ライフサイエンスコーパス: arsenic trioxide

1 feriority and P=0.02 for superiority of ATRA-arsenic trioxide).

2 s such as ATRA (all trans retinoic acid) and arsenic trioxide.

3 of the transport of the trivalent metalloid arsenic trioxide.

4 of QT prolongation in patients treated with arsenic trioxide.

5 lates induction of antileukemic responses by arsenic trioxide.

6 thmia developed while they were treated with arsenic trioxide.

7 treatment with 0.1 mg/kg per day intravenous arsenic trioxide.

8 le, and kidney were relatively unaffected by arsenic trioxide.

9 ose of (131)I-MIBG plus a 0.15 mg/kg dose of arsenic trioxide.

10 locytic leukemia that have been treated with arsenic trioxide.

11 treated with all-trans retinoic acid and/or arsenic trioxide.

12 4 or 666 MBq/kg) intravenously on day 1 plus arsenic trioxide (0.15 or 0.25 mg/m(2)) intravenously on

13 A single administration of arsenic trioxide (10 mg/kg i.p.) produced a preferential

14 We show here that arsenic trioxide (a potent inducer of apoptosis that ind

15 Importantly, addition of arsenic trioxide, a compound capable of causing reactive

16 colleagues provide preclinical evidence that arsenic trioxide, a drug FDA approved for the treatment

17 Arsenic trioxide, a drug for patients with acute promyel

18 Here we found that arsenic trioxide, a frontline agent for acute promyelocy

19 Furthermore, we found that arsenic trioxide activates the Pirh2 promoter and conseq

20 ethasone, doxorubicin, melphalan) and novel (arsenic trioxide) agents augment apoptosis induced by at

21 Itraconazole and arsenic trioxide, alone or in combination, inhibit the g

22 tly, anticancer drugs, such as cisplatin and arsenic trioxide, also induce KSHV reactivation and PEL

23 s of SIRT2 sensitized breast cancer cells to arsenic trioxide, an approved therapeutic agent, along w

24 ssential for induction of its degradation by arsenic trioxide, an effective APL treatment.

25 suggest that treatment with a combination of arsenic trioxide and imatinib can eliminate refractory M

26 ent synergistic effect of the combination of arsenic trioxide and interferon alpha (As/IFN-alpha) wit

27 Arsenic trioxide and itraconazole antagonize the hedgeho

28 Overall, arsenic trioxide and itraconazole reduced GLI1 messenger

29 Targeting the HH pathway with sequential arsenic trioxide and itraconazole treatment is a feasibl

30 Arsenic trioxide and liposomally encapsulated all-trans-

31 Arsenic trioxide and sodium arsenite did not directly mo

32 We discovered that arsenicals, including arsenic trioxide and sodium arsenite, inhibited activati

33 Arsenic trioxide and stem cell transplantation are effec

34 factors that increase the stability of ND10, arsenic trioxide and the proteasome inhibitor MG132, inh

35 hed on allogeneic stem cell transplantation, arsenic trioxide, and bortezomib for this condition.

36 including agents such as all- retinoic acid, arsenic trioxide, and inhibitors of DNA methylation and

37 IkappaB superrepressor, lactacystin, MG132, arsenic trioxide, and phenylarsine oxide reverse the pro

38 ose of (131)I-MIBG plus a 0.15 mg/kg dose of arsenic trioxide; and 3 patients received a 666 MBq/kg d

39 and are treated with a ROS-inducer, such as arsenic trioxide (ARS), N-(4-hydroxyphenyl) retinamide (

40 uisitely sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell diff

41 -terminal kinase (JNK) reciprocally regulate arsenic trioxide (arsenite)-induced, p53-independent exp

42 indings further support the use of ATRA plus arsenic trioxide as preferred first-line treatment in pa

43 Arsenic trioxide (As(2)O(3)) and gamma interferon (IFN-g

44 Exposure to a low dose (0.5 mum) of arsenic trioxide (As(2)O(3)) caused transformation of BA

45 Recent clinical data shows that arsenic trioxide (As(2)O(3)) causes remission in patient

46 Arsenic trioxide (As(2)O(3)) exhibits potent antitumor e

47 Arsenic trioxide (As(2)O(3)) has been found to induce ap

48 Arsenic trioxide (As(2)O(3)) has potent antileukemic pro

49 Arsenic trioxide (As(2)O(3)) has recently been used succ

50 Arsenic trioxide (As(2)O(3)) has shown considerable effi

51 xposed acute promyelocytic leukemia cells to arsenic trioxide (As(2)O(3)) in the presence and absence

52 Arsenic trioxide (As(2)O(3)) increased human immunodefic

53 All-trans retinoic acid (tRA) and arsenic trioxide (As(2)O(3)) induce non-cross-resistant

54 Arsenic trioxide (As(2)O(3)) induces differentiation and

55 Recent data indicate that arsenic trioxide (As(2)O(3)) induces remission of refrac

56 Arsenic trioxide (As(2)O(3)) is a highly effective treat

57 Arsenic trioxide (As(2)O(3)) is a potent inducer of apop

58 Arsenic trioxide (As(2)O(3)) is a potent inducer of apop

59 Arsenic trioxide (As(2)O(3)) is an effective agent for t

60 Arsenic trioxide (As(2)O(3)) is an effective therapeutic

61 Arsenic trioxide (As(2)O(3)) is highly effective for the

62 Arsenic trioxide (As(2)O(3)) produces dramatic remission

63 They show that the therapeutic drug arsenic trioxide (AS(2)O(3)) targets BCR-ABL for autopha

64 We provide evidence that arsenic trioxide (As(2)O(3)) targets the BCR-ABL oncopro

65 In this study, arsenic trioxide (As(2)O(3)) was shown to increase the a

66 reactive oxygen species, could be killed by arsenic trioxide (As(2)O(3)), a chemotherapeutic drug us

67 We have discovered that arsenic trioxide (As(2)O(3)), a very potent antineoplast

68 Arsenic trioxide (As(2)O(3)), an agent that accentuates

69 transduction, we investigated the effect of arsenic trioxide (As(2)O(3)), an FDA-approved chemothera

70 On the other hand, one arsenic derivative, arsenic trioxide (As(2)O(3)), has important antitumor pr

71 Positive and negative ion mass spectra of arsenic trioxide (As2O3) and arsenic pentaoxide (As2O5)

72 Inorganic arsenic trioxide (As2O3) and the organic arsenical, mela

73 vestigated the impact of tolerated and toxic arsenic trioxide (As2O3) exposure in human embryonic kid

74 The use of arsenic trioxide (As2O3) has been shown to effectively t

75 orbic acid (AA) will enhance the efficacy of arsenic trioxide (As2O3) in myeloma.

76 Arsenic trioxide (As2O3) induces clinical remission in a

77 Arsenic trioxide (As2O3) is a potent inducer of apoptosi

78 ance to imatinib would alter the efficacy of arsenic trioxide (As2O3) or 5-aza-2-deoxycytidine (decit

79 Arsenic trioxide (As2O3) treatment results in the total

80 Inorganic arsenic trioxide (As2O3) was recently shown to induce ap

81 es, and sudden death have been reported with arsenic trioxide (As2O3), a highly effective agent for a

82 (dTMP) biosynthesis is a sensitive target of arsenic trioxide (As2O3), leading to uracil misincorpora

83 er extensive prior therapy were treated with arsenic trioxide at doses ranging from 0.06 to 0.2 mg pe

84 sent studies demonstrate that treatment with arsenic trioxide (AT) lowered ectopically expressed or e

85 While arsenic trioxide (ATO) can induce remissions in 95% of r

86 determine the survival of patients receiving arsenic trioxide (ATO) consolidation and reduced doses o

87 Arsenic trioxide (ATO) has been found to be an effective

88 ation of all-trans-retinoic acid (ATRA) plus arsenic trioxide (ATO) has been shown to be superior to

89 Arsenic trioxide (ATO) has been shown to induce differen

90 Arsenic trioxide (ATO) has been successfully used as a t

91 Arsenic trioxide (ATO) has been successfully used for th

92 Arsenic trioxide (ATO) has been tested in relapsed/refra

93 combination therapy of decitabine (DAC) and arsenic trioxide (ATO) have demonstrated synergy on MDS

94 kemia clearance is different with the use of arsenic trioxide (ATO) in the treatment of APL.

95 on and more cell death than the FDA-approved arsenic trioxide (ATO) in vitro, but exhibits less syste

96 Arsenic trioxide (ATO) induces remission in 85% of adult

97 Arsenic trioxide (ATO) is a highly effective agent for t

98 Arsenic trioxide (ATO) is a potent anti-leukemic chemoth

99 ation of all- trans-retinoic acid (ATRA) and arsenic trioxide (ATO) is at least not inferior to stand

100 Arsenic in the form of arsenic trioxide (ATO) is used as a therapeutic drug for

101 combining all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) might be an alternative to ATRA +

102 We controlled the size of arsenic trioxide (ATO) nanocrystals by simply changing t

103 We have shown previously that arsenic trioxide (ATO) preferentially shutsdown tumor bl

104 Arsenic trioxide (ATO) resistance is a challenging probl

105 In this study, we present evidence that arsenic trioxide (ATO) suppresses human cancer cell grow

106 The use of arsenic trioxide (ATO) to treat multiple myeloma (MM) is

107 ated with all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) with or without gemtuzumab ozogam

108 cals active in Hh pathway antagonism include arsenic trioxide (ATO), a curative agent in clinical use

109 edgehog-pathway activity can be inhibited by arsenic trioxide (ATO), an anti-leukemia drug approved b

110 s: 5-aza-2'-deoxycytidine (DAC; decitabine), arsenic trioxide (ATO), and MS-275 [entinostat; N-(2-ami

111 e to both all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent understanding

112 ent with all-trans retinoic acid (ATRA) plus arsenic trioxide (ATO), which degrade the promyelocytic

113 ombining all-trans retinoic acid (ATRA) with arsenic trioxide (ATO).

114 ATRA), anthracycline-based chemotherapy, and arsenic trioxide (ATO).

115 Arsenic trioxide (ATO, As2 O3 ) is currently used to tre

116 Treatment with arsenic trioxide (ATO; 2-200 microM) inhibited NF-kappaB

117 other received only 6 of 10 planned doses of arsenic trioxide because of grade 3 diarrhea and vomitin

118 One did not receive arsenic trioxide because of transient central line-induc

119 Fourteen patients received (131)I-MIBG and arsenic trioxide, both at maximal dosages; 2 patients re

120 he use of all-trans-retinoic acid (ATRA) and arsenic trioxide, both of which induce degradation of th

121 of electrolytes and concomitant medications, arsenic trioxide can be safely administered in patients

122 Two reports from China have suggested that arsenic trioxide can induce complete remissions in patie

123 Low doses of arsenic trioxide can induce complete remissions in patie

124 This analysis shows that arsenic trioxide can prolong the QTc interval.

125 uencies and the combination of imatinib with arsenic trioxide cured a large fraction of mice with MPN

126 In addition, we found that arsenic trioxide decreases the stability of DeltaNp63 pr

127 We also found that arsenic trioxide decreases the stability of mutant p53 p

128 ators for signals that control generation of arsenic trioxide-dependent apoptosis and antileukemic re

129 1 and Akt2 genes, we found that induction of arsenic trioxide-dependent apoptosis is strongly enhance

130 ls before the second course, signifying that arsenic trioxide does not permanently prolong the QTc in

131 ood, Iland et al report that the addition of arsenic trioxide during induction and consolidation can

132 andomly assigned to receive either ATRA plus arsenic trioxide for induction and consolidation therapy

133 I/II study was initiated in June 1998 using arsenic trioxide for relapsed APL to determine the maxim

134 relapsed or refractory APL were treated with arsenic trioxide for remission induction at daily doses

135 ent-free survival rates were 97% in the ATRA-arsenic trioxide group and 86% in the ATRA-chemotherapy

136 Patients in the ATRA and arsenic trioxide group had significantly less requiremen

137 ubicin group and 40 patients in the ATRA and arsenic trioxide group reported grade 3-4 toxicities.

138 was achieved in all 77 patients in the ATRA-arsenic trioxide group who could be evaluated (100%) and

139 In the ATRA and arsenic trioxide group, arsenic trioxide was given intra

140 in group versus 5 (5%) of 95 in the ATRA and arsenic trioxide group, raised liver alanine transaminas

141 in group versus 2 (3%) of 77 in the ATRA and arsenic trioxide group; no other toxicities reached the

142 Arsenic trioxide had complex and TRIM5alpha-independent

143 Arsenic trioxide has also surfaced as an effective induc

144 Arsenic trioxide has been shown to be effective in treat

145 Arsenic trioxide has in vitro and in vivo radiosensitizi

146 Arsenic trioxide has shown great promise in the treatmen

147 ng bortezomib, thalidomide, lenalidomide and arsenic trioxide, have been found to block activation of

148 ng mda-7/IL-24 mRNA, a single treatment with arsenic trioxide, HPR or NSC656240 induces apoptosis, wh

149 nts undergoing assessment at present include arsenic trioxide, hsp90 inhibitors and histone deacetyla

150 r ibrutinib in chronic lymphocytic leukemia, arsenic trioxide in acute promyelocytic leukemia, and th

151 The expanded use of arsenic trioxide in APL for postremission therapy, in co

152 o use exogenous ROS-producing agents such as arsenic trioxide in combination with 2-ME to enhance the

153 ced malignancies who received 170 courses of arsenic trioxide in either a phase I or phase II investi

154 The further study of arsenic trioxide in MDS, particularly in combination wit

155 As experience with ATRA and arsenic trioxide in patients with APL accumulates, a num

156 paring ATRA plus chemotherapy with ATRA plus arsenic trioxide in patients with APL classified as low-

157 id (ATRA) plus chemotherapy versus ATRA plus arsenic trioxide in patients with newly diagnosed, low-

158 To investigate the antitumor action of arsenic trioxide in solid tumors, we carried out quantit

159 The success of arsenic trioxide in the treatment of acute promyelocytic

160 y, we found that wild type p53 is induced by arsenic trioxide in tumor cells, consistent with publish

161 Arsenic trioxide induced the expression of the proenzyme

162 e pathway, acting as a negative regulator of arsenic trioxide-induced apoptosis and inhibition of mal

163 ng of reactive oxygen species, which prevent arsenic trioxide-induced apoptosis, also prevent the for

164 tion of topoisomerase I expression decreases arsenic trioxide-induced apoptotic DNA fragmentation.

165 or, benzyloxycarbonyl-VAD partially prevents arsenic trioxide-induced topoisomerase I-DNA complexes a

166 n the present study we provide evidence that arsenic trioxide induces activation of the small G-prote

167 In clinical trials, arsenic trioxide induces complete remission in 87% of pa

168 Arsenic trioxide induces differentiation and apoptosis o

169 Thus, we propose that arsenic trioxide induces topoisomerase I-DNA complexes t

170 ATRA and arsenic trioxide is a feasible treatment in low-risk and

171 Arsenic trioxide is a toxic metalloid and carcinogen tha

172 The finding that arsenic trioxide is an effective treatment for acute pro

173 Arsenic trioxide is an effective treatment for patients

174 duction therapy of APL with all-trans RA and arsenic trioxide is associated with leukocytosis and the

175 ATRA plus arsenic trioxide is at least not inferior and may be sup

176 iscontinuation of all-trans retinoic acid or arsenic trioxide is indicated only for patients in very

177 Arsenic trioxide is used in clinical trials in the treat

178 Arsenic trioxide, like all-trans-retinoic acid (RA), ind

179 Treatment with arsenic trioxide may be associated with the APL differen

180 These observations suggest that arsenic trioxide may be significantly or even fatally to

181 ertain arsenic complexes (i.e., arsenate and arsenic trioxide) may inactivate RhoA by bridging the cy

182 Arsenic trioxide monotherapy has moderate activity again

183 d to ATRA and idarubicin (n=119) or ATRA and arsenic trioxide (n=116).

184 onversely, agents augmenting ROS production (arsenic trioxide, NSC656240, and PK11195) facilitate Ad.

185 of mTOR enhances the suppressive effects of arsenic trioxide on leukemic progenitor colony formation

186 activity enhances the suppressive effects of arsenic trioxide on primary leukemic progenitors from pa

187 F) enhances the antiproliferative effects of arsenic trioxide on target cells.

188 mised 1:1 to receive treatment with ATRA and arsenic trioxide or ATRA and idarubicin.

189 ed incorporation of novel therapies, such as arsenic trioxide or histone deacetylase inhibitors.

190 Bcr-Abl by inhibiting its translation, e.g., arsenic trioxide, or promoting its proteasomal degradati

191 Overall survival was also better with ATRA-arsenic trioxide (P=0.02).

192 n cancer cells of four anticancer compounds, arsenic trioxide, phosphoaspirin, phosphosulindac, and n

193 LLG APML4 (single arm of ATRA + idarubicin + arsenic trioxide + prednisone), CALGB C9710 (single arm

194 onitoring, early treatment intervention with arsenic trioxide prevented progression to overt relapse

195 ith granulocyte colony-stimulating factor or arsenic trioxide reduced MPN-initiating cell frequencies

196 stablish that activation of Mnk1 and Mnk2 by arsenic trioxide regulates downstream phosphorylation of

197 regulatory manner, to control generation of arsenic trioxide responses.

198 radation, such as all-trans retinoic acid or arsenic trioxide, restore nuclear PTEN.

199 The multiple mechanisms of action of arsenic trioxide suggest that it may have antitumor acti

200 In addition, downregulation of PML by arsenic trioxide suppressed monosodium urate (MSU)-induc

201 Arsenic trioxide suppressed the growth of leukemic myelo

202 Here, we found that RA or arsenic trioxide synergistically induce proteasomal degr

203 ules for ATRA plus chemotherapy, the role of arsenic trioxide, the use of current molecular monitorin

204 for APL and additional molecular targets for arsenic trioxide therapy.

205 The addition of arsenic trioxide to (131)I-MIBG did not significantly im

206 This article reviews the clinical use of arsenic trioxide to date and discusses new therapeutic s

207 We reviewed our clinical experience with arsenic trioxide to determine the incidence of these two

208 , PIAS1 suppression abrogated the ability of arsenic trioxide to trigger apoptosis in APL cells.

209 One hypokalemic, arsenic trioxide-treated patient with relapsed APL devel

210 MO inhibitor treatment underwent intravenous arsenic trioxide treatment for 5 days, every 28 days, an

211 udy, we compare a chemotherapy-free ATRA and arsenic trioxide treatment regimen with the standard che

212 Our result showed 0.4 ppm, 2 ppm, and 4 ppm arsenic trioxide treatment through drinking water for 30

213 Here, we report that itraconazole and arsenic trioxide, two agents in clinical use that inhibi

214 ability of hexose transporters to facilitate arsenic trioxide uptake in Saccharomyces cerevisiae was

215 As compared with ATRA-chemotherapy, ATRA-arsenic trioxide was associated with less hematologic to

216 In the ATRA and arsenic trioxide group, arsenic trioxide was given intravenously at 0.3 mg/kg on

217 (131)I-MIBG plus arsenic trioxide was well tolerated, with an adverse eve

218 ce, favoring patients treated with ATRA plus arsenic trioxide, was found for fatigue severity (mean s

219 n CT at baseline and after administration of arsenic trioxide, which is known to cause acute reductio

220 Pilot studies of treatment with arsenic trioxide with or without ATRA have shown high ef

221 However, the combination of ATRA and arsenic trioxide, with minimal chemotherapy to control l

222 d in being more active than the FDA-approved arsenic trioxide, with the most lipophilic molecule in t

223 We hypothesized that arsenic trioxide would enhance the efficacy of the targe