP-16 to produce equivalent damage to DNA.

127 tein is toxic in 293 cells, we used the tetR/VP 16 transactivator and teto minimal promoter system fo

128 ls detached from the monolayer; untreated or VP-16-treated attached cells retained a normal morpholog

129 ASSF6 depletion delays DNA repair in UV- and VP-16-treated cells and increases polyploid cells after

130 In detached VP-16-treated cells, there was accrual of 30-50-kbp DNA

131 gocytosis by monocyte-derived macrophages of VP-16-treated lymphoma cells is also inhibited by H(2)O(

132 the development of acute myeloid leukemia in VP-16-treated patients.

133 progression, indicating a synergism between VP-16 treatment and the loss of Star-PAP.

134 th MG-132, exposure to MG-132 after SN-38 or VP-16 treatment of neo or mIkappaBalpha cells decreased

135 ed cells and increases polyploid cells after VP-16 treatment.

136 s in response to either Fas-cross-linking or VP-16 treatment.

137 The accumulation of [3H]VP-16 was 2-3-fold lower in the resistant cells (HL-60/D

138 The response rate of 2-CDA/VP-16 was 8%.

139 VP-16 was administered orally as repeated 21-day courses

140 The major toxicity of oral VP-16 was hematologic, with two patients requiring plate

141 The resistance of Bak-deficient cells to VP-16 was reversed by transduction of the Bak gene into

142 This form of administration of oral VP-16 was well tolerated and produced modest toxicity.

143 merase inhibitors camptothecin or etoposide (VP-16), we find that RPA2, the middle-sized subunit of R

144 in, 0.3-3 microM topotecan, and 10-90 microM VP-16), which was caspase dependent but Fas independent.

145 utic agents, including parenteral etoposide (VP-16), who showed responses to the administration of re