ライフサイエンスコーパス: acute promyelocytic leukemia

1 de (ATO, As2 O3 ) is currently used to treat acute promyelocytic leukemia.

2 alpha fusion proteins have been described in acute promyelocytic leukemia.

3 ions in patients with relapsed or refractory acute promyelocytic leukemia.

4 ic by its dramatic clinical efficacy against acute promyelocytic leukemia.

5 mplified by the prototypical RA treatment of acute promyelocytic leukemia.

6 ioxide (As2O3), a highly effective agent for acute promyelocytic leukemia.

7 nd likely responsible for the development of acute promyelocytic leukemia.

8 interacts with the PLZF protein of t(11;17) acute promyelocytic leukemia.

9 ently disrupted by t(15;17) in patients with acute promyelocytic leukemia.

10 lpha (RARalpha), causes a refractory form of acute promyelocytic leukemia.

11 nes and clinical remissions in patients with acute promyelocytic leukemia.

12 its efficacy as a chemotherapeutic agent for acute promyelocytic leukemia.

13 cription factor that is fused to RARalpha in acute promyelocytic leukemia.

14 (15;17), a consistent cytogenetic feature of acute promyelocytic leukemia.

15 hus contribute to its therapeutic effects on acute promyelocytic leukemia.

16 tations can contribute to the development of acute promyelocytic leukemia.

17 Arsenic is effective in the treatment of acute promyelocytic leukemia.

18 treatment of relapsed and resistant cases of acute promyelocytic leukemia.

19 are commonly associated with development of acute promyelocytic leukemia.

20 d in several pathogenic conditions including acute promyelocytic leukemia.

21 n patients with t(11;17)(q23;q21)-associated acute promyelocytic leukemia.

22 l function of PML and in the pathogenesis of acute promyelocytic leukemia.

23 ohort comprising 280 adults with primary non-acute promyelocytic leukemia.

24 the continuing problem with early deaths in acute promyelocytic leukemia.

25 l counts after chemotherapy in patients with acute promyelocytic leukemia.

26 for acute myeloid leukemia (AML), excluding acute promyelocytic leukemia.

27 emotherapeutic drug used in the treatment of acute promyelocytic leukemia.

28 that is disrupted during the pathogenesis of acute promyelocytic leukemia, a disease characterized by

29 eukemogenic chromatin signature, we analyzed acute promyelocytic leukemia, a subtype of leukemia char

30 cedent chemotherapy were varied and included acute promyelocytic leukemia, acute myeloid leukemia wit

31 (As(2)O(3)) induces remission of refractory acute promyelocytic leukemia and apoptosis of cell lines

32 wth which is characteristically disrupted in acute promyelocytic leukemia and by a variety of viruses

33 (2)O(3)) is an effective therapeutic against acute promyelocytic leukemia and certain solid tumors.

34 he authors summarize current mouse models of acute promyelocytic leukemia and describe current knowle

35 y been used successfully in the treatment of acute promyelocytic leukemia and has been shown to induc

36 a tumor suppressor originally identified in acute promyelocytic leukemia and implicated in tumorigen

37 mmunomodulatory effects and is used to treat acute promyelocytic leukemia and inflammatory disorders

38 As(2)O(3)) causes remission in patients with acute promyelocytic leukemia and multiple myeloma withou

39 useful adjuvant with ATRA for patients with acute promyelocytic leukemia and possibly retinoid-resis

40 tential contributions to the pathogenesis of acute promyelocytic leukemia and variety of viral infect

41 ed in a variety of human disorders including acute promyelocytic leukemia and viral infections, sugge

42 ic lymphocytic leukemia, arsenic trioxide in acute promyelocytic leukemia, and the BH3-mimetic ABT199

43 rative syndrome, but only 15% to 20% develop acute promyelocytic leukemia (APL) after a latent period

44 Here, we used a mouse model of acute promyelocytic leukemia (APL) and a small molecule

45 eviously related to poorer prognosis in both acute promyelocytic leukemia (APL) and acute myeloid leu

46 been successfully used for the treatment of acute promyelocytic leukemia (APL) and has activity in m

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

48 plays a critical role in the pathogenesis of acute promyelocytic leukemia (APL) and non-Hodgkin's lym

49 sociated with increased penetrance of murine acute promyelocytic leukemia (APL) and the frequent acqu

50 , we elucidated the DNA methylome in primary acute promyelocytic leukemia (APL) and the role of promy

51 minimal residual disease (MRD) monitoring in acute promyelocytic leukemia (APL) are available only in

52 More effective treatments for acute promyelocytic leukemia (APL) are needed.

53 rans-retinoic acid (ATRA) -based therapy for acute promyelocytic leukemia (APL) averages 70% at 5 yea

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

55 e the gap in quality of care and outcomes in acute promyelocytic leukemia (APL) between developed and

56 on of p70 S6 kinase was inducible in primary acute promyelocytic leukemia (APL) blasts and RA-sensiti

57 rentiation of normal hematopoietic cells and acute promyelocytic leukemia (APL) blasts by transcripti

58 ed fibrinolysis is an important component of acute promyelocytic leukemia (APL) bleeding diathesis.

59 ide (AS) has excellent cytotoxic activity in acute promyelocytic leukemia (APL) but its activity in s

60 ously generated a transgenic mouse model for acute promyelocytic leukemia (APL) by expressing the pro

61 We previously developed a murine model of acute promyelocytic leukemia (APL) by using human cathep

62 clinical remission in patients with t(15;17) acute promyelocytic leukemia (APL) carrying leukemogenic

63 Acute promyelocytic leukemia (APL) cases expressing the

64 ic acid (RA) treatment induces remissions in acute promyelocytic leukemia (APL) cases expressing the

65 In most acute promyelocytic leukemia (APL) cases, translocons pr

66 ell differentiation and apoptosis of the NB4 acute promyelocytic leukemia (APL) cell line.

67 on induced monocytic differentiation of NB-4 acute promyelocytic leukemia (APL) cells and HL-60 AML c

68 n to induce differentiation and apoptosis in acute promyelocytic leukemia (APL) cells concomitant wit

69 Acute promyelocytic leukemia (APL) cells contain one of

70 In contrast, acute promyelocytic leukemia (APL) cells do not express

71 We here report that primary acute promyelocytic leukemia (APL) cells express high le

72 Acute promyelocytic leukemia (APL) cells express promyel

73 Acute promyelocytic leukemia (APL) cells invariably expr

74 ) can induce myeloid cell differentiation in acute promyelocytic leukemia (APL) cells.

75 r, HK3 expression was significantly lower in acute promyelocytic leukemia (APL) compared with non-APL

76 The PML gene of acute promyelocytic leukemia (APL) encodes a cell-growth

77 Most patients with acute promyelocytic leukemia (APL) express PML-RAR alpha

78 as been successfully used as a treatment for acute promyelocytic leukemia (APL) for more than a decad

79 The t(5;17) variant of acute promyelocytic leukemia (APL) fuses the genes for n

80 The t(15;17) chromosomal translocation in acute promyelocytic leukemia (APL) generates the PML-RAR

81 Acute promyelocytic leukemia (APL) has been recognized a

82 all-trans retinoic acid (ATRA) treatment in acute promyelocytic leukemia (APL) has been the paradigm

83 sive promyelocytic leukemia (PML) protein of acute promyelocytic leukemia (APL) has served as one of

84 pha (PR) and RARalpha-PML frequently develop acute promyelocytic leukemia (APL) in association with a

85 ents with the microgranular variant (M3V) of acute promyelocytic leukemia (APL) in the all-trans reti

86 Acute promyelocytic leukemia (APL) is a distinct and par

87 Acute promyelocytic leukemia (APL) is a distinct subtype

88 Acute promyelocytic leukemia (APL) is a hematological ma

89 Acute promyelocytic leukemia (APL) is a hematopoietic ma

90 Acute promyelocytic leukemia (APL) is a malignancy of th

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

92 Acute promyelocytic leukemia (APL) is a subtype of acute

93 Acute promyelocytic leukemia (APL) is a subtype of AML i

94 A hallmark of acute promyelocytic leukemia (APL) is altered nuclear ar

95 ptor (RAR) activity that characterizes human acute promyelocytic leukemia (APL) is associated with a

96 Acute promyelocytic leukemia (APL) is associated with ch

97 Acute promyelocytic leukemia (APL) is associated with ch

98 Acute promyelocytic leukemia (APL) is associated with ch

99 Acute promyelocytic leukemia (APL) is associated with re

100 Acute promyelocytic leukemia (APL) is associated with re

101 Acute promyelocytic leukemia (APL) is characterized by a

102 Acute promyelocytic leukemia (APL) is characterized by a

103 Acute promyelocytic leukemia (APL) is characterized by a

104 Acute promyelocytic leukemia (APL) is characterized by g

105 Acute promyelocytic leukemia (APL) is characterized by s

106 Acute promyelocytic leukemia (APL) is characterized by t

107 Acute promyelocytic leukemia (APL) is characterized by t

108 Acute promyelocytic leukemia (APL) is characterized by t

109 Acute promyelocytic leukemia (APL) is characterized by t

110 Acute promyelocytic leukemia (APL) is commonly complicat

111 Acute promyelocytic leukemia (APL) is driven by a chromo

112 yelocytic leukemia (PML) tumor suppressor of acute promyelocytic leukemia (APL) is essential for a nu

113 Acute promyelocytic leukemia (APL) is now the most curab

114 th all-trans retinoic acid and chemotherapy, acute promyelocytic leukemia (APL) is now the most curab

115 Acute promyelocytic leukemia (APL) is often associated w

116 cid receptor alpha (PML-RARalpha) protein of acute promyelocytic leukemia (APL) is oncogenic in vivo.

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

118 lpha (RARalpha) gene in the vast majority of acute promyelocytic leukemia (APL) patients as a consequ

119 ve demonstrated that the immense majority of acute promyelocytic leukemia (APL) patients can be defin

120 Up to 15% of acute promyelocytic leukemia (APL) patients fail to achi

121 e retinoic acid receptor alpha (RARalpha) in acute promyelocytic leukemia (APL) patients.

122 fourth of five fusion proteins identified in acute promyelocytic leukemia (APL) patients.

123 Acute promyelocytic leukemia (APL) remains the best exam

124 large population of unselected patients with acute promyelocytic leukemia (APL) remains unknown becau

125 transplantation advantage and development of acute promyelocytic leukemia (APL) required DNMT3A.

126 ll-trans retinoic acid (ATRA)--a therapy for acute promyelocytic leukemia (APL) that is considered th

127 ent anti-leukemic chemotherapeutic agent for acute promyelocytic leukemia (APL) that results from a t

128 We utilized a mouse model of acute promyelocytic leukemia (APL) to investigate how ab

129 the outcome of patients with newly diagnosed acute promyelocytic leukemia (APL) treated with all-tran

130 AAML0631 trial for newly diagnosed pediatric acute promyelocytic leukemia (APL) was a phase III histo

131 study, the possible role of angiogenesis in acute promyelocytic leukemia (APL) was explored.

132 Acute promyelocytic leukemia (APL) was originally distin

133 is an effective treatment for patients with acute promyelocytic leukemia (APL) who have relapsed fro

134 mples from 406 patients with newly diagnosed acute promyelocytic leukemia (APL) who were receiving al

135 protein PML-RARalpha in 5 of 8 patients with acute promyelocytic leukemia (APL) with 2 or more relaps

136 (As2O3) has been shown to effectively treat acute promyelocytic leukemia (APL) with greater than 80%

137 The t(15;17) translocation in acute promyelocytic leukemia (APL) yields a PML/RAR-alph

138 Acute promyelocytic leukemia (APL), a cytogenetically di

139 In one such disease, acute promyelocytic leukemia (APL), a promyelocytic leuk

140 In acute promyelocytic leukemia (APL), all-trans retinoic a

141 In acute promyelocytic leukemia (APL), both isoforms are ex

142 protein is the initiating genetic event for acute promyelocytic leukemia (APL), but the molecular me

143 by the chromosomal translocation t(15;17) in acute promyelocytic leukemia (APL), encodes a multifunct

144 in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL), encodes a protein wh

145 signaling in leukemogenesis, particularly in acute promyelocytic leukemia (APL), has started to emerg

146 17)(q22;q11.2) translocation associated with acute promyelocytic leukemia (APL), initiates APL when e

147 ith a retinoic acid (RA)-insensitive form of acute promyelocytic leukemia (APL), involving the produc

148 In acute promyelocytic leukemia (APL), NTAL depletion from

149 PML) gene, a tumor suppressor inactivated in acute promyelocytic leukemia (APL), regulates apoptosis

150 In acute promyelocytic leukemia (APL), repression by the PM

151 ith chemotherapy is the standard of care for acute promyelocytic leukemia (APL), resulting in cure ra

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

153 The most common chromosomal translocation in acute promyelocytic leukemia (APL), t15;17(q22;q21), cre

154 c acid (RA)-based differentiation therapy in acute promyelocytic leukemia (APL), the broad promise of

155 In acute promyelocytic leukemia (APL), the promyelocytic le

156 In acute promyelocytic leukemia (APL), the translocation t(

157 e commonly dysregulated in a murine model of acute promyelocytic leukemia (APL), we first defined gen

158 e has been shown to be effective in treating acute promyelocytic leukemia (APL), with minimal overall

159 psy was performed, yielding the diagnosis of acute promyelocytic leukemia (APL), with t(15;17)(q23;q2

160 is of chronic myelogenous leukemia (CML)- or acute promyelocytic leukemia (APL)-derived cell lines.

161 We found PMLRARalpha interaction with Fas in acute promyelocytic leukemia (APL)-derived cells and APL

162 standard-risk patients with newly diagnosed acute promyelocytic leukemia (APL).

163 sed to guide molecularly targeted therapy in acute promyelocytic leukemia (APL).

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

165 RARalpha oncogene is the central effector of acute promyelocytic leukemia (APL).

166 uence of t(15;17)(q22;q21) translocations in acute promyelocytic leukemia (APL).

167 lpha (PR), the fusion protein that initiates acute promyelocytic leukemia (APL).

168 e late 1980s and only in one subtype of AML, acute promyelocytic leukemia (APL).

169 sixth RARalpha-containing fusion protein in acute promyelocytic leukemia (APL).

170 s remission in 85% of adults with refractory acute promyelocytic leukemia (APL).

171 st-line therapy of low- or intermediate-risk acute promyelocytic leukemia (APL).

172 (promyelocytic leukemia) that is involved in acute promyelocytic leukemia (APL).

173 in the t(15;17) chromosomal translocation of acute promyelocytic leukemia (APL).

174 ment of patients with relapsed or refractory acute promyelocytic leukemia (APL).

175 a locus on chromosome 17 are the hallmark of acute promyelocytic leukemia (APL).

176 on, and apoptosis in cancer cells, including acute promyelocytic leukemia (APL).

177 (ATRA)-induced neutrophil differentiation in acute promyelocytic leukemia (APL).

178 on protein is central to the pathogenesis of acute promyelocytic leukemia (APL).

179 ith retinoic acid receptor alpha in t(11;17) acute promyelocytic leukemia (APL).

180 pediatric AML and are particularly common in acute promyelocytic leukemia (APL).

181 ha is the fifth fusion protein identified in acute promyelocytic leukemia (APL).

182 ic acid (ATRA) to 19 patients with untreated acute promyelocytic leukemia (APL).

183 ion and maintenance therapy in patients with acute promyelocytic leukemia (APL).

184 nuclear hormone receptor implicated in human acute promyelocytic leukemia (APL).

185 (2)D(3)) is interrupted during the course of acute promyelocytic leukemia (APL).

186 acid receptor (RARalpha) is associated with acute promyelocytic leukemia (APL).

187 by the chromosomal translocation t(15;17) in acute promyelocytic leukemia (APL).

188 ARalpha) chimeric protein is associated with acute promyelocytic leukemia (APL).

189 clin A1 overexpression is especially high in acute promyelocytic leukemia (APL).

190 a) in the t(15;17) translocation that causes acute promyelocytic leukemia (APL).

191 ses myeloid differentiation genes and drives acute promyelocytic leukemia (APL).

192 highly effective agent for the treatment of acute promyelocytic leukemia (APL).

193 cid receptor-alpha (PML-RARalpha)-associated acute promyelocytic leukemia (APL).

194 h newly diagnosed, low- or intermediate-risk acute promyelocytic leukemia (APL).

195 did we experience as many surprises as with acute promyelocytic leukemia (APL).

196 n PML-RAR is involved in the pathogenesis of acute promyelocytic leukemia (APL).

197 es with distinct outcomes in newly diagnosed acute promyelocytic leukemia (APL).

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

199 a PML-RARalpha fusion protein causative for acute promyelocytic leukemia (APL).

200 umoylate PML and the PML-RARA oncoprotein of acute promyelocytic leukemia (APL).

201 understanding of the coagulopathy present in acute promyelocytic leukemia (APL).

202 cid (ATRA) was evaluated in 69 patients with acute promyelocytic leukemia (APL): 32 new diagnoses, 35

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

204 fective treatment for patients with relapsed acute promyelocytic leukemia (APL); its role as consolid

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

206 nt outcomes in patients with newly diagnosed acute promyelocytic leukemia (APL; see figure).

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

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

209 in blast-phase chronic myeloid leukemia and acute promyelocytic leukemia arguing against this strate

210 aired for corepressor release and operate in acute promyelocytic leukemia as dominant-negative inhibi

211 xide (ATO), an established agent in treating acute promyelocytic leukemia, as cysteine-reactive compo

212 tor fused to retinoic acid receptor alpha in acute promyelocytic leukemia associated with the (11;17)

213 tinoic acid decreased plasminogen binding to acute promyelocytic leukemia blasts.

214 ling by all-trans RA, an anticancer drug for acute promyelocytic leukemia, blocked SMC transition to

215 MRP8 promoter recapitulated the phenotype of acute promyelocytic leukemia but had the unexpected resu

216 zumab ozogamicin is efficacious not only for acute promyelocytic leukemia but, in combination with co

217 G (Rig-G) as a tumor suppressor in not only acute promyelocytic leukemia, but also in other solid tu

218 for the treatment of relapsed and refractory acute promyelocytic leukemia by induction of partial dif

219 ccessful strategy to treat AML, as proved in acute promyelocytic leukemia by treatment with all-trans

220 the dominant molecular signatures of murine acute promyelocytic leukemia can be influenced by severa

221 Lack of LF expression in the acute promyelocytic leukemia cell line NB4, which harbor

222 imexon in several myeloma cell lines and an acute promyelocytic leukemia cell line.

223 myl-transpeptidase (gamma-GT) protects human acute promyelocytic leukemia cells (NB4) from Dar, but n

224 phosphorylation was also observed in primary acute promyelocytic leukemia cells and resulted in activ

225 proliferation and induces differentiation of acute promyelocytic leukemia cells in vitro and in vivo.

226 In humans, overexpression of A2 by acute promyelocytic leukemia cells is associated with ex

227 suggesting that the expression signature of acute promyelocytic leukemia cells reflects the genetic

228 ccumulation of oxidized proteins, we exposed acute promyelocytic leukemia cells to arsenic trioxide (

229 es including NCI-H929 myeloma cells and NB-4 acute promyelocytic leukemia cells, whereas normal lymph

230 lpha (PML-RARalpha) fusion gene, and primary acute promyelocytic leukemia cells.

231 d in the passive selection of ATRA-resistant acute promyelocytic leukemia clones leading to disease r

232 The t(11;17)(q21;q23)-associated acute promyelocytic leukemia creates the promyelocytic l

233 If one excludes acute promyelocytic leukemia, current AML management sti

234 have been shown to be capable of initiating acute promyelocytic leukemia development, and dictate th

235 reciprocal translocation fusion proteins on acute promyelocytic leukemia development, and have demon

236 is, cytarabine-induced cellebellar toxicity, acute promyelocytic leukemia differentiation syndrome, t

237 While acute promyelocytic leukemia displays marked sensitivity

238 3)) is highly effective for the treatment of acute promyelocytic leukemia, even in patients who are u

239 e then focus on a discussion of RARalpha and acute promyelocytic leukemia followed by a discussion of

240 with acute myeloid leukemia (AML; excluding acute promyelocytic leukemia) from 1990 to 2006 who rece

241 In acute promyelocytic leukemia, granulocytic differentiati

242 The treatment of acute promyelocytic leukemia has improved considerably a

243 cess of arsenic trioxide in the treatment of acute promyelocytic leukemia has renewed interest in the

244 senic trioxide is an effective treatment for acute promyelocytic leukemia has renewed interest in the

245 ties of our method not only by screening two acute promyelocytic leukemia human cells lines (NB4 and

246 according to the International Consortium on Acute Promyelocytic Leukemia (IC-APL) study.

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

248 lishments of the International Consortium on Acute Promyelocytic Leukemia (IC-APL), an initiative of

249 ts), and 2% for SPT (one patient), which was acute promyelocytic leukemia (ie, not of the upper aerod

250 associated with remissions in patients with acute promyelocytic leukemia, implying that G0S2 may pos

251 emission therapy in the setting of high-risk acute promyelocytic leukemia in first remission.

252 and Drug Administration for the treatment of acute promyelocytic leukemia in humans.

253 alterations that occur during development of acute promyelocytic leukemia in the mouse.

254 , 282 were excluded, including patients with acute promyelocytic leukemia, incorrect diagnosis, or no

255 that arsenic trioxide, a frontline agent for acute promyelocytic leukemia, inhibits DeltaNp63 but not

256 de, a drug FDA approved for the treatment of acute promyelocytic leukemia, inhibits the growth of Ewi

257 L-RARalpha) oncofusion protein, which causes acute promyelocytic leukemia, inhibits TNFalpha induced

258 Acute promyelocytic leukemia is associated with chromoso

259 Human acute promyelocytic leukemia is causally linked to chrom

260 Acute promyelocytic leukemia is one of the few hematolog

261 Acute promyelocytic leukemia is the first malignant dise

262 ein, the leukemogenic product of t(15,17) in acute promyelocytic leukemia, is cleaved into a truncate

263 Arsenic trioxide, a drug for patients with acute promyelocytic leukemia, is found to target and deg

264 antineoplastic compound for the treatment of acute promyelocytic leukemia, is proarrhythmic via two s

265 ion syndrome, thrombohemorrhagic syndrome in acute promyelocytic leukemia, L-asparaginase-associated

266 man subjects, overexpression of annexin 2 in acute promyelocytic leukemia leads to a bleeding diathes

267 ofiles of fully transformed cells from three acute promyelocytic leukemia model systems were all diff

268 biomarkers of differentiation therapy in an acute promyelocytic leukemia model treated with all-tran

269 14e were further tested in vivo in a murine acute promyelocytic leukemia model, resulting 14d the mo

270 sion events, we compared two high-penetrance acute promyelocytic leukemia models that both commonly a

271 y resuscitation (n=116) and to patients with acute promyelocytic leukemia (n=83).

272 clinically achievable doses of As(2)O(3) in acute promyelocytic leukemia NB4 cells.

273 on in NB4 cells, a cell line derived from an acute promyelocytic leukemia patient with t(15;17) trans

274 Here, we report the expression of miRNAs in acute promyelocytic leukemia patients and cell lines dur

275 been found to be an effective treatment for acute promyelocytic leukemia patients and is being teste

276 sseminated intravascular coagulation scores, acute promyelocytic leukemia patients had higher fibrino

277 All registered non-acute promyelocytic leukemia patients with intensive ind

278 01) than both nondrowning cardiac arrest and acute promyelocytic leukemia patients.

279 eported that As(2)O(3), a drug used to treat acute promyelocytic leukemia (PML), stimulates HIV-1 rep

280 However, acute promyelocytic leukemia represents only a small min

281 All-trans retinoic acid therapy of acute promyelocytic leukemia represents the most success

282 Acute promyelocytic leukemia should be considered in any

283 However, with notable exceptions such as acute promyelocytic leukemia, significant improvements i

284 e chromatin marks generated by the aberrant, acute promyelocytic leukemia specific promyelocytic locu

285 The acute promyelocytic leukemia specific repressive chromat

286 fied 2 additional cases of t(15;17)-negative acute promyelocytic leukemia that had cytogenetically in

287 from arsenic poisoning and in patients with acute promyelocytic leukemia that have been treated with

288 ly severe complication seen in patients with acute promyelocytic leukemia treated with all-trans reti

289 atus in 1333 young adult patients, excluding acute promyelocytic leukemia, treated in the United King

290 427 young adult patients with AML, excluding acute promyelocytic leukemia, using denaturing high-perf

291 tPCR]) measurements of PML-RAR alpha mRNA in acute promyelocytic leukemia was retrospectively assesse

292 In an animal model of acute promyelocytic leukemia, we developed a DNA-based v

293 Investigating arsenic sensitivity of acute promyelocytic leukemia, we proposed that PML oxida

294 tailed analyses of the abnormalities seen in acute promyelocytic leukemia were examined.

295 uding those with core binding factor AML and acute promyelocytic leukemia, were randomly assigned to

296 including subclones) has been exemplified by acute promyelocytic leukemia, where successful targeting

297 rentiation therapy has been the treatment of acute promyelocytic leukemia with all-trans retinoic aci

298 were referred a difficult diagnostic case of acute promyelocytic leukemia with no pathogenic X-RARA f

299 complete clinical remission in patients with acute promyelocytic leukemia with t(15;17) translocation

300 Seven were acute myeloid leukemia (2 acute promyelocytic leukemia with t(15;17), 2 with confi