ライフサイエンスコーパス: promyelocytic

1 ranulocytic differentiation of HL-60 and NB4 promyelocytic cell lines and of human CD34(+) primary ce

2 yeloid progenitor cells and CDllb(lo)Gr1(lo) promyelocytic cells within the bone marrow, as well as r

3 Importantly, in human promyelocytic cells, H3K27me3 is also dependent on mC.

4 hanges in acute myeloid leukemia (AML) human promyelocytic cells.

5 ransferases (ST6GalNAc1, -2, or -4) in human promyelocytic HL-60 cells altered glycan structures and

6 tives 4a, 4d, and 4f were evaluated in human promyelocytic HL-60, breast carcinoma MCF-7, and neurobl

7 ellular carcinoma (Hep 3B 2.1-7 and Hep G2), promyelocytic (HL-60) and chronic myelogenous (K-562) le

8 Here we show that, in acute promyelocytic leukaemia (APL), ILC2s are increased and h

9 previously unknown role for the cytoplasmic promyelocytic leukaemia (cPML) tumour suppressor in TGF-

10 (CBMNCyt) assay conducted with respectively, promyelocytic leukaemia (HL-60) and colon adenocarcinoma

11 myelomonocytic leukaemia (WEHI-3) and Human promyelocytic leukaemia (HL-60) cell lines.

12 Furthermore, the cytoplasmic localization of promyelocytic leukaemia (PML) is mediated by its nuclear

13 The promyelocytic leukaemia (PML) protein controls multiple

14 Here, we show that the tumour suppressor promyelocytic leukaemia (PML) protein is a circadian clo

15 signatures, including the linear form of the promyelocytic leukaemia (PML)-defined structure in iPSCs

16 c acid (RA)-induced differentiation of acute promyelocytic leukaemia and HL-60 cells, CD38 is one of

17 Acute promyelocytic leukaemia is a chemotherapy-sensitive subg

18 Here we report that promyelocytic leukaemia zinc finger (PLZF), the BTB-zinc

19 istinct lineage that originates from a novel promyelocytic leukaemia zinc finger (PLZF)-expressing IL

20 for acute myeloid leukaemia (excluding acute promyelocytic leukaemia) compared with chemotherapy alon

21 gible patients (aged >/=16 years) with acute promyelocytic leukaemia, confirmed by the presence of th

22 We excluded those with acute promyelocytic leukaemia, those seen only for a one-time

23 Here the authors show that, in acute promyelocytic leukaemia, tumour-activated ILC2s secrete

24 n low-risk and high-risk patients with acute promyelocytic leukaemia, with a high cure rate and less

25 h high-risk and low-risk patients with acute promyelocytic leukaemia.

26 We also observed robust engraftment of acute promyelocytic leukemia (APL) and myelofibrosis (MF) samp

27 lucidated the DNA methylome in primary acute promyelocytic leukemia (APL) and the role of promyelocyt

28 l residual disease (MRD) monitoring in acute promyelocytic leukemia (APL) are available only in the c

29 etinoic acid (ATRA) -based therapy for acute promyelocytic leukemia (APL) averages 70% at 5 years.

30 study, we investigated the dynamics of acute promyelocytic leukemia (APL) before and during therapy w

31 gap in quality of care and outcomes in acute promyelocytic leukemia (APL) between developed and devel

32 rinolysis is an important component of acute promyelocytic leukemia (APL) bleeding diathesis.

33 S) has excellent cytotoxic activity in acute promyelocytic leukemia (APL) but its activity in solid t

34 In most acute promyelocytic leukemia (APL) cases, translocons produce

35 expression was significantly lower in acute promyelocytic leukemia (APL) compared with non-APL patie

36 n successfully used as a treatment for acute promyelocytic leukemia (APL) for more than a decade.

37 rans retinoic acid (ATRA) treatment in acute promyelocytic leukemia (APL) has been the paradigm of ta

38 Acute promyelocytic leukemia (APL) is a distinct subtype of ac

39 Acute promyelocytic leukemia (APL) is a hematological malignan

40 Acute promyelocytic leukemia (APL) is a malignancy of the bone

41 Because PML-RARA-induced acute promyelocytic leukemia (APL) is a morphologically differ

42 Acute promyelocytic leukemia (APL) is a subtype of acute myelo

43 A hallmark of acute promyelocytic leukemia (APL) is altered nuclear architec

44 Acute promyelocytic leukemia (APL) is characterized by a block

45 Acute promyelocytic leukemia (APL) is characterized by granulo

46 Acute promyelocytic leukemia (APL) is characterized by the t(1

47 Acute promyelocytic leukemia (APL) is commonly complicated by

48 Acute promyelocytic leukemia (APL) is driven by a chromosomal

49 -trans retinoic acid and chemotherapy, acute promyelocytic leukemia (APL) is now the most curable typ

50 Acute promyelocytic leukemia (APL) is rare in children.

51 onstrated that the immense majority of acute promyelocytic leukemia (APL) patients can be definitivel

52 Up to 15% of acute promyelocytic leukemia (APL) patients fail to achieve or

53 Acute promyelocytic leukemia (APL) remains the best example of

54 population of unselected patients with acute promyelocytic leukemia (APL) remains unknown because of

55 lantation advantage and development of acute promyelocytic leukemia (APL) required DNMT3A.

56 ns retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered the firs

57 31 trial for newly diagnosed pediatric acute promyelocytic leukemia (APL) was a phase III historicall

58 Acute promyelocytic leukemia (APL), a cytogenetically distinct

59 In acute promyelocytic leukemia (APL), all-trans retinoic acid (A

60 In acute promyelocytic leukemia (APL), both isoforms are expresse

61 In acute promyelocytic leukemia (APL), repression by the PML-RARa

62 emotherapy is the standard of care for acute promyelocytic leukemia (APL), resulting in cure rates ex

63 In PML/RARA-driven acute promyelocytic leukemia (APL), retinoic acid (RA) induces

64 s performed, yielding the diagnosis of acute promyelocytic leukemia (APL), with t(15;17)(q23;q21.1) i

65 nd PMLRARalpha interaction with Fas in acute promyelocytic leukemia (APL)-derived cells and APL prima

66 eloid differentiation genes and drives acute promyelocytic leukemia (APL).

67 y effective agent for the treatment of acute promyelocytic leukemia (APL).

68 ceptor-alpha (PML-RARalpha)-associated acute promyelocytic leukemia (APL).

69 y diagnosed, low- or intermediate-risk acute promyelocytic leukemia (APL).

70 e experience as many surprises as with acute promyelocytic leukemia (APL).

71 RAR is involved in the pathogenesis of acute promyelocytic leukemia (APL).

72 -RARalpha fusion protein causative for acute promyelocytic leukemia (APL).

73 h distinct outcomes in newly diagnosed acute promyelocytic leukemia (APL).

74 as a therapeutic drug for treatment of acute promyelocytic leukemia (APL).

75 e therapy of low- or intermediate-risk acute promyelocytic leukemia (APL).

76 te PML and the PML-RARA oncoprotein of acute promyelocytic leukemia (APL).

77 tanding of the coagulopathy present in acute promyelocytic leukemia (APL).

78 guide molecularly targeted therapy in acute promyelocytic leukemia (APL).

79 that contributes to the development of acute promyelocytic leukemia (APL).

80 ard-risk patients with newly diagnosed acute promyelocytic leukemia (APL).

81 , a curative agent in clinical use for acute promyelocytic leukemia (APL); in our studies, ATO inhibi

82 e treatment for patients with relapsed acute promyelocytic leukemia (APL); its role as consolidation

83 es (IRR = 2.20) to nearly equal IRs of acute promyelocytic leukemia (APL; IRR = 1.08).

84 comes in patients with newly diagnosed acute promyelocytic leukemia (APL; see figure).

85 n assayed for cytotoxicity against the human promyelocytic leukemia (HL-60) cell line.

86 To validate our method, we mechanotype human promyelocytic leukemia (HL-60) cells and thereby confirm

87 We used human promyelocytic leukemia (HL-60) cells as a model system t

88 bed here is toxic toward cancer cells (human promyelocytic leukemia (HL-60), IC(50) = 9 muM, and huma

89 ing to the International Consortium on Acute Promyelocytic Leukemia (IC-APL) study.

90 The International Consortium on Acute Promyelocytic Leukemia (IC-APL) was established to creat

91 nts of the International Consortium on Acute Promyelocytic Leukemia (IC-APL), an initiative of the In

92 scitation (n=116) and to patients with acute promyelocytic leukemia (n=83).

93 ssociation of the major organizer of ND10, a promyelocytic leukemia (PML) and ND10 constituent, Sp100

94 egradation of both sumoylated and unmodified promyelocytic leukemia (PML) and other sumoylated cellul

95 The effective BGLF4-mediated dispersion of promyelocytic leukemia (PML) bodies was dependent on SUM

96 We identified a metabolic function for the promyelocytic leukemia (PML) gene, uncovering an unexpec

97 Promyelocytic Leukemia (PML) is a nuclear protein that f

98 Promyelocytic leukemia (PML) is a pleiotropic tumor supp

99 The tumor-suppressor protein promyelocytic leukemia (PML) is aberrantly degraded in m

100 red nuclear architecture, with disruption of promyelocytic leukemia (PML) nuclear bodies (NBs) mediat

101 Promyelocytic leukemia (PML) nuclear bodies (NBs) recrui

102 at K120 and K382 and colocalizes with p53 in promyelocytic leukemia (PML) nuclear bodies following ce

103 Promyelocytic leukemia (PML) nuclear bodies selectively

104 the proviral chromatin in close proximity to promyelocytic leukemia (PML) nuclear bodies, a reversibl

105 iction mediated by one or more components of promyelocytic leukemia (PML) nuclear bodies, and IE1 and

106 d on IFN-induced gene products associated to promyelocytic leukemia (PML) nuclear bodies, and we show

107 atin remodeling complexes and associate with promyelocytic leukemia (PML) nuclear bodies.

108 from the nucleolus, but it also disorganizes promyelocytic leukemia (PML) nuclear bodies.

109 Promyelocytic leukemia (PML) plays a tumor suppressive r

110 The promyelocytic leukemia (PML) protein has been implicated

111 etreated with siX3, but not siUL54, retained promyelocytic leukemia (PML) protein in cellular PML bod

112 The promyelocytic leukemia (PML) protein is a tumor suppress

113 The promyelocytic leukemia (PML) protein is a tumor suppress

114 The promyelocytic leukemia (PML) protein is an essential com

115 The promyelocytic leukemia (PML) protein organizes PML nucle

116 is found in punctate domains associated with promyelocytic leukemia (PML) protein within the nucleus.

117 n 10 (ND10) components, including hDaxx, the promyelocytic leukemia (PML) protein, and Sp100.

118 The promyelocytic leukemia (PML) protein, initially discover

119 CV LTA as well as an increased expression of promyelocytic leukemia (PML) protein, which is known to

120 8) promotes the degradation of the antiviral promyelocytic leukemia (PML) protein.

121 tein mediates functional inactivation of the promyelocytic leukemia (PML) tumor suppressor pathway.

122 Here we identify a previously unknown promyelocytic leukemia (PML)-peroxisome proliferator-act

123 us arsenic trioxide (ATO), which degrade the promyelocytic leukemia (PML)-retinoic acid receptor fusi

124 s expression of the tumor suppressor protein promyelocytic leukemia (PML).

125 mias (MLL-AF9;Nras(G12D); PML-RARalpha acute promyelocytic leukemia [APL] cells) and Emicro-Myc lymph

126 onic myeloblastic leukemia and ATRA in acute promyelocytic leukemia [APL]).

127 )) is an effective therapeutic against acute promyelocytic leukemia and certain solid tumors.

128 The interior of the spheres contained promyelocytic leukemia and HSP70 proteins.

129 or suppressor originally identified in acute promyelocytic leukemia and implicated in tumorigenesis i

130 odulatory effects and is used to treat acute promyelocytic leukemia and inflammatory disorders such a

131 tric acute myeloid leukemia (AML), excluding promyelocytic leukemia and myeloid neoplasms of patients

132 translocation (15:17) and expression of the promyelocytic leukemia and the retinoic receptor alpha (

133 ast-phase chronic myeloid leukemia and acute promyelocytic leukemia arguing against this strategy.

134 acid decreased plasminogen binding to acute promyelocytic leukemia blasts.

135 hsaki et al. show that the nuclear membrane, promyelocytic leukemia bodies, and the protein PML-II pl

136 ozogamicin is efficacious not only for acute promyelocytic leukemia but, in combination with conventi

137 ul strategy to treat AML, as proved in acute promyelocytic leukemia by treatment with all-trans retin

138 pendent and -independent manner in the human promyelocytic leukemia cell line HL-60.

139 Cells of human promyelocytic leukemia cell line-60 were differentiated

140 toxicity (IC50) of the prodrugs toward human promyelocytic leukemia cells (HL-60) from 52 to 12 muM.

141 anspeptidase (gamma-GT) protects human acute promyelocytic leukemia cells (NB4) from Dar, but not fro

142 th the accumulation of Hsp70 protein in HL60 promyelocytic leukemia cells recovering from acute therm

143 ted chemotaxis of differentiated HL-60 human promyelocytic leukemia cells was blocked by PPTN with a

144 the combination of the two methods on human promyelocytic leukemia cells, our results surprisingly r

145 d in breast and prostate cancer cells and in promyelocytic leukemia cells.

146 gulated Oct4 during differentiation of HL-60 promyelocytic leukemia cells.

147 he passive selection of ATRA-resistant acute promyelocytic leukemia clones leading to disease relapse

148 tarabine-induced cellebellar toxicity, acute promyelocytic leukemia differentiation syndrome, thrombo

149 ominant-negative-acting transcription factor promyelocytic leukemia gene (PML)/RARalpha, which is gen

150 The treatment of acute promyelocytic leukemia has improved considerably after r

151 trioxide is an effective treatment for acute promyelocytic leukemia has renewed interest in the pharm

152 us cell cancer FaDu (intermediate EpCAM) and promyelocytic leukemia HL60 (EpCAM-negative) xenografts.

153 f our method not only by screening two acute promyelocytic leukemia human cells lines (NB4 and AP-106

154 on therapy in the setting of high-risk acute promyelocytic leukemia in first remission.

155 Human acute promyelocytic leukemia is causally linked to chromosomal

156 rkers of differentiation therapy in an acute promyelocytic leukemia model treated with all-trans reti

157 ere further tested in vivo in a murine acute promyelocytic leukemia model, resulting 14d the most eff

158 ct nuclear bodies, including nucleoli (148), promyelocytic leukemia nuclear bodies (38), nuclear spec

159 Using promyelocytic leukemia nuclear bodies (PML NBs) as a mod

160 ported that MORC3, a protein associated with promyelocytic leukemia nuclear bodies (PML NBs), is a ta

161 irus 1 (HSV-1) is conferred by components of promyelocytic leukemia nuclear bodies (PML NBs), which r

162 ral cellular proteins that are components of promyelocytic leukemia nuclear bodies (PML NBs, also kno

163 Promyelocytic leukemia nuclear bodies (PML-NB) are sub-n

164 ge-limited human fibroblasts by dissociating promyelocytic leukemia nuclear bodies (PML-NBs).

165 Promyelocytic leukemia nuclear bodies (PML-NBs)/nuclear

166 , ErbB4 colocalized with PIAS3 and SUMO-1 in promyelocytic leukemia nuclear bodies, nuclear domains i

167 tivity-induced increase in the expression of promyelocytic leukemia nuclear bodies, which decreases G

168 intrinsic antiviral immunity are mediated by promyelocytic leukemia nuclear body (PML-NB) constituent

169 in E1A/E1B-55K-mediated tumorigenesis, other promyelocytic leukemia nuclear body (PML-NB)/PML oncogen

170 ated intravascular coagulation scores, acute promyelocytic leukemia patients had higher fibrinogen bu

171 fferentiation will be useful for identifying promyelocytic leukemia patients who are eligible for new

172 an both nondrowning cardiac arrest and acute promyelocytic leukemia patients.

173 We report here an interaction between promyelocytic leukemia protein (PML) and ASC.

174 dation during lytic infection, including the promyelocytic leukemia protein (PML) and its small ubiqu

175 e residues and vicinal thiol groups, such as promyelocytic leukemia protein (PML) and PML-retinoic ac

176 P0, via degradation of the ND10 constituents promyelocytic leukemia protein (PML) and Sp100 and the s

177 ontains an E3 ubiquitin ligase that degrades promyelocytic leukemia protein (PML) and Sp100, two majo

178 unctional activities of the tumor suppressor promyelocytic leukemia protein (PML) are mostly associat

179 We identified promyelocytic leukemia protein (PML) as a Fas-interactin

180 and it directly targets the tumor-suppressor promyelocytic leukemia protein (PML) for proteasomal deg

181 The tumor suppressor promyelocytic leukemia protein (PML) functions as a stre

182 Promyelocytic leukemia protein (PML) has been implicated

183 PK2 in nuclear speckles and association with promyelocytic leukemia protein (PML) in response to DNA

184 Promyelocytic leukemia protein (PML) is a tumor suppress

185 Promyelocytic leukemia protein (PML) is an essential org

186 Promyelocytic leukemia protein (PML) modulates the p53 t

187 infection, the virus genome is localized to promyelocytic leukemia protein (PML) nuclear bodies (NB)

188 moylation pathway, and both proteins disrupt promyelocytic leukemia protein (PML) nuclear bodies (NBs

189 Promyelocytic leukemia protein (PML) nuclear bodies (NBs

190 P0 localizes to cellular structures known as promyelocytic leukemia protein (PML) nuclear bodies or N

191 The latter enforces promyelocytic leukemia protein (PML) nuclear body (NB) f

192 ed to HSV-1 genomes but had no effect on the promyelocytic leukemia protein (PML) or Sp100.

193 3 ubiquitin ligase E6AP in the regulation of promyelocytic leukemia protein (PML) stability and forma

194 Promyelocytic leukemia protein (PML) was originally iden

195 ization with ICP0 are distinct from those of promyelocytic leukemia protein (PML), a well-characteriz

196 olve direct interactions between ATO and the promyelocytic leukemia protein (PML), as well as acceler

197 r structures containing both constant [e.g., promyelocytic leukemia protein (PML), SP100, death domai

198 lear structures contain both constant [e.g., promyelocytic leukemia protein (PML), Sp100, death-domai

199 used to an N-terminal partner, most commonly promyelocytic leukemia protein (PML).

200 Specifically, the promyelocytic leukemia protein (TRIM19; also called PML)

201 mutations of which lead to BS, localizes to promyelocytic leukemia protein bodies and to the nucleol

202 zed by multitelomere clusters and associated promyelocytic leukemia protein bodies.

203 by translocating to the nucleus, increasing promyelocytic leukemia protein expression and decreasing

204 The promyelocytic leukemia protein is a well known tumor sup

205 n size and ultimately became juxtaposed with promyelocytic leukemia protein nuclear bodies.

206 a characterized intrinsic antiviral factor, promyelocytic leukemia protein, and are antagonized by I

207 bination with the intrinsic antiviral factor promyelocytic leukemia protein, significantly impairs th

208 leukemia (APL) cases, translocons produce a promyelocytic leukemia protein-retinoic acid receptor al

209 isruption and colocalize with Mdm2, p53, and promyelocytic leukemia protein.

210 INs abrogated arsenic-induced degradation of promyelocytic leukemia protein.

211 scence by activating the histone repressor A/promyelocytic leukemia senescence pathway.

212 additional cases of t(15;17)-negative acute promyelocytic leukemia that had cytogenetically invisibl

213 arsenic poisoning and in patients with acute promyelocytic leukemia that have been treated with arsen

214 ere complication seen in patients with acute promyelocytic leukemia treated with all-trans retinoic a

215 eferred a difficult diagnostic case of acute promyelocytic leukemia with no pathogenic X-RARA fusion

216 Seven were acute myeloid leukemia (2 acute promyelocytic leukemia with t(15;17), 2 with confirmed p

217 and IL-12Rbeta and the transcription factors promyelocytic leukemia zinc finger (PLZF) and RAR-relate

218 Two transcription factors, promyelocytic leukemia zinc finger (PLZF) and Slug were

219 e dependent on the transcriptional regulator promyelocytic leukemia zinc finger (PLZF) and the adapto

220 that RORgammat and the transcription factor promyelocytic leukemia zinc finger (PLZF) are valuable n

221 ave shown that the transcriptional regulator promyelocytic leukemia zinc finger (PLZF) controls the d

222 tigated the role of the transcription factor promyelocytic leukemia zinc finger (plzf) in HSC fate us

223 The transcription factor promyelocytic leukemia zinc finger (PLZF) is transiently

224 Here, we show that the transcription factor Promyelocytic Leukemia Zinc Finger (PLZF) plays a critic

225 We found that E proteins directly bound the promyelocytic leukemia zinc finger (PLZF) promoter and w

226 Expression of promyelocytic leukemia zinc finger (PLZF) protein direct

227 CRPC) reveals that 5% to 7% of tumors harbor promyelocytic leukemia zinc finger (PLZF) protein homozy

228 The transcription factor promyelocytic leukemia zinc finger (PLZF) seemed to cont

229 Most MAIT cells express the promyelocytic leukemia zinc finger (PLZF) transcription

230 Surprisingly, both promyelocytic leukemia zinc finger (PLZF)(+) and NK1.1(+

231 increase in the frequency of IL-4-producing promyelocytic leukemia zinc finger (PLZF)(hi) immature i

232 ctions with CD1d ligands prior to expressing promyelocytic leukemia zinc finger (PLZF), a broad compl

233 tional CD4 T cells by the sole expression of promyelocytic leukemia zinc finger (PLZF), a transcripti

234 acked expression of the transcription factor promyelocytic leukemia zinc finger (PLZF), as well as ex

235 gher expression of the transcription factors promyelocytic leukemia zinc finger (PLZF), eomesodermin,

236 essed the NKT lineage-specific transcription promyelocytic leukemia zinc finger (PLZF), indicating a

237 s, kallikrein related peptidase 4 (KLK4) and promyelocytic leukemia zinc finger (PLZF), integrate opt

238 Mechanistically, expression of Egr2 and promyelocytic leukemia zinc finger (PLZF), two key trans

239 T cells expressing the transcription factor promyelocytic leukemia zinc finger (PLZF), which confers

240 1 and beta-catenin regulate the frequency of promyelocytic leukemia zinc finger (PLZF)-expressing, IL

241 ce IL-4 and express the transcription factor promyelocytic leukemia zinc finger (PLZF).

242 aling, and the cells expressed both IL-4 and promyelocytic leukemia zinc finger (PLZF).

243 transcription factors Sal-like 4 (SALL4) and promyelocytic leukemia zinc finger (PLZF; also known as

244 Moreover, we show that promyelocytic leukemia zinc finger and IL-4 are also req

245 her analyses reveal that Hox5 interacts with promyelocytic leukemia zinc finger biochemically and gen

246 nip1(-/-) iNKT cells failed to down-regulate Promyelocytic leukemia zinc finger compared with their W

247 ugh binding of the transcriptional repressor promyelocytic leukemia zinc finger protein (PLZF) at the

248 bric-a-brac-zinc finger transcription factor promyelocytic leukemia zinc finger protein (PLZF).

249 PLZF (Promyelocytic Leukemia Zinc Finger protein), a member of

250 eroid-responsive transcription factor, PLZF (promyelocytic leukemia zinc finger protein), which media

251 h the expression of the transcription factor promyelocytic leukemia zinc finger protein.

252 yelocytic leukemia zinc finger; however, the promyelocytic leukemia zinc finger transgene does not re

253 nsion of a usually rare population of CD4(+) promyelocytic leukemia zinc finger(+) "gammadelta NKT" c

254 LRF was originally identified as a PLZF (promyelocytic leukemia zinc finger) homolog that physica

255 -/-) T cells require the presence of a novel promyelocytic leukemia zinc finger-expressing, SLAM fami

256 translocation produces two fusion proteins, promyelocytic leukemia zinc finger-retinoic acid recepto

257 tes expressing the transcriptional regulator promyelocytic leukemia zinc finger.

258 howed a significant upregulation of IL-4 and promyelocytic leukemia zinc finger.

259 dependent on the BTB-ZF transcription factor promyelocytic leukemia zinc finger.

260 pment is rescued by transgenic expression of promyelocytic leukemia zinc finger; however, the promyel

261 The transcription factor PLZF (promyelocytic leukemia zinc finger; zbtb16) is essential

262 However, promyelocytic leukemia zinc-finger (PLZF), a critical tr

263 ar localization and functional impairment of promyelocytic leukemia zinc-finger, a transcription fact

264 cancer), MCF-7 (breast cancer), HL-60 (Human promyelocytic leukemia), HepG2 (Hepatocellular carcinoma

265 sed Rara(+/-) mice with mice expressing PML (promyelocytic leukemia)-RARA from the cathepsin G locus

266 genic chromatin signature, we analyzed acute promyelocytic leukemia, a subtype of leukemia characteri

267 phocytic leukemia, arsenic trioxide in acute promyelocytic leukemia, and the BH3-mimetic ABT199 in ly

268 If one excludes acute promyelocytic leukemia, current AML management still rel

269 In acute promyelocytic leukemia, granulocytic differentiation is

270 iated with remissions in patients with acute promyelocytic leukemia, implying that G0S2 may possess t

271 were excluded, including patients with acute promyelocytic leukemia, incorrect diagnosis, or no adequ

272 rsenic trioxide, a frontline agent for acute promyelocytic leukemia, inhibits DeltaNp63 but not TAp63

273 lpha) oncofusion protein, which causes acute promyelocytic leukemia, inhibits TNFalpha induced gene e

274 nic trioxide, a drug for patients with acute promyelocytic leukemia, is found to target and degrade a

275 ndrome, thrombohemorrhagic syndrome in acute promyelocytic leukemia, L-asparaginase-associated thromb

276 n 1333 young adult patients, excluding acute promyelocytic leukemia, treated in the United Kingdom MR

277 ung adult patients with AML, excluding acute promyelocytic leukemia, using denaturing high-performanc

278 Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxidation p

279 those with core binding factor AML and acute promyelocytic leukemia, were randomly assigned to treatm

280 ing subclones) has been exemplified by acute promyelocytic leukemia, where successful targeting of th

281 The gene product of this ORF localizes to promyelocytic leukemia-adjacent nuclear bodies.

282 We show that Nrf2 traffics, in part, to promyelocytic leukemia-nuclear bodies (PML-NBs).

283 promyelocytic leukemia (APL) and the role of promyelocytic leukemia-retinoic acid receptor alpha (PML

284 ) chromosomal translocation that creates the promyelocytic leukemia-retinoic acid receptor alpha (PML

285 emia that results from the expression of the promyelocytic leukemia-retinoic acid receptor alpha (PML

286 nslocation that generates the fusion protein promyelocytic leukemia-retinoic acid receptor alpha (PML

287 n oncoproteins, as recently demonstrated for promyelocytic leukemia-retinoic acid receptor alpha and

288 comprising 280 adults with primary non-acute promyelocytic leukemia.

289 O, As2 O3 ) is currently used to treat acute promyelocytic leukemia.

290 ontinuing problem with early deaths in acute promyelocytic leukemia.

291 ts after chemotherapy in patients with acute promyelocytic leukemia.

292 cute myeloid leukemia (AML), excluding acute promyelocytic leukemia.

293 rapeutic drug used in the treatment of acute promyelocytic leukemia.

294 ion characterize the epigenetic landscape of promyelocytic leukemia/retinoic acid receptor-alpha (PML

295 rigger ER-stress induced cell death of acute promyelocytic leukemic (APL) cells by intercepting the d

296 Overexpression of UTX in promyelocytic NB4 cells results in enhanced cellular dif

297 Because treatment of acute promyelocytic patients with all-trans retinoic acid (ATR

298 loid cells and regulates transition from the promyelocytic stage to the myelocytic stage of neutrophi

299 granulopoietic differentiation arrest at the promyelocytic stage.

300 The promyelocytic zinc finger transcription factor (PLZF) is