ライフサイエンスコーパス: ATRA

1 ATRA also reduced tumor burden of mutant IDH1 AML cells

2 ATRA and arsenic trioxide is a feasible treatment in low

3 ATRA and NaBu promoted global acetylation of histones H3

4 ATRA effects on DRA expression appeared to be mediated v

5 ATRA inhibits the expansion of CD25(+) DCs and gammadelt

6 ATRA plus arsenic trioxide is at least not inferior and

7 ATRA reduced mammosphere-forming ability of a subset of

8 ATRA sensitivity depends on the enzymatic activity and p

9 ATRA treatment specifically decreased cell viability and

10 ATRA triggered the differentiation of Gr1(+) cells into

11 ATRA was given to participants in both groups in a daily

12 ATRA-induced Pin1 ablation also potently inhibits triple

13 ATRA-induced Pin1 ablation degrades the protein encoded

14 ATRA-induced Pin1 degradation inhibited the growth of HC

15 ATRA-PLLA microparticles exerted its efficacy likely thr

16 ATRA-PLLA microparticles had good biocompatibility, and

17 ATRA-treated cGVHD B cells had elevated TLR9 and PAX5, b

18 ant contributor to RA-DC function because 1) ATRA potentiated the expression of IFN-gamma-induced iNO

19 -1) was found promote suppression because 1) ATRA was a potent inducer of Arg-1 protein and activity,

20 Loss of NPC2 expression ablated ATRA-induced antimicrobial activity.

21 Indeed, Pin1 knock-down abolished ATRA inhibitory effects on HCC cells and ATRA-PLLA did n

22 els, combination of all-trans retinoic acid (ATRA) and AEG-1 knockdown synergistically inhibited grow

23 the combination of all- trans-retinoic acid (ATRA) and arsenic trioxide (ATO) is at least not inferio

24 s sensitive to both all-trans-retinoic acid (ATRA) and arsenic trioxide (ATO), and the subsequent und

25 We used all-trans retinoic acid (ATRA) and histone deacetylase (HDAC) inhibitor, sodium b

26 retinoids, such as all trans retinoic acid (ATRA) and its precursor all trans retinaldehyde (Rald),

27 l pathway involving all-trans retinoic acid (ATRA) and its receptor (RARgamma) signaling that inhibit

28 t identification of all-trans retinoic acid (ATRA) as a Pin1 inhibitor.

29 e identification of all-trans retinoic acid (ATRA) as a potent Pin1 inhibitor provides a promising ca

30 rials that included all-trans retinoic acid (ATRA) as part of induction, we assessed known determinan

31 that treatment with all-trans retinoic acid (ATRA) at clinically achievable doses markedly enhanced t

32 l patients received all-trans retinoic acid (ATRA) during induction, each consolidation course, and m

33 eatment of AML with all-trans retinoic acid (ATRA) enhanced FRbeta expression, resulting in improved

34 All-trans retinoic acid (ATRA) has been used in several clinical trials for the t

35 cytic patients with all-trans retinoic acid (ATRA) has improved the survival of these patients substa

36 fferentiation agent all-trans-retinoic acid (ATRA) has revolutionized the therapy for a subset of leu

37 ough treatment with all-trans retinoic acid (ATRA) have yielded limited success, partially due to the

38 All-trans retinoic acid (ATRA) increased IRF4 expression, restored the IRF4-to-IR

39 itamin A metabolite all-trans retinoic acid (ATRA) induces a gut-homing phenotype in activated CD4(+)

40 All-trans retinoic acid (ATRA) induces differentiation in various cell types and

41 idence showing that all-trans retinoic acid (ATRA) induces the interaction and chromatin recruitment

42 rmacologic doses of all trans retinoic acid (ATRA) inducing differentiation and cell death at the exp

43 mechanism by which all-trans retinoic acid (ATRA) inhibits experimental autoimmune uveitis (EAU) and

44 All-trans-retinoic acid (ATRA) is a natural compound proposed for the treatment/c

45 All-trans-retinoic acid (ATRA) is an active vitamin A derivative known to modulat

46 All-trans retinoic acid (ATRA) neutralizes the differentiation block and decrease

47 a blunted effect of all-trans-retinoic acid (ATRA) on body weight and fat mass, lipid metabolism, and

48 and the effects of all-trans retinoic acid (ATRA) on these processes.

49 tes stimulated with all-trans retinoic acid (ATRA) or 1,25-dihydroxyvitamin D3 (1,25D3), the biologic

50 The combination of all-trans-retinoic acid (ATRA) plus arsenic trioxide (ATO) has been shown to be s

51 a by treatment with all-trans retinoic acid (ATRA) plus arsenic trioxide (ATO), which degrade the pro

52 oxicity of standard all-trans-retinoic acid (ATRA) plus chemotherapy versus ATRA plus arsenic trioxid

53 We used all-trans retinoic acid (ATRA) to differentiate MDSCs in mice bearing metastatic

54 While all-trans retinoic acid (ATRA) treatment in acute promyelocytic leukemia (APL) ha

55 tic leukemia (APL), all-trans retinoic acid (ATRA) treatment induces granulocytic maturation and comp

56 All-trans retinoic acid (ATRA) was negatively connected with gene expression in C

57 strategy combining all-trans retinoic acid (ATRA) with arsenic trioxide (ATO).

58 All-trans retinoic acid (ATRA) with chemotherapy is the standard of care for acut

59 All-trans retinoic acid (ATRA), a derivative of vitamin A, is a common component

60 rabine (Ara-C), and all-trans retinoic acid (ATRA), and complete remission was documented 5 weeks lat

61 e by treatment with all-trans-retinoic acid (ATRA), leading to complete clinical remission.

62 e, chemotherapy and all-trans retinoic acid (ATRA), results in a high proportion of patients being cu

63 ectin and show that all trans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the

64 gulatory metabolite all-trans retinoic acid (ATRA), which may contribute to the generation of tolerog

65 , here we find that all-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL)

66 he great success of all-trans retinoic acid (ATRA)-based therapy, which results in a clinical remissi

67 nesis, and inhibits all-trans-retinoic acid (ATRA)-induced AML cell differentiation, through regulati

68 an effective model All-Trans Retinoic Acid (ATRA)-induced differentiation of HL-60 cells.

69 enes, including the all-trans-retinoic acid (ATRA)-responsive ones, through its modified histone-bind

70 pression profile of all-trans retinoic acid (ATRA)-treated human CD4(+) T cells.

71 essential morphogen all-trans-retinoic acid (ATRA).

72 east cancer cells, likely due to more active ATRA metabolism in liver cells.

73 the sustained controlled delivery of active ATRA.

74 approach was demonstrated to release active ATRA out to 10days in vitro while significantly enhancin

75 ons, such as atom transfer radical addition (ATRA) and atom transfer radical polymerization (ATRP).

76 n asymmetric atom-transfer radical addition (ATRA) mechanism in which the stereodetermining step invo

77 s through an atom transfer radical addition (ATRA) process.

78 o efficient atom transfer radical additions (ATRA) to unactivated alkenes to form chloro, difluoromet

79 el describes reinforcing feedback between an ATRA-inducible signalsome complex involving many protein

80 iation module that sensed and transformed an ATRA signal into program activation signals; a signal in

81 complete remission (CR) in the ATRA-ATO and ATRA-CHT arms, respectively ( P = .12).

82 Knockdown of LZTFL1 reduced the basal- and ATRA-induced levels of IL-5 in CD4(+) T cells, and overe

83 hed ATRA inhibitory effects on HCC cells and ATRA-PLLA did not inhibit normal liver cells, as expecte

84 nance therapy with low-dose chemotherapy and ATRA.

85 elease formulation of anti-cancer drugs, and ATRA-PLLA microparticles might be a promising targeted d

86 RA-DCs were dependent on both IFN-gamma and ATRA.

87 ibitors in chronic myeloblastic leukemia and ATRA in acute promyelocytic leukemia [APL]).

88 onal pathway analysis of drug resistance and ATRA-induced cell differentiation will be useful for ide

89 ATRA levels for retinol, retinaldehyde, and ATRA-oxidizing enzymes; however, the contribution of ret

90 n mice following treatment with FLT3 TKI and ATRA in combination, with evidence of cellular different

91 acid, and beta-apo-13-carotenone antagonized ATRA-induced transactivation of RARs.

92 diated via the RAR-beta receptor subtype, as ATRA remarkably induced RAR-beta mRNA levels, whereas RA

93 more sustained antileukemic efficacy of ATO-ATRA compared with ATRA-CHT in low- and intermediate-ris

94 trikingly, NPM1 mutant downregulation by ATO/ATRA was shown to potentiate response to the anthracycli

95 erimental evidence for further exploring ATO/ATRA in preclinical NPM1-mutated AML in vivo models and

96 erlying these observations and show that ATO/ATRA induce proteasome-dependent degradation of NPM1 leu

97 ibit normal liver cells, as expected because ATRA selectively inhibits active Pin1 in cancer cells.

98 number of patients still relapse and become ATRA resistant.

99 e findings reveal a novel difference between ATRA signaling and chemokine receptor induction in Treg

100 Blocking ATRA-induced cellular cholesterol reduction inhibits ant

101 The expression of LZTFL1 depended on both ATRA and TCR signaling.

102 This PVA bound ATRA can then act as a pro-drug and accumulate within th

103 dentify the molecular mechanism that bridges ATRA differentiation and resistance in cancer, we select

104 nulocytic differentiation program induced by ATRA in APL.

105 Being itself inducible by ATRA, this zinc finger transcription factor is involved

106 is involved in the inhibition of motility by ATRA.

107 c upregulation of Npr1 gene transcription by ATRA and NaBu leads to attenuation of renal fibrotic mar

108 on factor-like 1 (LZTFL1) was upregulated by ATRA in a dose- and time-dependent manner.

109 As compared with ATRA-chemotherapy, ATRA-arsenic trioxide was associated with less hematolog

110 We explored the efficacy of combining ATRA and FLT3 TKIs to eliminate FLT3/internal tandem dup

111 sensitive to ATRA, suggesting that combining ATRA with the currently used conventional chemotherapy m

112 ucted a phase 3, multicenter trial comparing ATRA plus chemotherapy with ATRA plus arsenic trioxide i

113 acycline, and maintenance therapy comprising ATRA, oral methotrexate, and mercaptopurine.

114 In conclusion, ATRA may act as an antidiarrheal agent by increasing DRA

115 In contrast, ATRA triggered a reduction in the total cellular cholest

116 trategies, when applied to the skin, deliver ATRA as a single bolus, which is immediately taken up in

117 Although bone marrow-derived ATRA-treated DCs (RA-DCs) and conventional DCs had compa

118 eaction conditions allowed for the efficient ATRA of perfluoroalkyl iodides onto alkenes and alkynes

119 nts were randomly assigned to receive either ATRA plus arsenic trioxide for induction and consolidati

120 ritical roles in the regulation of embryonic ATRA levels for retinol, retinaldehyde, and ATRA-oxidizi

121 itical carbon dioxide process to encapsulate ATRA in largely uniform poly L-lactic acid (PLLA) microp

122 PKA-I but also PKA-II in attempts to enhance ATRA-induced APL maturation in a clinical setting.

123 in retinoid treatment efficacy: it enhances ATRA-induced maturation in ATRA-sensitive APL cells (inc

124 reatment of TNBC xenografts with entinostat, ATRA, and doxorubicin (EAD) resulted in significant tumo

125 Excess ATRA also leads to alterations (40-80%) in the expressio

126 critical for preventing formation of excess ATRA during embryonic development.

127 Furthermore, accumulation of excess ATRA is accompanied by a compensatory 30-50% reduction i

128 n this study, we compare a chemotherapy-free ATRA and arsenic trioxide treatment regimen with the sta

129 plication site inflammation compared to free ATRA and retains the drug at the application site at mea

130 transferred gammadelta T cells isolated from ATRA-treated mice showed a diminished ability to promote

131 del parameters using measurements taken from ATRA-induced HL-60 cells.

132 Furthermore, ATRA treatment resulted in a significant increase in HNF

133 o-amplification of the ERBB2 and RARA genes, ATRA activates a RARalpha-dependent epithelial different

134 lsions to incorporate the highly hydrophobic ATRA drug.

135 ression of several developmentally important ATRA target genes.

136 vating agents can restore differentiation in ATRA maturation-resistant APL cells.

137 profiles suggests that NPC2 is a key gene in ATRA-induced cholesterol regulation.

138 1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression.

139 cacy: it enhances ATRA-induced maturation in ATRA-sensitive APL cells (including NB4 cells) and resto

140 ies exhibited enhanced kinetic reactivity in ATRA with no significant difference in overall product y

141 Ai-mediated attenuation of RASSF1A inhibited ATRA-induced granulocytic differentiation via regulation

142 estigate functions of Pin1 and its inhibitor ATRA in the development and treatment of HCC.

143 gs provide important molecular insights into ATRA response and a promising avenue for overcoming ATRA

144 lexes that could be rapidly transformed into ATRA-active species could successfully catalyze ATRP, wh

145 Moreover ATRA-PLLA microparticles significantly enhanced the effi

146 ene complexes are rapidly converted into new ATRA-active, metathesis-inactive species under typical A

147 down substantially attenuated the ability of ATRA to increase DRA expression.

148 The ability of ATRA to induce DRA expression was inhibited in the prese

149 that Lcn2 is required for the full action of ATRA on the induction of UCP1 and PGC-1alpha expression

150 plays a role in the anti-migratory action of ATRA; it is relevant also for the anti-proliferative act

151 Adjunct of ATRA to chemotherapy was reported to be beneficial for N

152 Administration of ATRA to B6 mice in which EAU was induced suppressed the

153 In KPC mice, administration of ATRA, which renders PSCs quiescent, increased numbers of

154 on These results show that the advantages of ATRA-ATO over ATRA-CHT increase over time and that there

155 Bioinformatic analysis of ATRA- and 1,25D3-induced gene profiles suggests that NPC

156 formulations for the topical application of ATRA rely on creams and emulsions to incorporate the hig

157 de + prednisone), CALGB C9710 (single arm of ATRA + cytarabine + daunorubicin), Eastern Cooperative O

158 n +/- prednisone), ALLG APML4 (single arm of ATRA + idarubicin + arsenic trioxide + prednisone), CALG

159 dies included were ALLG APML3 (single arm of ATRA + idarubicin +/- prednisone), ALLG APML4 (single ar

160 ve clinical trials, using the combination of ATRA and ATO, with or without GO.

161 his effect is enhanced by the combination of ATRA and the gamma-secretase inhibitor N-(N-(3,5-difluor

162 A combination of ATRA-NaBu promoted recruitment of activator-complex cont

163 reveal that pharmacological concentration of ATRA effectively downregulates PKCzeta through activatio

164 Consolidation comprised 2 cycles of ATRA and ATO without chemotherapy, followed by 2 years o

165 ete remission, patients received 4 cycles of ATRA plus ATO consolidation.

166 f patients relapse due to the development of ATRA resistance.

167 The protective effect of ATRA in gut inflammation and diarrheal diseases has been

168 l, revealing a potent antileukemic effect of ATRA in the presence of IDH1 mutation.

169 contributes to the anti-migratory effect of ATRA.

170 es were undertaken to examine the effects of ATRA on DRA expression.

171 The effects of ATRA on EMT are largely unknown.

172 ve T cells were compared, and the effects of ATRA on gammadelta T cells and CD25(+) dendritic cell (D

173 to many of the known adverse side effects of ATRA treatment, including skin irritation and hair loss.

174 icles significantly enhanced the efficacy of ATRA against HCC tumor growth in mice through reducing P

175 However, the efficacy of ATRA against solid tumors is limited due to its short ha

176 satory 30-50% reduction in the expression of ATRA synthetic genes and a 120% increase in the expressi

177 non-toxic controlled release formulation of ATRA for effective HCC therapy.

178 APK activation was bistable as a function of ATRA exposure.

179 RA), and SWOG S0521 (single-arm induction of ATRA + cytarabine + daunorubicin).

180 Indeed, inhibition of ATRA metabolism enhanced the sensitivity of HCC cells to

181 RS3 leads to a 40% increase in the levels of ATRA and a 60% and 55% decrease in the levels of retinol

182 9 when stimulated by physiological levels of ATRA, even though Tconv and Treg express similar levels

183 selective targeting by a hybrid molecule of ATRA with a 2-aminoanilide tail of the HDAC inhibitor MS

184 intensity combined with the orthogonality of ATRA chemistry allows well-defined chemically differenti

185 ificantly enhanced the inhibitory potency of ATRA on HCC cell growth, improving IC50 by over 3-fold.

186 ing that LZTFL1 is an important regulator of ATRA-induced T cell response.

187 noninferiority and P=0.02 for superiority of ATRA-arsenic trioxide).

188 y, we provide evidence that the synergism of ATRA and FLT3 TKIs is at least in part due to the observ

189 nt HRQOL findings further support the use of ATRA plus arsenic trioxide as preferred first-line treat

190 PRalpha/LBD mutant patients who relapsed off-ATRA (n = 5) had associated ACA.

191 y assigned to ATRA and idarubicin (n=119) or ATRA and arsenic trioxide (n=116).

192 ere randomly assigned to receive ATRA-ATO or ATRA-CHT between October 2007 and January 2013.

193 treatment with ATRA and arsenic trioxide or ATRA and idarubicin.

194 ption factor is involved in modulating other ATRA-inducible genes.

195 ts show that the advantages of ATRA-ATO over ATRA-CHT increase over time and that there is significan

196 sponse and a promising avenue for overcoming ATRA resistance.

197 and general method based on a photomediated ATRA reaction for the spatially controlled functionaliza

198 adjuvant (CFA), with or without a preceding ATRA treatment.

199 Prolonged ATRA treatment after chemotherapy can cure patients with

200 6 patients were randomly assigned to receive ATRA-ATO or ATRA-CHT between October 2007 and January 20

201 For induction, all patients received ATRA (45 mg/m(2) daily) and ATO (0.15 mg/kg daily) with

202 ion of 2-HG production significantly reduced ATRA effects in mutant IDH1 cells.

203 ith the standard chemotherapy-based regimen (ATRA and idarubicin) in both high-risk and low-risk pati

204 A slow-releasing ATRA formulation inhibits solid tumors such as HCC, but

205 ith a better potency than the slow-releasing ATRA formulation, consistent with its improved pharmacok

206 higher Cmax and AUC over the slow-releasing ATRA formulation.

207 Moreover, slow-releasing ATRA potently and dose-dependently inhibited HCC growth

208 Forced expression of PHF8 resensitizes ATRA-resistant APL cells, whereas its downregulation con

209 e pharmacologically manipulated to resurrect ATRA sensitivity to resistant cells.

210 Similarly, ATRA increased DRA protein expression by approximately 5

211 including NB4 cells) and restores it in some ATRA-resistant cells (including NB4-LR1 cells).

212 n is able to restore differentiation in some ATRA-resistant cells and eradicate leukemia-initiating c

213 uction and consolidation therapy or standard ATRA-idarubicin induction therapy followed by three cycl

214 e (ATO) is at least not inferior to standard ATRA and chemotherapy (CHT) in first-line therapy of low

215 Conformational experiments supported ATRA-induced bistability.

216 Thus, we conclude that ATRA enhances both Arg-1 and iNOS expression in IFN-gamm

217 nist (LE-135) studies further confirmed that ATRA exerts its effects through RAR-beta.

218 Knockdown experiments demonstrate that ATRA-mediated decrease in total cellular cholesterol con

219 and vitamin D, respectively, indicates that ATRA and 1,25D3 induce mechanistically distinct antimicr

220 Here we report that ATRA, an active metabolite of vitamin A, restores mechan

221 We show that ATRA reduces the ability of PSCs to generate high tracti

222 Moreover, Lcn2 deficiency abolished the ATRA effect on RBP4 expression in adipocytes.

223 functional differentiation markers from the ATRA-inducible transcription factors.

224 Patients in the ATRA and arsenic trioxide group had significantly less r

225 and idarubicin group and 40 patients in the ATRA and arsenic trioxide group reported grade 3-4 toxic

226 In the ATRA and arsenic trioxide group, arsenic trioxide was gi

227 idarubicin group versus 5 (5%) of 95 in the ATRA and arsenic trioxide group, raised liver alanine tr

228 idarubicin group versus 2 (3%) of 77 in the ATRA and arsenic trioxide group; no other toxicities rea

229 Overall, 57 patients in the ATRA and idarubicin group and 40 patients in the ATRA an

230 s reported in 25 (28%) of 89 patients in the ATRA and idarubicin group versus 2 (3%) of 77 in the ATR

231 s reported in 23 (23%) of 98 patients in the ATRA and idarubicin group versus 5 (5%) of 95 in the ATR

232 In the ATRA and idarubicin group, idarubicin was given intraven

233 cts of supportive care than did those in the ATRA and idarubicin group.

234 ar event-free survival rates were 97% in the ATRA-arsenic trioxide group and 86% in the ATRA-chemothe

235 ssion was achieved in all 77 patients in the ATRA-arsenic trioxide group who could be evaluated (100%

236 ents achieved complete remission (CR) in the ATRA-ATO and ATRA-CHT arms, respectively ( P = .12).

237 uded two relapses and one death in CR in the ATRA-ATO arm and two instances of molecular resistance a

238 ll survival at 50 months for patients in the ATRA-ATO versus ATRA-CHT arms were 97.3% v 80%, 1.9% v 1

239 e ATRA-arsenic trioxide group and 86% in the ATRA-chemotherapy group (95% confidence interval for the

240 uated (100%) and in 75 of 79 patients in the ATRA-chemotherapy group (95%) (P=0.12).

241 Two patients in the ATRA-CHT arm developed a therapy-related myeloid neoplas

242 n, 15 relapses, and five deaths in CR in the ATRA-CHT arm.

243 and a 120% increase in the expression of the ATRA catabolic enzyme Cyp26a1 in Dhrs3(-/-) embryos vs.

244 icantly enhancing dermal accumulation of the ATRA in explant pig skin.

245 gations revealed that miR-181a/b targets the ATRA-regulated tumor suppressor gene RASSF1A by direct b

246 Therefore, ATRA inhibits the ability of PSCs to mechanically releas

247 X-ray crystallography, we suspect that this ATRA-active species is a RuxCly(PCy3)z complex.

248 Thus, ATRA alone or in combination can be tested for efficacy

249 Thus, ATRA simultaneously blocks multiple Pin1-regulated cance

250 ients were enrolled and randomly assigned to ATRA and idarubicin (n=119) or ATRA and arsenic trioxide

251 2-HG sensitized wild-type IDH1 AML cells to ATRA-induced myeloid differentiation, whereas inhibition

252 ism enhanced the sensitivity of HCC cells to ATRA.

253 eukemia cell line HL-60[R] by exposing it to ATRA, followed by sequential increases of one-half log c

254 he enzyme responsible for converting Rald to ATRA in adult animals.

255 contribution of retinaldehyde reductases to ATRA metabolism is not completely understood.

256 d or refractory disease that is resistant to ATRA is a clinically significant problem.

257 that HL-60[R] cells were highly resistant to ATRA, doxorubicin, and etoposide.

258 ation sustain a CSC pool highly resistant to ATRA, where inhibition of PKCzeta directs the resistant

259 cell line enriched for CSCs was resistant to ATRA, which was reversed by MAP kinase inhibitors.

260 dy, using NB4 APL cell variants resistant to ATRA-induced differentiation, we reveal distinct functio

261 t of the EVI-1-positive AML cases respond to ATRA by induction of differentiation and decreased clono

262 y was significantly increased in response to ATRA indicating transcriptional activation.

263 vated ( approximately 4-fold) in response to ATRA with induction starting as early as 8 h of incubati

264 which catalyzes the conversion of retinal to ATRA, was preferentially expressed by small intestine CD

265 -positive primary AML cases are sensitive to ATRA, suggesting that combining ATRA with the currently

266 at least not inferior and may be superior to ATRA plus chemotherapy in the treatment of patients with

267 oxide (ATO) has been shown to be superior to ATRA plus chemotherapy in the treatment of standard-risk

268 and interferes with protein translation, to ATRA sharply increases APL cell killing to the extent th

269 relapse than, and survival not different to, ATRA and idarubicin, with a low incidence of liver toxic

270 etical (and practical) basis for translating ATRA/ATO-based strategies to non-APL acute myelocytic le

271 This suggests that in Treg, ATRA-induced upregulation of CCR9 and alpha4beta7 is dep

272 e, metathesis-inactive species under typical ATRA conditions.

273 er in APL blasts and NB4 leukemia cells upon ATRA treatment as a key event in the drug response.

274 expression of their downstream targets upon ATRA treatment.

275 Our findings also caution against using ATRA to modulate myeloid cell differentiation and functi

276 0 months for patients in the ATRA-ATO versus ATRA-CHT arms were 97.3% v 80%, 1.9% v 13.9%, and 99.2%

277 etinoic acid (ATRA) plus chemotherapy versus ATRA plus arsenic trioxide in patients with newly diagno

278 , consisting of daunorubicin + cytarabine vs ATRA), and SWOG S0521 (single-arm induction of ATRA + cy

279 We show that MC2392 elicits weak ATRA and essentially no HDACi activity in vitro or in vi

280 ients substantially, we investigated whether ATRA might also be effective for the subgroup of AML pat

281 findings elucidate mechanisms through which ATRA may contribute to liver immune tolerance.

282 ks to clarify the mechanism(s) through which ATRA promotes the development of tolerogenic DCs.

283 treatment of primary EVI-1-positive AML with ATRA leads to a significant reduction in leukemic engraf

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

285 n HL-60[R] cells and repressed in cells with ATRA-induced differentiation were related to mismatch re

286 trial comparing ATRA plus chemotherapy with ATRA plus arsenic trioxide in patients with APL classifi

287 , which may be augmented by combination with ATRA.

288 As compared with ATRA-chemotherapy, ATRA-arsenic trioxide was associated

289 ileukemic efficacy of ATO-ATRA compared with ATRA-CHT in low- and intermediate-risk APL.

290 However, cotreatment with ATRA reduces Bcl6 expression to baseline levels through

291 apy, followed by 2 years of maintenance with ATRA, oral methotrexate, and 6-mercaptopurine.

292 Stimulation of primary human monocytes with ATRA did not result in expression of the antimicrobial p

293 he increased metastatic growth observed with ATRA treatment.

294 nockdown of CXCL12 or treatment of PSCs with ATRA.

295 y three cycles of consolidation therapy with ATRA plus chemotherapy and maintenance therapy with low-

296 t difference, favoring patients treated with ATRA plus arsenic trioxide, was found for fatigue severi

297 and randomised 1:1 to receive treatment with ATRA and arsenic trioxide or ATRA and idarubicin.

298 Treatment with ATRA and NaBu synergistically attenuated the expression

299 ity of FLT3/ITD(+) cells upon treatment with ATRA and TKI.

300 atment with arsenic trioxide with or without ATRA have shown high efficacy and reduced hematologic to