ライフサイエンスコーパス: trioxide

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

2 n insertion into MTO, forming methoxyrhenium trioxide.

3 s ATRA (all trans retinoic acid) and arsenic trioxide.

4 transport of the trivalent metalloid arsenic trioxide.

5 rolongation in patients treated with arsenic trioxide.

6 duction of antileukemic responses by arsenic trioxide.

7 veloped while they were treated with arsenic trioxide.

8 t with 0.1 mg/kg per day intravenous arsenic trioxide.

9 kidney were relatively unaffected by arsenic trioxide.

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

11 leukemia that have been treated with arsenic trioxide.

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

13 onite [Sb(III)] as microcrystals of antimony trioxide.

14 face carrier transfer method with molybdenum trioxides.

15 MBq/kg) intravenously on day 1 plus arsenic trioxide (0.15 or 0.25 mg/m(2)) intravenously on days 6-

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

17 ment with either H2O2 or Br2/H2O to give the trioxide 9-aneP3(O)3Et3 (8).

18 We show here that arsenic trioxide (a potent inducer of apoptosis that induces the

19 Importantly, addition of arsenic trioxide, a compound capable of causing reactive oxygen

20 es provide preclinical evidence that arsenic trioxide, a drug FDA approved for the treatment of acute

21 Arsenic trioxide, a drug for patients with acute promyelocytic l

22 Here we found that arsenic trioxide, a frontline agent for acute promyelocytic leuk

23 Furthermore, we found that arsenic trioxide activates the Pirh2 promoter and consequently i

24 , doxorubicin, melphalan) and novel (arsenic trioxide) agents augment apoptosis induced by atiprimod.

25 the materials were washed in either mineral trioxide aggregate (MTA) or hybrid ionomere composite re

26 eated with calcium hydroxide (CH) or mineral trioxide aggregate (MTA) showed an increased expression

27 Abbreviations: mineral trioxide aggregate (MTA), zinc-oxide eugenol cement (ZOE

28 ved and the defect was restored with mineral trioxide aggregate (MTA).

29 White mineral trioxide aggregate was used to seal one end of the tooth

30 capping in permanent teeth with MTA (mineral trioxide aggregate) or CaOH (calcium hydroxide).

31 strumentation, and retrofilling with mineral trioxide aggregate.

32 lable calcium silicate cement (white mineral trioxide aggregate; WMTA) after different aging periods.

33 Itraconazole and arsenic trioxide, alone or in combination, inhibit the growth of

34 icancer drugs, such as cisplatin and arsenic trioxide, also induce KSHV reactivation and PEL cell dea

35 T2 sensitized breast cancer cells to arsenic trioxide, an approved therapeutic agent, along with othe

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

37 that treatment with a combination of arsenic trioxide and imatinib can eliminate refractory MPN-initi

38 rgistic effect of the combination of arsenic trioxide and interferon alpha (As/IFN-alpha) with emodin

39 Arsenic trioxide and itraconazole antagonize the hedgehog (HH) p

40 Overall, arsenic trioxide and itraconazole reduced GLI1 messenger RNA lev

41 eting the HH pathway with sequential arsenic trioxide and itraconazole treatment is a feasible treatm

42 Arsenic trioxide and liposomally encapsulated all-trans-retinoic

43 s consecutive to the formation of dinitrogen trioxide and peroxynitrite.

44 Arsenic trioxide and sodium arsenite did not directly modify or

45 iscovered that arsenicals, including arsenic trioxide and sodium arsenite, inhibited activation of th

46 Arsenic trioxide and stem cell transplantation are effective tre

47 that increase the stability of ND10, arsenic trioxide and the proteasome inhibitor MG132, inhibited v

48 llogeneic stem cell transplantation, arsenic trioxide, and bortezomib for this condition.

49 g agents such as all- retinoic acid, arsenic trioxide, and inhibitors of DNA methylation and histone

50 superrepressor, lactacystin, MG132, arsenic trioxide, and phenylarsine oxide reverse the protection

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

52 dioxide), leading to the formation of sulfur trioxide anion radical ((.)SO(3)(-)).

53 Ferrous myoglobin was oxidized by sulfur trioxide anion radical (STAR) during the free radical ch

54 treated with a ROS-inducer, such as arsenic trioxide (ARS), N-(4-hydroxyphenyl) retinamide (HPR) or

55 sensitive to retinoic acid (RA) and arsenic trioxide (arsenic), which both trigger cell differentiat

56 l kinase (JNK) reciprocally regulate arsenic trioxide (arsenite)-induced, p53-independent expression

57 ting a minor yield of methanol or stabilized trioxide as a product.

58 further support the use of ATRA plus arsenic trioxide as preferred first-line treatment in patients w

59 An assignment of a heme-bound dinitrogen trioxide as the stable intermediate associated with the

60 Arsenic trioxide (As(2)O(3)) and gamma interferon (IFN-gamma), w

61 Exposure to a low dose (0.5 mum) of arsenic trioxide (As(2)O(3)) caused transformation of BALB/c 3T3

62 Recent clinical data shows that arsenic trioxide (As(2)O(3)) causes remission in patients with a

63 Arsenic trioxide (As(2)O(3)) exhibits potent antitumor effects i

64 Arsenic trioxide (As(2)O(3)) has been found to induce apoptosis

65 Arsenic trioxide (As(2)O(3)) has potent antileukemic properties

66 Arsenic trioxide (As(2)O(3)) has recently been used successfully

67 Arsenic trioxide (As(2)O(3)) has shown considerable efficacy in

68 cute promyelocytic leukemia cells to arsenic trioxide (As(2)O(3)) in the presence and absence of a ge

69 Arsenic trioxide (As(2)O(3)) increased human immunodeficiency vi

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

71 Arsenic trioxide (As(2)O(3)) induces differentiation and apoptos

72 Recent data indicate that arsenic trioxide (As(2)O(3)) induces remission of refractory acu

73 Arsenic trioxide (As(2)O(3)) is a highly effective treatment for

74 Arsenic trioxide (As(2)O(3)) is a potent inducer of apoptosis of

75 Arsenic trioxide (As(2)O(3)) is a potent inducer of apoptosis of

76 Arsenic trioxide (As(2)O(3)) is an effective agent for the treat

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

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

79 Arsenic trioxide (As(2)O(3)) produces dramatic remissions in pat

80 They show that the therapeutic drug arsenic trioxide (AS(2)O(3)) targets BCR-ABL for autophagic degr

81 We provide evidence that arsenic trioxide (As(2)O(3)) targets the BCR-ABL oncoprotein via

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

83 e oxygen species, could be killed by arsenic trioxide (As(2)O(3)), a chemotherapeutic drug used in th

84 We have discovered that arsenic trioxide (As(2)O(3)), a very potent antineoplastic compo

85 Arsenic trioxide (As(2)O(3)), an agent that accentuates POD form

86 ction, we investigated the effect of arsenic trioxide (As(2)O(3)), an FDA-approved chemotherapeutic a

87 other hand, one arsenic derivative, arsenic trioxide (As(2)O(3)), has important antitumor properties

88 ive and negative ion mass spectra of arsenic trioxide (As2O3) and arsenic pentaoxide (As2O5) have bee

89 Inorganic arsenic trioxide (As2O3) and the organic arsenical, melarsoprol,

90 ed the impact of tolerated and toxic arsenic trioxide (As2O3) exposure in human embryonic kidney (HEK

91 The use of arsenic trioxide (As2O3) has been shown to effectively treat acu

92 id (AA) will enhance the efficacy of arsenic trioxide (As2O3) in myeloma.

93 Arsenic trioxide (As2O3) induces clinical remission in acute pro

94 Arsenic trioxide (As2O3) is a potent inducer of apoptosis of leu

95 imatinib would alter the efficacy of arsenic trioxide (As2O3) or 5-aza-2-deoxycytidine (decitabine) a

96 Arsenic trioxide (As2O3) treatment results in the total degradat

97 Inorganic arsenic trioxide (As2O3) was recently shown to induce apoptosis

98 sudden death have been reported with arsenic trioxide (As2O3), a highly effective agent for acute pro

99 iosynthesis is a sensitive target of arsenic trioxide (As2O3), leading to uracil misincorporation int

100 sive prior therapy were treated with arsenic trioxide at doses ranging from 0.06 to 0.2 mg per kilogr

101 dies demonstrate that treatment with arsenic trioxide (AT) lowered ectopically expressed or endogenou

102 While arsenic trioxide (ATO) can induce remissions in 95% of relapsed

103 e the survival of patients receiving arsenic trioxide (ATO) consolidation and reduced doses of anthra

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

105 all-trans-retinoic acid (ATRA) plus arsenic trioxide (ATO) has been shown to be superior to ATRA plu

106 Arsenic trioxide (ATO) has been shown to induce differentiation

107 Arsenic trioxide (ATO) has been successfully used as a treatment

108 Arsenic trioxide (ATO) has been successfully used for the treatm

109 Arsenic trioxide (ATO) has been tested in relapsed/refractory mu

110 tion therapy of decitabine (DAC) and arsenic trioxide (ATO) have demonstrated synergy on MDS treatmen

111 earance is different with the use of arsenic trioxide (ATO) in the treatment of APL.

112 ore cell death than the FDA-approved arsenic trioxide (ATO) in vitro, but exhibits less systemic toxi

113 Arsenic trioxide (ATO) induces remission in 85% of adults with r

114 Arsenic trioxide (ATO) is a highly effective agent for the treat

115 Arsenic trioxide (ATO) is a potent anti-leukemic chemotherapeuti

116 all- trans-retinoic acid (ATRA) and arsenic trioxide (ATO) is at least not inferior to standard ATRA

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

118 g all-trans retinoic acid (ATRA) and arsenic trioxide (ATO) might be an alternative to ATRA + chemoth

119 We controlled the size of arsenic trioxide (ATO) nanocrystals by simply changing the conce

120 We have shown previously that arsenic trioxide (ATO) preferentially shutsdown tumor blood flow

121 Arsenic trioxide (ATO) resistance is a challenging problem in ch

122 this study, we present evidence that arsenic trioxide (ATO) suppresses human cancer cell growth and t

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

124 h all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO) with or without gemtuzumab ozogamicin (GO

125 ive in Hh pathway antagonism include arsenic trioxide (ATO), a curative agent in clinical use for acu

126 pathway activity can be inhibited by arsenic trioxide (ATO), an anti-leukemia drug approved by the US

127 -2'-deoxycytidine (DAC; decitabine), arsenic trioxide (ATO), and MS-275 [entinostat; N-(2-aminophenyl

128 h all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent understanding of the

129 all-trans retinoic acid (ATRA) plus arsenic trioxide (ATO), which degrade the promyelocytic leukemia

130 nthracycline-based chemotherapy, and arsenic trioxide (ATO).

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

132 Arsenic trioxide (ATO, As2 O3 ) is currently used to treat acute

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

134 ceived only 6 of 10 planned doses of arsenic trioxide because of grade 3 diarrhea and vomiting with c

135 One did not receive arsenic trioxide because of transient central line-induced cardi

136 en patients received (131)I-MIBG and arsenic trioxide, both at maximal dosages; 2 patients received a

137 f all-trans-retinoic acid (ATRA) and arsenic trioxide, both of which induce degradation of the progre

138 iethyl-1,4,7-triphosphacyclononane, from the trioxide by reduction proved unsuccessful.

139 rolytes and concomitant medications, arsenic trioxide can be safely administered in patients with rel

140 ports from China have suggested that arsenic trioxide can induce complete remissions in patients with

141 Low doses of arsenic trioxide can induce complete remissions in patients with

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

143 s oxidized quantitatively to NO2 by chromium trioxide (CrO3), before conversion to NO2(-) and NO3(-)

144 and the combination of imatinib with arsenic trioxide cured a large fraction of mice with MPNs.

145 In addition, we found that arsenic trioxide decreases the stability of DeltaNp63 protein vi

146 We also found that arsenic trioxide decreases the stability of mutant p53 protein t

147 r signals that control generation of arsenic trioxide-dependent apoptosis and antileukemic responses.

148 t2 genes, we found that induction of arsenic trioxide-dependent apoptosis is strongly enhanced in the

149 e the second course, signifying that arsenic trioxide does not permanently prolong the QTc interval.

150 nd et al report that the addition of arsenic trioxide during induction and consolidation can substant

151 ion of NO to NO2, using the oxidant chromium trioxide, followed by detection of chemiluminescence in

152 assigned to receive either ATRA plus arsenic trioxide for induction and consolidation therapy or stan

153 udy was initiated in June 1998 using arsenic trioxide for relapsed APL to determine the maximum toler

154 or refractory APL were treated with arsenic trioxide for remission induction at daily doses that ran

155 survival rates were 97% in the ATRA-arsenic trioxide group and 86% in the ATRA-chemotherapy group (9

156 Patients in the ATRA and arsenic trioxide group had significantly less requirement for mo

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

158 ieved in all 77 patients in the ATRA-arsenic trioxide group who could be evaluated (100%) and in 75 o

159 In the ATRA and arsenic trioxide group, arsenic trioxide was given intravenously

160 versus 5 (5%) of 95 in the ATRA and arsenic trioxide group, raised liver alanine transaminase in 11

161 versus 2 (3%) of 77 in the ATRA and arsenic trioxide group; no other toxicities reached the 10% leve

162 iously unknown oxidants including dihydrogen trioxide (H(2)O(3)) and ozone (O(3)) from singlet oxygen

163 ays proceeds via the formation of dihydrogen trioxide (H(2)O(3)), we now consider the possibility tha

164 ia the postulated intermediacy of dihydrogen trioxide (H2O3) and other trioxygen species.

165 Arsenic trioxide had complex and TRIM5alpha-independent enhancin

166 Arsenic trioxide has also surfaced as an effective induction the

167 Arsenic trioxide has been shown to be effective in treating acut

168 Arsenic trioxide has in vitro and in vivo radiosensitizing prope

169 Arsenic trioxide has shown great promise in the treatment of pat

170 zomib, thalidomide, lenalidomide and arsenic trioxide, have been found to block activation of NF-kapp

171 /IL-24 mRNA, a single treatment with arsenic trioxide, HPR or NSC656240 induces apoptosis, which corr

172 rgoing assessment at present include arsenic trioxide, hsp90 inhibitors and histone deacetylase inhib

173 nib in chronic lymphocytic leukemia, arsenic trioxide in acute promyelocytic leukemia, and the BH3-mi

174 The expanded use of arsenic trioxide in APL for postremission therapy, in conjunctio

175 ogenous ROS-producing agents such as arsenic trioxide in combination with 2-ME to enhance the antileu

176 gnancies who received 170 courses of arsenic trioxide in either a phase I or phase II investigational

177 The further study of arsenic trioxide in MDS, particularly in combination with other

178 As experience with ATRA and arsenic trioxide in patients with APL accumulates, a number of i

179 TRA plus chemotherapy with ATRA plus arsenic trioxide in patients with APL classified as low-to-inter

180 ) plus chemotherapy versus ATRA plus arsenic trioxide in patients with newly diagnosed, low- or inter

181 investigate the antitumor action of arsenic trioxide in solid tumors, we carried out quantitative tu

182 The success of arsenic trioxide in the treatment of acute promyelocytic leukemi

183 und that wild type p53 is induced by arsenic trioxide in tumor cells, consistent with published studi

184 Arsenic trioxide induced the expression of the proenzymes of cas

185 y, acting as a negative regulator of arsenic trioxide-induced apoptosis and inhibition of malignant c

186 active oxygen species, which prevent arsenic trioxide-induced apoptosis, also prevent the formation o

187 topoisomerase I expression decreases arsenic trioxide-induced apoptotic DNA fragmentation.

188 yloxycarbonyl-VAD partially prevents arsenic trioxide-induced topoisomerase I-DNA complexes and apopt

189 esent study we provide evidence that arsenic trioxide induces activation of the small G-protein Rac1

190 In clinical trials, arsenic trioxide induces complete remission in 87% of patients a

191 Arsenic trioxide induces differentiation and apoptosis of malign

192 Thus, we propose that arsenic trioxide induces topoisomerase I-DNA complexes that part

193 ATRA and arsenic trioxide is a feasible treatment in low-risk and high-ri

194 Arsenic trioxide is a toxic metalloid and carcinogen that is als

195 The finding that arsenic trioxide is an effective treatment for acute promyelocyt

196 Arsenic trioxide is an effective treatment for patients with acu

197 therapy of APL with all-trans RA and arsenic trioxide is associated with leukocytosis and the RA synd

198 ATRA plus arsenic trioxide is at least not inferior and may be superior to

199 uation of all-trans retinoic acid or arsenic trioxide is indicated only for patients in very poor cli

200 Arsenic trioxide is used in clinical trials in the treatment of

201 n opposite directions for lithium molybdenum trioxide (Li2MoO3).

202 Arsenic trioxide, like all-trans-retinoic acid (RA), induces dif

203 Treatment with arsenic trioxide may be associated with the APL differentiation

204 These observations suggest that arsenic trioxide may be significantly or even fatally toxic at d

205 rsenic complexes (i.e., arsenate and arsenic trioxide) may inactivate RhoA by bridging the cysteine r

206 a novel route for the production of antimony trioxide microcrystals of commercial significance to the

207 Arsenic trioxide monotherapy has moderate activity against MDS,

208 metal oxide layers, in particular molybdenum trioxide (MoO3), is studied combining photoemission spec

209 Methylrhenium trioxide (MTO) has the rare ability to stoichiometricall

210 for the selective oxidation of methylrhenium trioxide (MTO) to methanol in acidic aqueous solution.

211 on of 2 molecules of nitrite into dinitrogen trioxide (N(2)O(3)), an uncharged molecule that may be e

212 A and idarubicin (n=119) or ATRA and arsenic trioxide (n=116).

213 nitrosation by the .NO derivative dinitrogen trioxide (N2O3), RSNOs may be formed via intermediate on

214 anopaper, assembled via ultralong molybdenum trioxide nanobelts, displays an excellent average transm

215 A flexible transparent molybdenum trioxide nanopaper, assembled via ultralong molybdenum t

216 ndogenous nitrosating agent N2O3 (dinitrogen trioxide, nitrous anhydride) may be formed either by the

217 y, agents augmenting ROS production (arsenic trioxide, NSC656240, and PK11195) facilitate Ad.mda-7-in

218 enhances the suppressive effects of arsenic trioxide on leukemic progenitor colony formation.

219 enhances the suppressive effects of arsenic trioxide on primary leukemic progenitors from patients w

220 ces the antiproliferative effects of arsenic trioxide on target cells.

221 1 to receive treatment with ATRA and arsenic trioxide or ATRA and idarubicin.

222 poration of novel therapies, such as arsenic trioxide or histone deacetylase inhibitors.

223 by inhibiting its translation, e.g., arsenic trioxide, or promoting its proteasomal degradation, e.g.

224 l survival was also better with ATRA-arsenic trioxide (P=0.02).

225 cells of four anticancer compounds, arsenic trioxide, phosphoaspirin, phosphosulindac, and nitric ox

226 4 (single arm of ATRA + idarubicin + arsenic trioxide + prednisone), CALGB C9710 (single arm of ATRA

227 g, early treatment intervention with arsenic trioxide prevented progression to overt relapse in the m

228 d to its corresponding aldehyde using sulfur trioxide-pyridine.

229 HO3-/H2O3 may be the bactericidal trioxide recently identified in the antibody-catalyzed a

230 ulocyte colony-stimulating factor or arsenic trioxide reduced MPN-initiating cell frequencies and the

231 that activation of Mnk1 and Mnk2 by arsenic trioxide regulates downstream phosphorylation of the euk

232 ory manner, to control generation of arsenic trioxide responses.

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

234 visible leads to photolysis, forming sulfur trioxide (SO3) and water.

235 transfer of sulfuric acid (H2SO4) and sulfur trioxide (SO3) from an acidic sulfopeptide (sSE) to a ba

236 the influence of nitric oxide (NO) on sulfur trioxide (SO3) generation.

237 The multiple mechanisms of action of arsenic trioxide suggest that it may have antitumor activity in

238 n addition, downregulation of PML by arsenic trioxide suppressed monosodium urate (MSU)-induced IL-1b

239 Arsenic trioxide suppressed the growth of leukemic myeloid (CFU-

240 Here, we found that RA or arsenic trioxide synergistically induce proteasomal degradation

241 ATRA plus chemotherapy, the role of arsenic trioxide, the use of current molecular monitoring for mi

242 and additional molecular targets for arsenic trioxide therapy.

243 Molybdenum trioxide thin films of different thicknesses were prepar

244 The addition of arsenic trioxide to (131)I-MIBG did not significantly improve re

245 article reviews the clinical use of arsenic trioxide to date and discusses new therapeutic strategie

246 eviewed our clinical experience with arsenic trioxide to determine the incidence of these two phenome

247 suppression abrogated the ability of arsenic trioxide to trigger apoptosis in APL cells.

248 l but inert transition metal oxide, tungsten trioxide, to be an efficient electrocatalyst for hydroge

249 One hypokalemic, arsenic trioxide-treated patient with relapsed APL developed asy

250 itor treatment underwent intravenous arsenic trioxide treatment for 5 days, every 28 days, and oral i

251 compare a chemotherapy-free ATRA and arsenic trioxide treatment regimen with the standard chemotherap

252 ult showed 0.4 ppm, 2 ppm, and 4 ppm arsenic trioxide treatment through drinking water for 30 days an

253 ere, we report that itraconazole and arsenic trioxide, two agents in clinical use that inhibit Hedgeh

254 that is produced from formic acid and sulfur trioxide under supersonic jet conditions.

255 of hexose transporters to facilitate arsenic trioxide uptake in Saccharomyces cerevisiae was examined

256 ompared with ATRA-chemotherapy, ATRA-arsenic trioxide was associated with less hematologic toxicity a

257 the ATRA and arsenic trioxide group, arsenic trioxide was given intravenously at 0.3 mg/kg on days 1-

258 (131)I-MIBG plus arsenic trioxide was well tolerated, with an adverse event profi

259 ring patients treated with ATRA plus arsenic trioxide, was found for fatigue severity (mean score dif

260 baseline and after administration of arsenic trioxide, which is known to cause acute reduction in blo

261 Pilot studies of treatment with arsenic trioxide with or without ATRA have shown high efficacy a

262 However, the combination of ATRA and arsenic trioxide, with minimal chemotherapy to control leukocyto

263 ng more active than the FDA-approved arsenic trioxide, with the most lipophilic molecule in the serie

264 rganic oxide semiconductors such as tungsten trioxide (WO3) for photovoltaic or photocatalytic solar

265 ctural and electronic properties of tungsten trioxide (WO3) surfaces interfaced with an IrO2 thin fil

266 We hypothesized that arsenic trioxide would enhance the efficacy of the targeted radi