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

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

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

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

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

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

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

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

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

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

12 The promyelocytic leukaemia (PML) protein controls multiple

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

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

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

16 Acute promyelocytic leukaemia is a chemotherapy-sensitive subg

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

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

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

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

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

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

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

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

25 ly related to poorer prognosis in both acute promyelocytic leukemia (APL) and acute myeloid leukemia,

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

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

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

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

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

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

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

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

37 Acute promyelocytic leukemia (APL) is a hematological malignan

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

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

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

41 Acute promyelocytic leukemia (APL) is characterized by granulo

42 Acute promyelocytic leukemia (APL) is commonly complicated by

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

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

45 Acute promyelocytic leukemia (APL) is often associated with ac

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

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

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

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

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

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

52 31 trial for newly diagnosed pediatric acute promyelocytic leukemia (APL) was a phase III historicall

53 Acute promyelocytic leukemia (APL), a cytogenetically distinct

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

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

56 In acute promyelocytic leukemia (APL), NTAL depletion from lipid

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 LT-like phenotypes, including ALT-associated promyelocytic leukemia (PML) bodies (APBs), telomere sis

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

89 er is the excessively clustered telomeres in promyelocytic leukemia (PML) bodies, represented as larg

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

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

92 Promyelocytic leukemia (PML) is a pleiotropic tumor supp

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

94 reported that ICP0 differentially recognizes promyelocytic leukemia (PML) isoforms.

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

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

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

98 Upregulated Mad1 localizes to ProMyelocytic Leukemia (PML) nuclear bodies in breast ca

99 Promyelocytic leukemia (PML) nuclear bodies selectively

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

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

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

103 RL4-mediated degradation by associating with promyelocytic leukemia (PML) nuclear bodies, ensuring it

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

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

106 structurally organized, containing canonical promyelocytic leukemia (PML) nuclear body protein SP100

107 Promyelocytic leukemia (PML) plays a tumor suppressive r

108 In hBMECs, NBs formed by STAT2 and promyelocytic leukemia (PML) protein are present constit

109 The promyelocytic leukemia (PML) protein has been implicated

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

111 xible hinge domain containing 1 (SMCHD1), or promyelocytic leukemia (PML) protein increased basal lev

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

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

114 The promyelocytic leukemia (PML) protein organizes PML nucle

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

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

117 singly, mTRF1 suppresses the accumulation of promyelocytic leukemia (PML) protein, BRCA1 and the SMC5

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 suppresses intrinsic immunity driven by the promyelocytic leukemia (PML) protein, which limits ZIKV

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

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

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

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

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

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

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

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

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 The treatment of acute promyelocytic leukemia has improved considerably after r

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

151 Next, neutrophil-differentiated human promyelocytic leukemia HL-60 cells (HL60D) were treated

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

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

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

158 (ALT) pathway that depends on ALT-associated promyelocytic leukemia nuclear bodies (APBs), whose func

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 mponents involved in this innate process are promyelocytic leukemia nuclear bodies (PML-NBs), which a

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 All registered non-acute promyelocytic leukemia patients with intensive induction

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

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

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

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 ier (SUMO)-conjugating enzyme, UBC9, and the promyelocytic leukemia protein (PML) and thus was not du

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

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

181 o makes Aire susceptible to interaction with promyelocytic leukemia protein (PML) bodies, sites of ma

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

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

184 Promyelocytic leukemia protein (PML) has been implicated

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

186 Promyelocytic leukemia protein (PML) is a tumor suppress

187 Promyelocytic leukemia protein (PML) is an essential org

188 Promyelocytic leukemia protein (PML) modulates the p53 t

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

190 Promyelocytic leukemia protein (PML) nuclear bodies (NBs

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

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

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

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

195 3 ubiquitin ligase E6AP in the regulation of promyelocytic leukemia protein (PML) stability and forma

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

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

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

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

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

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

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

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

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

205 The promyelocytic leukemia protein is a well known tumor sup

206 se changes are associated with remodeling of promyelocytic leukemia protein nuclear bodies (PML NBs),

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

229 ess NK-inhibitory receptors, and 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 acked expression of the transcription factor promyelocytic leukemia zinc finger (PLZF), as well as ex

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

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

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

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

237 1 and beta-catenin regulate the frequency of promyelocytic leukemia zinc finger (PLZF)-expressing, IL

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

239 ed by expression of the transcription factor Promyelocytic Leukemia Zinc Finger (PLZF).

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

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

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

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

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

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

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

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

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

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

250 We also found that promyelocytic leukemia zinc finger seemed to play a role

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

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

253 ption factors (KLF), i.e., KLF4, KLF6, PLZF (promyelocytic leukemia zinc finger), and KLF15, are indu

254 (IFN-gamma)-producing PLZF(lo)RORgammat(lo) (promyelocytic leukemia zinc finger, retinoic acid-relate

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

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

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

262 The promyelocytic leukemia zinc-finger transcription factor

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 MDA-MB-231 breast adenocarcinoma, and HL-60 promyelocytic leukemia).

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 ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compounds t

269 y all-trans RA, an anticancer drug for acute promyelocytic leukemia, blocked SMC transition to SEM ce

270 g-G) as a tumor suppressor in not only acute promyelocytic leukemia, but also in other solid tumors.

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

272 In acute promyelocytic leukemia, granulocytic differentiation is

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

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

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

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

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

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

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

287 ontinuing problem with early deaths in acute promyelocytic leukemia.

288 ts after chemotherapy in patients with acute promyelocytic leukemia.

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

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

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

292 TRA) and arsenic both target and degrade its ProMyelocytic Leukemia/Retinoic Acid Receptor alpha (PML

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

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

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

296 induction in murine myeloblast 32D and human promyelocytic NB4 cells.

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