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 ng cytotoxicity in cancer cells treated with arsenic trioxide.

10 inhibitor U0126, cytarabine, azacitidine and arsenic trioxide.

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

12 locytic leukemia that have been treated with arsenic trioxide.

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

14 4 or 666 MBq/kg) intravenously on day 1 plus arsenic trioxide (0.15 or 0.25 mg/m(2)) intravenously on

15 ter calcine wastes (14.4 wt% Fe oxides), and arsenic trioxide (0.8 wt%) derived from an electrostatic

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

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

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

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

20 Arsenic trioxide, a drug for patients with acute promyel

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

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

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

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

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

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

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

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

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

30 Arsenic trioxide and itraconazole antagonize the hedgeho

31 Overall, arsenic trioxide and itraconazole reduced GLI1 messenger

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

33 Arsenic trioxide and liposomally encapsulated all-trans-

34 Arsenic trioxide and sodium arsenite did not directly mo

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

36 Arsenic trioxide and stem cell transplantation are effec

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

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

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

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

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

42 All-trans retinoic acid and arsenic trioxide are classic examples of differentiating

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

80 Arsenic trioxide (As2O3) induces clinical remission in a

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

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

83 Arsenic trioxide (As2O3) treatment results in the total

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

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

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

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

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

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

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

91 t and key senescence gene whose targeting by arsenic trioxide (ATO) drives eradication of acute promy

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

108 identified that extend the mode of action of arsenic trioxide (ATO) only when accounting for these me

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

110 Arsenic trioxide (ATO) resistance is a challenging probl

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

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

113 Arsenic trioxide (ATO) was used to investigate the effec

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

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

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

117 identification of small molecules, including arsenic trioxide (ATO), an established agent in treating

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

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

120 , such as all-trans retinoic acid (ATRA) and arsenic trioxide (ATO), are by and large curative in acu

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

122 rapy with all-trans retinoic acid (ATRA) and arsenic trioxide (ATO).

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

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

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

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

127 outcomes when treated with a novel ATRA and arsenic trioxide-based regimen that included 4 doses of

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

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

130 Acetylcysteine, arsenic-trioxide, beta-elemene, bortezomib and curcumin

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

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

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

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

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

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

137 All patients received ATRA and arsenic trioxide continuously during induction therapy a

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

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

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

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

142 1 and Akt2 genes, we found that induction of arsenic trioxide-dependent apoptosis is strongly enhance

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

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

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

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

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

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

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

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

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

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

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

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

155 Arsenic trioxide had complex and TRIM5alpha-independent

156 Arsenic trioxide has also surfaced as an effective induc

157 Arsenic trioxide has been shown to be effective in treat

158 Arsenic trioxide has in vitro and in vivo radiosensitizi

159 Arsenic trioxide has shown great promise in the treatmen

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

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

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

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

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

165 rofiles are important because the success of arsenic trioxide in blood cancers (such as APL) has not

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

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

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

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

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

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

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

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

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

175 Arsenic trioxide induced the expression of the proenzyme

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

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

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

179 nduce nuclear translation of G3BP2 and block arsenic trioxide-induced SG formation.

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

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

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

183 Arsenic trioxide induces differentiation and apoptosis o

184 As a result, low-dose arsenic trioxide induces ER-stress and inhibits prolifer

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

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

187 Arsenic trioxide is a toxic metalloid and carcinogen tha

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

189 Arsenic trioxide is an effective treatment for patients

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

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

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

193 s the standard of care in countries in which arsenic trioxide is not affordable.

194 Arsenic trioxide is used in clinical trials in the treat

195 Arsenic, in the simple form of arsenic trioxide, is currently marketed for the treatmen

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

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

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

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

200 Arsenic trioxide monotherapy has moderate activity again

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

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

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

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

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

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

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

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

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

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

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

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

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

214 treatment with a chemotherapy-free ATRA and arsenic trioxide regimen experienced positive outcomes.

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

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

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

218 Therapy with arsenic trioxide results in degradation of PML-RARA and

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

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

221 Arsenic trioxide suppressed the growth of leukemic myelo

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

223 ly important anticancer drugs, cisplatin and arsenic trioxide, that have a Pt(II) bond to an As(III)

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

225 All-trans retinoic acid (ATRA) and arsenic trioxide therapy without the use of maintenance

226 combined all-trans retinoic acid (ATRA) and arsenic trioxide therapy, which induces the destruction

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

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

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

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

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

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

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

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

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

236 ing to an increased apoptosis rate following arsenic trioxide treatment.

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

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

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

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

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

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

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

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

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

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

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