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 signaled through the retinoid X receptor to decreas

6 ATRA treatment specifically decreased cell viability and

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

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

9 ATRA-induced Pin1 ablation also potently inhibits triple

10 ATRA-induced Pin1 ablation degrades the protein encoded

11 ATRA-induced Pin1 degradation inhibited the growth of HC

12 ATRA-PLLA microparticles exerted its efficacy likely thr

13 ATRA-PLLA microparticles had good biocompatibility, and

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

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

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

17 s with advanced, unresectable PDAC (n = 27), ATRA is re-purposed as a stromal-targeting agent in comb

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

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

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

21 targeted therapies: all-trans retinoic acid (ATRA) and arsenic both target and degrade its ProMyelocy

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

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

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

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

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

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

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

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

30 1 and K10 by adding all-trans retinoic acid (ATRA) but increased for K2 in the absence of PR.

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

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

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

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

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

36 tients treated with all-trans retinoic acid (ATRA) in combination with anthracycline-based chemothera

37 bitor valproate and all-trans retinoic acid (ATRA) in treatment-naive elderly patients with acute mye

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 lly, we reveal that all trans retinoic acid (ATRA) induces VCP expression, creating a positive feedba

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

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

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

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

47 In mammals, all-trans retinoic acid (ATRA) is instrumental to spermatogenesis.

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

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

50 pact of exposure to all-trans retinoic acid (ATRA) on wild-type NK and CD38KO NK cell function and hi

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

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

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

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

55 ource of diffusible all-trans retinoic acid (ATRA) that allow their targeting by the EOMs in a tempor

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

57 ave also found that all-trans retinoic acid (ATRA) treatment increased AGAP2 protein levels in both c

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

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

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

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

62 active metabolite, all-trans retinoic acid (ATRA), exhibits a potent antiviral property by enhancing

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

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

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

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

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

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

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

70 ated with increased all-trans retinoic acid (ATRA)-induced differentiation, generation of reactive ox

71 ession and inhibits all-trans-retinoic acid (ATRA)-induced myeloid differentiation of AML cells.

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

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

74 neuronal cells with all-trans retinoic acid (ATRA).

75 stellate cells with all-trans-retinoic-acid (ATRA) reprograms pancreatic stroma to suppress pancreati

76 Vitamin A (all trans retinoic acid, ATRA) treated leukemic cells had increased apoptosis, de

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

78 the sustained controlled delivery of active ATRA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

93 ation of CBFA2T3 resulted in spontaneous and ATRA-induced activation of myeloid-specific genes in a m

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

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

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

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

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

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

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

101 modified receptor accumulation occurs before ATRA treatment; therefore, the transcritptional defect i

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

103 Blocking ATRA-induced cellular cholesterol reduction inhibits ant

104 ly demonstrate that FLT3-ITD severely blunts ATRA response.

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

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

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

108 We found that the engagement of CRABP1 by ATRA potently supported viral infection by promoting the

109 nulocytic differentiation program induced by ATRA in APL.

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

111 is involved in the inhibition of motility by ATRA.

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

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

114 The combined ATRA/arsenic regimen now cures virtually all patients wi

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

116 otential benefits and drawbacks of combining ATRA with DARA in patients with MM.

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

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

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

120 In contrast, ATRA binding to CRABP2 potently inhibited HCV via suppre

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

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

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

124 In contrast, knockdown of APLNR diminished ATRA-induced growth inhibition of NPC cells.

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

126 both necessary and sufficient for enhancing ATRA-induced myeloid gene expression and differentiation

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

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

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

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

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

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

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

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

135 D) was an adverse risk factor for historical ATRA/chemotherapy regimens, the molecular bases for this

136 lsions to incorporate the highly hydrophobic ATRA drug.

137 loitation of CRABP1 functionality.IMPORTANCE ATRA, a biologically active metabolite of vitamin A, exe

138 ression of several developmentally important ATRA target genes.

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

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

141 APLNR is involved in ATRA-induced growth inhibition of nasopharyngeal carcino

142 1beta siRNA indicative of its involvement in ATRA-induced effects on DRA expression.

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

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

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

146 though the transcriptional output of initial ATRA response is unaffected, ATRA-induced PML/RARA degra

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

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

149 ly enriched with retinoid and its metabolite ATRA, it supports the establishment of efficient hepatit

150 Moreover ATRA-PLLA microparticles significantly enhanced the effi

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

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

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

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

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

156 The addition of ATRA resulted in a higher remission rate (21.9% with ATR

157 The addition of ATRA to decitabine resulted in a higher remission rate a

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

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

160 ibuting to two-thirds of the total amount of ATRA present in the testis.

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

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

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

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

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

166 Critically, the combination of ATRA and arsenic fully rescues therapeutic response in F

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

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

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

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

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

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

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

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

175 contributes to the anti-migratory effect of ATRA.

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

177 The effects of ATRA on EMT are largely unknown.

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

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

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

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

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

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

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

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

186 9 when stimulated by physiological levels of ATRA, even though Tconv and Treg express similar levels

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

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

189 10 mRNAs are destabilised in the presence of ATRA.

190 s how HCV evades the antiviral properties of ATRA via the exploitation of CRABP1 functionality.IMPORT

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

192 the relative contributions of each source of ATRA, we have generated mice lacking all RALDH activitie

193 that both the SC- and GC-derived sources of ATRA cooperate to initiate and propagate spermatogenetic

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

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

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

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

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

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

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

201 sponse and a promising avenue for overcoming ATRA resistance.

202 Prolonged ATRA treatment after chemotherapy can cure patients with

203 Re-purposing ATRA as a stromal-targeting agent with gemcitabine-nab-p

204 istently, after treatment with all-trans-RA (ATRA), we found that APLNR was significantly up-regulate

205 6 patients were randomly assigned to receive ATRA-ATO or ATRA-CHT between October 2007 and January 20

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

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

208 cell lines whilst curcumin treatment reduced ATRA-mediated AGAP2 increase.

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

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

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

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

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

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

215 Similarly, ATRA increased DRA protein expression by approximately 5

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

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

218 Conformational experiments supported ATRA-induced bistability.

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

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

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

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

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

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

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

226 PML nuclear bodies in APL eradication by the ATRA/arsenic combination.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

245 ermatogonia differentiation depends upon the ATRA synthesized by RALDH inside the SE, whereas initiat

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 simultaneously blocks multiple Pin1-regulated cance

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

250 2-HG sensitized wild-type IDH1 AML cells to ATRA-induced myeloid differentiation, whereas inhibition

251 ism enhanced the sensitivity of HCC cells to ATRA.

252 Secondary outcomes show no detriment to ATRA pharmacokinetics..

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

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

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

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

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

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

259 scovered that the hepatocellular response to ATRA creates either a proviral or an antiviral environme

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

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

262 l target for enhancing AML responsiveness to ATRA differentiation therapies.

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

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

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

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

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

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

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

270 tput of initial ATRA response is unaffected, ATRA-induced PML/RARA degradation is blunted, as is PML

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

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

273 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%

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

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

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

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

278 e-specific cell-intrinsic mechanism by which ATRA exerts either a proviral or antiviral effect, depen

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

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

281 ulted in a higher remission rate (21.9% with ATRA v 13.5% without ATRA; odds ratio, 1.80; 95% CI, 0.8

282 ose of gemcitabine-nab-paclitaxel along-with ATRA (45 mg/m(2) orally, days 1-15/cycle).

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

284 less favorable outcome of FLT3-ITD APLs with ATRA-based regimens, and stress the key role of PML nucl

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

286 , which may be augmented by combination with ATRA.

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

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

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

290 Median overall survival was 8.2 months with ATRA v 5.1 months without ATRA (hazard ratio, 0.65; 95%

291 he increased metastatic growth observed with ATRA treatment.

292 At least for patients treated with ATRA and anthracycline-based chemotherapy, ISAPL modelin

293 ression in a cohort of patients treated with ATRA and anthracyclines, revealed that NTAL overexpressi

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

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

296 Treatment with ATRA and NaBu synergistically attenuated the expression

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

298 ission rate (21.9% with ATRA v 13.5% without ATRA; odds ratio, 1.80; 95% CI, 0.86 to 3.79; one-sided

299 as 8.2 months with ATRA v 5.1 months without ATRA (hazard ratio, 0.65; 95% CI, 0.48 to 0.89; two-side

300 of STRA8 by spermatocytes can occur without ATRA.