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 sting of graphene and alpha-phase molybdenum trioxide.

11 oxicity in cancer cells treated with arsenic trioxide.

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

13 leukemia that have been treated with arsenic trioxide.

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

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

16 face carrier transfer method with molybdenum trioxides.

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

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

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

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

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

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

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

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

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

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

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

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

29 Mineral trioxide aggregate (MTA), a first-generation bioceramic

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

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

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

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

34 e including calcium hydroxide paste, mineral trioxide aggregate, and glass ionomer resin, are used wi

35 strumentation, and retrofilling with mineral trioxide aggregate.

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

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

38 n time-of-flight mass spectrometry, hydrogen trioxide along with hydrogen peroxide and the hydroperox

39 r Waals semiconductor alpha-phase molybdenum trioxide (alpha-MoO(3) ) has recently received significa

40 ntours in bilayers of alpha-phase molybdenum trioxide (alpha-MoO(3)), arising when the rotation betwe

41 oron nitride (hBN) or alpha-phase molybdenum trioxide (alpha-MoO(3)), transferred on nanoscale oxygen

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

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

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

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

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

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

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

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

50 Arsenic trioxide and liposomally encapsulated all-trans-retinoic

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

52 Arsenic trioxide and sodium arsenite did not directly modify or

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

54 Arsenic trioxide and stem cell transplantation are effective tre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

97 n on the structural properties of molybdenum trioxide, as a representative, and its impact on redox c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

134 Arsenic trioxide (ATO) was used to investigate the effects and m

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

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

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

138 cation of small molecules, including arsenic trioxide (ATO), an established agent in treating acute p

139 -2'-deoxycytidine (DAC; decitabine), arsenic trioxide (ATO), and MS-275 [entinostat; N-(2-aminophenyl

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

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

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

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

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

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

146 s when treated with a novel ATRA and arsenic trioxide-based regimen that included 4 doses of idarubic

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

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

149 Acetylcysteine, arsenic-trioxide, beta-elemene, bortezomib and curcumin were ide

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

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

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

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

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

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

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

157 e uptake of three stable isomers of chlorine trioxide (Cl(2)O(3)), namely, ClOCl(O)O, ClClO(3), and C

158 All patients received ATRA and arsenic trioxide continuously during induction therapy and inter

159 de (CrOOH) was oxidized to metastable Cr(VI) trioxide (CrO(3)) up to 600 degrees C, which spontaneous

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

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

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

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

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

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

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

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

168 oratory simulation experiments that hydrogen trioxide effectively forms in water-molecular oxygen ice

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 Arsenic trioxide had complex and TRIM5alpha-independent enhancin

184 Arsenic trioxide has also surfaced as an effective induction the

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

186 Arsenic trioxide has in vitro and in vivo radiosensitizing prope

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

188 , the abiotic formation pathways to hydrogen trioxide have remained elusive.

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

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

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

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

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

194 are important because the success of arsenic trioxide in blood cancers (such as APL) has not been see

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

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

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

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

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

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

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

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

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

204 Arsenic trioxide induced the expression of the proenzymes of cas

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

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

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

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

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

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

211 Arsenic trioxide induces differentiation and apoptosis of malign

212 As a result, low-dose arsenic trioxide induces ER-stress and inhibits proliferation in

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

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

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

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

217 Arsenic trioxide is an effective treatment for patients with acu

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

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

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

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

222 Arsenic, in the simple form of arsenic trioxide, is currently marketed for the treatment of acu

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

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

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

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

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

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

229 Arsenic trioxide monotherapy has moderate activity against MDS,

230 , we introduce a highly efficient molybdenum trioxide (MoO(3))-catalyzed polymerization of n-PBDF.

231 Molybdenum trioxides (MoO(3)) are one of the most prominent solid-s

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

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

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

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

236 *), nitrogen dioxide (NO(2) (*)), dinitrogen trioxide (N(2)O(3)), nitroxyl (HNO), and peroxynitrite (

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

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

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

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

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

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

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

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

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

246 1 to receive treatment with ATRA and arsenic trioxide or ATRA and idarubicin.

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

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

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

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

251 4 (single arm of ATRA + idarubicin + arsenic trioxide + prednisone), CALGB C9710 (single arm of ATRA

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

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

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

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

256 nt with a chemotherapy-free ATRA and arsenic trioxide regimen experienced positive outcomes.

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

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

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

260 n reaction in which CH(3) (+) adds to sulfur trioxide (SO(3)) to form CH(3)-S(O)(2)O(+) This mechanis

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

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

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

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

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

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

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

268 tant anticancer drugs, cisplatin and arsenic trioxide, that have a Pt(II) bond to an As(III) hydroxid

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

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

271 d all-trans retinoic acid (ATRA) and arsenic trioxide therapy, which induces the destruction of PML-R

272 and additional molecular targets for arsenic trioxide therapy.

273 Molybdenum trioxide thin films of different thicknesses were prepar

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

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

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

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

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

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

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

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

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

283 n increased apoptosis rate following arsenic trioxide treatment.

284 This method, which employs the sulfur trioxide-trimethylamine complex as the electrophile, has

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

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

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

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

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

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

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

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

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

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

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

296 e research reports the synthesis of tungsten trioxide (WO(3)) and cobalt oxide (Co(3)O(4)) nanostruct

297 tercalation governs the activity of tungsten trioxide (WO(3)) toward the hydrogen evolution reaction

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

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

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