ライフサイエンスコーパス: myelogenous

1 ent of most human cancers, including chronic myelogenous and acute lymphoblastic leukemias initiated

2 s from patients with multiple myeloma, acute myelogenous and lymphoblastic leukemia, and ovarian canc

3 -Abl fusion protein that causes most chronic myelogenous and some acute lymphocytic leukemias (CML an

4 oliferative neoplasms (MPNs) such as chronic myelogenous (CML) and chronic myelomonocytic leukemias (

5 e of immune competence and predisposition to myelogenous diseases in the elderly.

6 d Hep G2), promyelocytic (HL-60) and chronic myelogenous (K-562) leukemias, histiocytic lymphoma (U-9

7 Acute myelogenous leukaemia (AML) is associated with risk fact

8 BCR-ABL1, is the defining lesion of chronic myelogenous leukaemia (CML) and a subset of acute lympho

9 l renewal and decreases induction of chronic myelogenous leukaemia (CML) by the BCR-ABL1 oncoprotein.

10 Chronic myelogenous leukaemia (CML) can progress from a slow gro

11 ng the specific survival of the rare chronic myelogenous leukaemia (CML) stem cell population could p

12 ors (TKI) are front-line therapy for chronic myelogenous leukaemia and are among the best-known examp

13 cover' the BCR-ABL1 gene fusion in a chronic myelogenous leukaemia cell line and the TMPRSS2-ERG gene

14 Myelodysplasia resulted and acute myelogenous leukaemia emerged that had acquired several

15 iladelphia chromosome (Ph+)-positive chronic myelogenous leukaemia.

16 level of 27 C&Ckines in serum from 176 acute myelogenous leukemia (AML) and 114 myelodysplastic syndr

17 tein levels were robustly expressed in acute myelogenous leukemia (AML) and acute lymphoblastic leuke

18 hosphatase, is overexpressed in 50% of acute myelogenous leukemia (AML) and associated with poor surv

19 potent in vivo anticancer activity in acute myelogenous leukemia (AML) and endemic Burkitt lymphoma

20 by platelet defects, predisposition to acute myelogenous leukemia (AML) and germ-line heterozygous RU

21 ) expression is frequently observed in acute myelogenous leukemia (AML) and has been implicated in le

22 , especially in patients with relapsed acute myelogenous leukemia (AML) and multiple myeloma.

23 PURPOSE Acute myelogenous leukemia (AML) and myelodysplastic syndrome

24 are important for the pathogenesis of acute myelogenous leukemia (AML) and represent a reservoir of

25 Patients with acute myelogenous leukemia (AML) and those undergoing bone mar

26 One patient developed acute myelogenous leukemia (AML) at 6 years of age.

27 a well-defined cohort of patients with acute myelogenous leukemia (AML) at diagnosis and relapse to a

28 ion factor family member, is linked to acute myelogenous leukemia (AML) by chromosomal events at the

29 xpression of IGF1R and IR isoform A in acute myelogenous leukemia (AML) cell lines as well as in >80%

30 ntly, AEG-1 markedly protected HCC and acute myelogenous leukemia (AML) cells from retinoid- and rexi

31 strategies to eradicate primary human acute myelogenous leukemia (AML) cells is a major challenge to

32 eraction between the integrin VLA-4 on acute myelogenous leukemia (AML) cells with stromal fibronecti

33 d panobinostat) were examined in human acute myelogenous leukemia (AML) cells.

34 naling cues in the microenvironment of acute myelogenous leukemia (AML) contribute to disease progres

35 Acute myelogenous leukemia (AML) frequently relapses after com

36 he chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion tra

37 stic syndrome (MDS) that progresses to acute myelogenous leukemia (AML) in association with overexpre

38 (Trib2) is a pseudokinase that induces acute myelogenous leukemia (AML) in mice and is highly express

39 We studied LSCs in mouse models of acute myelogenous leukemia (AML) induced either by coexpressio

40 nthracyclines used in the treatment of acute myelogenous leukemia (AML) inhibit the activity of the m

41 As the pathophysiology of acute myelogenous leukemia (AML) involves a block of myeloid m

42 Acute Myelogenous Leukemia (AML) is an aggressive cancer that

43 Acute myelogenous leukemia (AML) is an aggressive disease asso

44 The microenviroment of acute myelogenous leukemia (AML) is suppressive for immune eff

45 d implement therapeutic approaches for acute myelogenous leukemia (AML) originated primarily from adu

46 Using acute myelogenous leukemia (AML) patient-derived xenograft (PD

47 tate in primary specimens derived from acute myelogenous leukemia (AML) patients.

48 toimmune disorders and in NPM1-mutated acute myelogenous leukemia (AML) patients.

49 DH1 mutations were identified in 8% of acute myelogenous leukemia (AML) patients.

50 were also screened against M9-ENL1 and acute myelogenous leukemia (AML) primary cell lines and exhibi

51 The survival of most patients with acute myelogenous leukemia (AML) remains poor, and novel thera

52 leukemogenesis in T cells, its role in acute myelogenous leukemia (AML) remains unclear.

53 d next-generation sequencing to assess acute myelogenous leukemia (AML) response to induction chemoth

54 series of 260 newly diagnosed primary acute myelogenous leukemia (AML) samples.

55 ty was observed in four of six primary acute myelogenous leukemia (AML) specimens.

56 ver, the interactions and influence of acute myelogenous leukemia (AML) stem cells with the microenvi

57 regimen that selectively targets human acute myelogenous leukemia (AML) stem cells.

58 Acute myelogenous leukemia (AML) subtypes that result from onc

59 a panel of cell lines representing all acute myelogenous leukemia (AML) subtypes using selective, rev

60 nding protein 2 (SSBP2) is a candidate acute myelogenous leukemia (AML) suppressor gene located at ch

61 9 presented by cell lines, and primary acute myelogenous leukemia (AML) targets that endogenously exp

62 stic syndrome (MDS) transforms into an acute myelogenous leukemia (AML) with associated increased bon

63 ssion of the MLL-AF9 fusion results in acute myelogenous leukemia (AML) with different behaviors depe

64 topoietic progenitor cells and induces acute myelogenous leukemia (AML) with long latency in bone mar

65 Interestingly, patients with acute myelogenous leukemia (AML), acute lymphoblastic leukemia

66 or acute lymphoblastic leukemia (ALL), acute myelogenous leukemia (AML), and chronic myelogenous leuk

67 and clinical outcome of patients with acute myelogenous leukemia (AML), and conventional karyotype-b

68 been implicated in the pathogenesis of acute myelogenous leukemia (AML), but the functional significa

69 Among 5394 cases with acute myelogenous leukemia (AML), the 2-year cumulative incide

70 ssful use of cytotoxic chemotherapy in acute myelogenous leukemia (AML), the biological basis for its

71 In acute myelogenous leukemia (AML), the FLT3 receptor tyrosine k

72 understanding of the genetic basis of acute myelogenous leukemia (AML), we determined the coding exo

73 lt3, an additional important target in acute myelogenous leukemia (AML), with pharmacologically usefu

74 B, would titrate NK reactivity against acute myelogenous leukemia (AML).

75 of myelodysplastic syndromes (MDS) and acute myelogenous leukemia (AML).

76 nd long-term survival of patients with acute myelogenous leukemia (AML).

77 ssed in subsets of pediatric and adult acute myelogenous leukemia (AML).

78 ll survival (OS) for older adults with acute myelogenous leukemia (AML).

79 ansplantation (alloSCT) in adults with acute myelogenous leukemia (AML).

80 in elderly adults with newly diagnosed acute myelogenous leukemia (AML).

81 nduction chemotherapy for treatment of acute myelogenous leukemia (AML).

82 ients with less-than-favorable risk of acute myelogenous leukemia (AML).

83 ncluding 31 patients with nonremission acute myelogenous leukemia (AML).

84 overy after intensive chemotherapy for acute myelogenous leukemia (AML).

85 initiating cells (SL-ICs), are rare in acute myelogenous leukemia (AML).

86 in myelodysplastic syndrome (MDS) and acute myelogenous leukemia (AML).

87 The majority of patients (76%) had acute myelogenous leukemia (AML).

88 ineage dysplasia and susceptibility to acute myelogenous leukemia (AML).

89 several human malignancies, including acute myelogenous leukemia (AML).

90 sis in multiple human tumors including acute myelogenous leukemia (AML).

91 rs from 1409 unrelated transplants for acute myelogenous leukemia (AML; n = 1086) and acute lymphobla

92 emotherapy in patients with refractory acute myelogenous leukemia (and other hematologic malignancies

93 nst acute leukemias and blast-crisis chronic myelogenous leukemia (BC-CML).

94 mg twice daily in chronic-phase (CP) chronic myelogenous leukemia (CML) after imatinib treatment fail

95 parts, leukemia stem cells (LSCs) in chronic myelogenous leukemia (CML) and acute myeloid leukemia (A

96 elf-renewal in p210(BCR-ABL)-induced chronic myelogenous leukemia (CML) and exhibits synergistic effe

97 Cancer stem cells lie at the root of chronic myelogenous leukemia (CML) and mediate its continued gro

98 rine fashion, their possible role in chronic myelogenous leukemia (CML) and resistance to imatinib me

99 ment, and prognostic significance in chronic myelogenous leukemia (CML) are largely unknown.

100 We use chronic myelogenous leukemia (CML) as a model of LIC-dependent m

101 repressed in 32D-BCR/ABL, K562, and chronic myelogenous leukemia (CML) blast crisis (BC) primary cel

102 effective therapy for patients with chronic myelogenous leukemia (CML) but is now mostly indicated f

103 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by covalently immobilizing th

104 mical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine termina

105 Exposure to chronic myelogenous leukemia (CML) caused normal mouse hematopoi

106 BCR/ABL kinase-positive chronic myelogenous leukemia (CML) cells display genomic instabi

107 ere assessed in cell-free medium and chronic myelogenous leukemia (CML) cells overexpressing BCR-Abl

108 regulator of imatinib sensitivity in chronic myelogenous leukemia (CML) cells through an unknown mech

109 er65 as RI-mTORC1 signals in primary chronic myelogenous leukemia (CML) cells.

110 A subset of patients with chronic myelogenous leukemia (CML) do not respond to the tyrosin

111 The imatinib paradigm in chronic myelogenous leukemia (CML) established continuous BCR-AB

112 Chronic myelogenous leukemia (CML) in children is relatively rar

113 Chronic myelogenous leukemia (CML) invariably progresses to blas

114 Although chronic myelogenous leukemia (CML) is effectively controlled by

115 chromosomal abnormalities (ACAs) in chronic myelogenous leukemia (CML) is generally associated with

116 Effective treatment of chronic myelogenous leukemia (CML) largely depends on the eradic

117 of OBs in regulating normal HSCs and chronic myelogenous leukemia (CML) LSCs.

118 lance of minimal residual disease in chronic myelogenous leukemia (CML) may be relevant for long-term

119 donor lymphocyte infusion (DLI) for chronic myelogenous leukemia (CML) may result from immunologic a

120 ukemias in recipient mice resembling chronic myelogenous leukemia (CML) myeloid blast crisis.

121 effective in inducing remissions in chronic myelogenous leukemia (CML) patients but do not eliminate

122 We previously demonstrated that chronic myelogenous leukemia (CML) patients treated with DLI dev

123 Chronic myelogenous leukemia (CML) patients treated with imatini

124 g primitive leukemic precursors from chronic myelogenous leukemia (CML) patients.

125 changed the therapeutic strategy for chronic myelogenous leukemia (CML) patients.

126 uces the burden of leukemia cells in chronic myelogenous leukemia (CML) patients.

127 se gene signatures in cell lines and chronic myelogenous leukemia (CML) patients.

128 bility to chromosomal aberrations in chronic myelogenous leukemia (CML) progenitors after exposure to

129 Chronic myelogenous leukemia (CML) results from a chromosomal tr

130 Chronic myelogenous leukemia (CML) results from transformation o

131 ely active mutant of Abl that causes chronic myelogenous leukemia (CML) stimulated the expression and

132 Progression of chronic myelogenous leukemia (CML) to accelerated (AP) and blast

133 ia stem cells (LSC) in chronic phase chronic myelogenous leukemia (CML) using a transgenic mouse mode

134 selenium has been shown to alleviate chronic myelogenous leukemia (CML) via the elimination of leukem

135 e in CLL, GRN was not upregulated in chronic myelogenous leukemia (CML) where miR-107 paralogs are no

136 ction (QPCR) levels in patients with chronic myelogenous leukemia (CML) who are in complete cytogenet

137 Treatment of chronic myelogenous leukemia (CML) with BCR-ABL tyrosine kinase

138 imatinib is remarkably effective in chronic myelogenous leukemia (CML), although drug resistance is

139 complete remissions in patients with chronic myelogenous leukemia (CML), and evidence supports an imm

140 a major role in the pathogenesis of chronic myelogenous leukemia (CML), and is the target of the bre

141 highly effective in the treatment of chronic myelogenous leukemia (CML), but primary and acquired res

142 ion in the majority of patients with chronic myelogenous leukemia (CML), but the persistence of CML s

143 hibitors are effective therapies for chronic myelogenous leukemia (CML), but these inhibitors target

144 se inhibitors (TKIs), a treatment of chronic myelogenous leukemia (CML), has largely replaced curativ

145 eted therapies, such as imatinib for chronic myelogenous leukemia (CML), represent the first agents t

146 b at inhibiting Bcr-Abl and treating chronic myelogenous leukemia (CML), resistance to the therapy oc

147 ncogene homolog 1 (BCR-ABL1)-induced chronic myelogenous leukemia (CML)-like myeloproliferative neopl

148 ine kinase (BCR-ABL) oncogene causes chronic myelogenous leukemia (CML).

149 stability, leading to development of chronic myelogenous leukemia (CML).

150 ntestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

151 e chronic and blast crisis phases of chronic myelogenous leukemia (CML).

152 iescent leukemia stem cells (LSC) in chronic myelogenous leukemia (CML).

153 in patients with advanced stages of chronic myelogenous leukemia (CML).

154 the treatment of imatinib-resistant chronic myelogenous leukemia (CML).

155 kinase inhibitor (TKI) therapies in chronic myelogenous leukemia (CML).

156 tial mediator of the pathogenesis of chronic myelogenous leukemia (CML).

157 ntestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

158 a causative tyrosine kinase (TK) of chronic myelogenous leukemia (CML).

159 successful front-line treatment for chronic myelogenous leukemia (CML).

160 tiated by the BCR-ABL1 kinase causes chronic myelogenous leukemia (CML).

161 R-ABL inhibitor imatinib in treating chronic myelogenous leukemia (CML).

162 esis of many human cancers including chronic myelogenous leukemia (CML).

163 /progenitor cells from patients with chronic myelogenous leukemia (CML).

164 nase inhibitor that is used to treat chronic myelogenous leukemia (CML).

165 ine kinase inhibitors and relapse of chronic myelogenous leukemia (CML).

166 gene networks that are important for chronic myelogenous leukemia (CML).

167 ors (TKI) have improved treatment of chronic myelogenous leukemia (CML); however, most patients are n

168 and revolutionized the treatment of chronic myelogenous leukemia (CML); in 2006 and 2007, approval o

169 e long-term response in blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia chromosom

170 ss of miR-328 occurs in blast crisis chronic myelogenous leukemia (CML-BC) in a BCR/ABL dose- and kin

171 Leukemic stem cells in chronic phase chronic myelogenous leukemia (CP-CML) are responsible for diseas

172 half of patients with chronic-phase chronic myelogenous leukemia (CP-CML) in complete molecular resp

173 leukemia (GVL) against chronic-phase chronic myelogenous leukemia (CP-CML) is potent, but it is less

174 SCT) is potent against chronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-

175 used the experimental data from immortalised myelogenous leukemia (K562) and healthy lymphoblastoid (

176 amster Ovary (CHO) cells, Human Immortalized Myelogenous Leukemia (K562) cells and hematopoietic stem

177 cs of DNA damage by 1 and 3 in human chronic myelogenous leukemia (K562) cells.

178 l lines isolated from a patient with chronic myelogenous leukemia (KBM7 and HAP1), as well as haploid

179 mples from 15 myelodysplastic syndrome/acute myelogenous leukemia (MDS/AML) patients undergoing decit

180 cute myelogenous leukemia (AML), and chronic myelogenous leukemia (RR = 26.9, 66.5, and 93.1, respect

181 tive neoplasms (MDS/MPN), or secondary acute myelogenous leukemia (sAML) and may point toward genes h

182 Therapy-related acute myelogenous leukemia (t-AML) is an important late advers

183 -related myelodysplastic syndromes and acute myelogenous leukemia (t-MDS/AML) comprise an increasingl

184 Therapy-related myelodysplasia or acute myelogenous leukemia (t-MDS/AML) is a lethal complicatio

185 t myeloid leukemia blasts (including chronic myelogenous leukemia [CML]-blast crisis cells) rely on c

186 both acute lymphoblastic leukemia and acute myelogenous leukemia achieve remission with upfront chem

187 We report a patient with relapsed acute myelogenous leukemia after allogeneic stem cell transpla

188 re previously avoided in patients with acute myelogenous leukemia aged more than 55 years because of

189 Here, we identify two patients with acute myelogenous leukemia and B-cell acute lymphoblastic leuk

190 ating bone metastatic cancers, such as acute myelogenous leukemia and breast cancer.

191 s the history of transplantation for chronic myelogenous leukemia and defines the new natural history

192 The trail blazed by imatinib for chronic myelogenous leukemia and GIST has become a desired route

193 increasing the time to progression to acute myelogenous leukemia and improving overall response rate

194 of inactivating mutations of DNMT3A in acute myelogenous leukemia and myelodysplastic syndrome, our r

195 erapeutic response for patients with chronic myelogenous leukemia and Philadelphia chromosome-positiv

196 ioned drug candidates against breast cancer, myelogenous leukemia and prostate cancer by looking for

197 94 and 88 candidate drugs for breast cancer, myelogenous leukemia and prostate cancer, 32%, 13% and 1

198 ndous impact on clinical outcomes in chronic myelogenous leukemia and revolutionized the field of tar

199 xpressed in breast cancer), BCR-ABL (chronic myelogenous leukemia and some cases of acute lymphoblast

200 ole caregiver for her husband, who has acute myelogenous leukemia and was undergoing allogeneic hemat

201 therapies and immune checkpoint therapies in myelogenous leukemia are desired.

202 genic KIT in systemic mastocytosis and acute myelogenous leukemia are poorly understood.

203 oblastic leukemia (ALL) and lymphoid chronic myelogenous leukemia blast crisis.

204 This procedure remains an option in chronic myelogenous leukemia but its use will become more sparin

205 the clinical outcome for patients with acute myelogenous leukemia by reducing the incidence of leukem

206 nd broad H3K4me3 domains in the K562 chronic myelogenous leukemia cell line as well as the MCF-7 brea

207 dentify essential genes in the human chronic myelogenous leukemia cell line K562.

208 ere cellular membrane fragments of a chronic myelogenous leukemia cell line, KU-812, were immobilized

209 ilar to native GCSF using the mouse M-NFS-60 myelogenous leukemia cell line.

210 s Crk was robustly phosphorylated in chronic myelogenous leukemia cell lines and in A431 and MDA-MB-4

211 they potently induced cell death in chronic myelogenous leukemia cell lines.

212 eration of the effects of As(2)O(3) on acute myelogenous leukemia cells and raise the potential of mo

213 TF-1 erythroleukemia and primary human acute myelogenous leukemia cells in vitro.

214 It is also used to sort K562 human chronic myelogenous leukemia cells that have either been treated

215 Treatment of K562 chronic myelogenous leukemia cells with phorbol-12-myristate-13-

216 ential for development and survival of acute myelogenous leukemia cells.

217 n of hematopoietic stem/progenitor and acute myelogenous leukemia cells.

218 s with acute lymphoblastic leukemia or acute myelogenous leukemia compared with normal bone marrow.

219 A 33-year-old woman with chronic myelogenous leukemia developed widespread alopecia invol

220 cell transplantation was the goal in chronic myelogenous leukemia for over 20 years and remains an op

221 n patients with autoimmune diseases or acute myelogenous leukemia illustrate the potential use of the

222 PURPOSE Patients with chronic myelogenous leukemia in accelerated phase (CML-AP) that

223 nd in CD34+ cells from patients with chronic myelogenous leukemia in blast crisis.

224 lated tyrosine kinase BCR-ABL causes chronic myelogenous leukemia in humans and forms a large multipr

225 amily kinase inhibitor used to treat chronic myelogenous leukemia in humans.

226 eased risk of development of secondary acute myelogenous leukemia involving the mixed-lineage leukemi

227 Successful treatment of chronic myelogenous leukemia is based on inhibitors binding to t

228 Acute myelogenous leukemia is propagated by a subpopulation of

229 Chronic myelogenous leukemia is typified by constitutive activat

230 of human tumor cell lines and clinical acute myelogenous leukemia isolates, which express abundant PK

231 in lymphohematopoietic cell lines and acute myelogenous leukemia isolates.

232 ukemia virus or those expressing the chronic myelogenous leukemia oncoprotein BCR-ABL in the hematopo

233 ary blasts isolated from patients with acute myelogenous leukemia or acute lymphocytic leukemia.

234 ears (range, 18-69 years), and 95% had acute myelogenous leukemia or high-risk myelodysplastic syndro

235 ne kinase FLT3 are frequently found in acute myelogenous leukemia patients and confer poor clinical p

236 acinus are overexpressed in some human acute myelogenous leukemia patients and correlate with elevate

237 ue, we analyzed outcomes of 2223 adult acute myelogenous leukemia patients who underwent allogeneic H

238 gene give rise to drug resistance in chronic myelogenous leukemia patients.

239 and primary leukemic progenitors from acute myelogenous leukemia patients.

240 cluding therapy-refractory B-ALL and chronic myelogenous leukemia samples, and inhibits growth of hum

241 corepressors originally identified in acute myelogenous leukemia that have recently been linked to e

242 could act as prognostic biomarkers of acute myelogenous leukemia though influencing cancer-related b

243 orrelates with sensitivity of clinical acute myelogenous leukemia to chemotherapy, whereas low BAK le

244 -Abl tyrosine kinase associated with chronic myelogenous leukemia to small molecule inhibitors that t

245 Finally, in patients with acute myelogenous leukemia treated with hematopoietic stem cel

246 e been reported in patients who have chronic myelogenous leukemia treated with the tyrosine kinase in

247 In human acute myelogenous leukemia we showed that all preleukemic muta

248 1 case in which neoplastic cells of chronic myelogenous leukemia were intermingled with the cells of

249 ed by the Philadelphia chromosome in chronic myelogenous leukemia were unraveled, and these have led

250 ders, 7 nonresponders) with relapsed chronic myelogenous leukemia who received CD4(+) DLI in the pre-

251 one marrow or peripheral blood HCT for acute myelogenous leukemia, acute lymphoblastic leukemia, chro

252 tive anaplastic large cell lymphoma, chronic myelogenous leukemia, and acute leukemias.

253 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome betwe

254 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndrome enrol

255 ified as chromosomal translocations in acute myelogenous leukemia, are transcriptional corepressors t

256 IDH1), frequently found in gliomas and acute myelogenous leukemia, creates a neoenzyme that produces

257 atment in HL-60 cells, a cell model of acute myelogenous leukemia, decreased miR181b expression and i

258 n patients developed myelodysplasia or acute myelogenous leukemia, four of those being the rare but u

259 R-ABL inhibitor for the treatment of chronic myelogenous leukemia, has created a great impetus for th

260 well-known therapeutic agent against chronic myelogenous leukemia, is an effective inhibitor of Abl t

261 kemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, or myelodysplastic syndrome; 98% r

262 he BCR-Abl translocation involved in chronic myelogenous leukemia, reportedly produces alopecia accor

263 ma, colorectal and prostate cancers, chronic myelogenous leukemia, small cell lung cancer, and medull

264 In chronic myelogenous leukemia, the constitutive activation of the

265 (-/-) mouse model of engrafted human chronic myelogenous leukemia, we now demonstrate the complete el

266 Using a murine model of chronic myelogenous leukemia, we show that malignant and nonmali

267 ntiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs), thereb

268 m a very early age a more aggressive chronic myelogenous leukemia-like disease than mice deficient in

269 nic fusion protein characteristic of chronic myelogenous leukemia.

270 xtended life to the degree seen with chronic myelogenous leukemia.

271 rosine kinase inhibitor approved for chronic myelogenous leukemia.

272 lance and result in the development of acute myelogenous leukemia.

273 ces similar survival for patients with acute myelogenous leukemia.

274 milar survival times for patients with acute myelogenous leukemia.

275 in patients with imatinib-resistant chronic myelogenous leukemia.

276 transform to myelodysplastic syndrome/acute myelogenous leukemia.

277 re implicated in leukemias, especially acute myelogenous leukemia.

278 n a syndrome highly similar to human chronic myelogenous leukemia.

279 inib for the first-line treatment of chronic myelogenous leukemia.

280 eukemic progenitors from patients with acute myelogenous leukemia.

281 some hematopoietic cancers, such as chronic myelogenous leukemia.

282 ainst a mouse model of chronic-phase chronic myelogenous leukemia.

283 a substrate of the BCR-ABL kinase in chronic myelogenous leukemia.

284 nificant activity in patients with MDS/acute myelogenous leukemia.

285 the current role of the procedure in chronic myelogenous leukemia.

286 to myelodysplastic syndrome (MDS) and acute myelogenous leukemia.

287 titutively active kinase that causes chronic myelogenous leukemia.

288 incidence of myelodysplastic syndrome/acute myelogenous leukemia.

289 in the development of both acute and chronic myelogenous leukemia.

290 n 6 years after HCT for treatment of chronic myelogenous leukemia.

291 hematopoietic cell transplantation for acute myelogenous leukemia.

292 may be a potent candidate for treating acute myelogenous leukemia.

293 n chromosome translocations that cause acute myelogenous leukemia.

294 as the cause of some familial cases of acute myelogenous leukemia/myelodysplastic syndrome and in Mon

295 Acute myelogenous leukemias (AMLs) and endothelial cells depen

296 on kinase is the driving mutation of chronic myelogenous leukemias and is also expressed in a subset

297 condary glioblastomas, and a subset of acute myelogenous leukemias but have not been detected in othe

298 optosis of CSC derived from chronic or acute myelogenous leukemias when administered at supraphysiolo

299 lymphoblastoid B cell (GM12878) and chronic myelogenous leukemic (K562) ENCODE Tier 1 cell lines.

300 Despite positive staining, acute myelogenous leukemic cells were not killed by IMMU-114.