ライフサイエンスコーパス: chronic myeloid leukemia

1 h tyrosine kinase inhibitor (TKI) failure in chronic myeloid leukemia.

2 to be critical to maintain CSC in a model of chronic myeloid leukemia.

3 60% to 78% (P < .001) for AML, ALL, MDS, and chronic myeloid leukemia.

4 R) in CNL and in some patients with atypical chronic myeloid leukemia.

5 is lost in Bcr-Abl(+) cells, which underlie chronic myeloid leukemia.

6 predicts clinical outcomes for patients with chronic myeloid leukemia.

7 kinases may be therapeutically useful in BC chronic myeloid leukemia.

8 inhibitors has transformed the treatment of chronic myeloid leukemia.

9 nilotinib is very effective in chronic-phase chronic myeloid leukemia.

10 for leukemic stem cell (LSC) maintenance in chronic myeloid leukemia.

11 and the emergence of imatinib resistance in chronic myeloid leukemia.

12 control as imatinib mesylate has produced in chronic myeloid leukemia.

13 ;22) chromosomal translocation causative for chronic myeloid leukemia.

14 as the clinically related diagnosis atypical chronic myeloid leukemia.

15 kemia, and in blast crisis transformation of chronic myeloid leukemia.

16 monocytes of patients receiving imatinib for chronic myeloid leukemia.

17 blast crisis, similar to the course of human chronic myeloid leukemia.

18 oglitazone) is proposed for the treatment of chronic myeloid leukemia.

19 SL biosynthesis affects the MDR phenotype of chronic myeloid leukemias.

20 well as acute myeloid leukemia (AML, 1.19), chronic myeloid leukemia (1.54), and myelodysplastic syn

21 phocytic Leukemia, 1 Non-Hodgkin Lymphoma, 1 Chronic Myeloid Leukemia, 2 Severe Aplastic Anemia) unde

22 Atypical chronic myeloid leukemia (aCML) is a rare subtype of mye

23 ukemia (CNL) and atypical (BCR-ABL-negative) chronic myeloid leukemia (aCML) patients.

24 mia (CNL) and to a lesser extent in atypical chronic myeloid leukemia (aCML) resulting in constitutiv

25 hronic neutrophilic leukemia (CNL), atypical chronic myeloid leukemia (aCML), and myelodysplastic/mye

26 liferative disease resembling human atypical chronic myeloid leukemia (aCML), preceded by ROCK hypera

27 consistent with a recent report on atypical chronic myeloid leukemia (aCML).

28 monocytic leukemia (CMML; n = 119), atypical chronic myeloid leukemia (aCML; n = 71), MDS/MPN with ri

29 an B cell leukemia cell lines, primary human chronic myeloid leukemia, acute myeloid leukemia with no

30 e (BCR-Abl) is a driver oncogene that causes chronic myeloid leukemia and a subset of acute lymphoid

31 tant subclones and experience in blast-phase chronic myeloid leukemia and acute promyelocytic leukemi

32 01 for treatment of many different stages of chronic myeloid leukemia and in 2002 for treatment of ga

33 PK activators in the treatment of refractory chronic myeloid leukemia and Ph(+) acute lymphoblastic l

34 In chronic myeloid leukemia and Philadelphia chromosome-pos

35 e inhibitor used to treat imatinib-resistant chronic myeloid leukemia and Philadelphia chromosome-pos

36 Expression of Icsbp is decreased in chronic myeloid leukemia, and Icsbp(-/-) mice exhibit pr

37 across inv(3)/t(3;3) acute myeloid leukemia, chronic myeloid leukemia, and myelodysplastic syndrome c

38 ll cycle progression and cooperates with the chronic myeloid leukemia-associated BCR-ABL1 oncoprotein

39 In one case of chronic myeloid leukemia, at blast crisis, most of the c

40 In blast crisis chronic myeloid leukemia (BC CML), we show that increase

41 ouse chronic-phase (CP-CML) and blast crisis chronic myeloid leukemia (BC-CML).

42 hput screen using Msi2-reporter blast crisis chronic myeloid leukemia (bcCML) and identify several ad

43 ine regulation, whereas it decreases that of chronic myeloid leukemia BCR-ABL(+) K-562 cells.

44 omal tumors (PDGFRA mutations) as well as in chronic myeloid leukemia (BCR-PDGFRA translocation), and

45 In patients with chronic myeloid leukemia, BCR-ABL mutations contribute t

46 Atypical chronic myeloid leukemia, BCR-ABL1 negative (aCML) is a

47 tinib Efficacy and Safety in Newly Diagnosed Chronic Myeloid Leukemia (BELA) trial compared bosutinib

48 syndromes (MDS), acute myeloid leukemia, and chronic myeloid leukemia, blast crisis.

49 ve therapy for newly diagnosed patients with chronic myeloid leukemia, but not all patients respond w

50 ibility that mutation-mediated resistance in chronic myeloid leukemia can be fully controlled; howeve

51 plied rMATS-DVR to RNA-seq data of the human chronic myeloid leukemia cell line K562 in response to s

52 sionMap to characterize fusion genes in K562 chronic myeloid leukemia cell line, we further demonstra

53 and open chromatin, all derived from a human chronic myeloid leukemia cell line.

54 17f inhibited the growth of acute and chronic myeloid leukemia cells and the phosphorylation a

55 h siRNAs reduced proliferation of human K562 chronic myeloid leukemia cells because of reduced IGF-II

56 azaspiro compounds reduced the viability of chronic myeloid leukemia cells in the micromolar range.

57 t, Gfi-1 short hairpin RNA-tranduced CD34(+) chronic myeloid leukemia cells were markedly more clonog

58 characterization of iPSCs derived from human chronic myeloid leukemia cells.

59 mutations conferring imatinib resistance in chronic myeloid leukemia cells.

60 Chronic myeloid leukemia chronic phase (CML-CP) CD34(+)

61 Unlike chronic myeloid leukemia, chronic lymphocytic leukemia (

62 criteria were categorized by 4 cancer types (chronic myeloid leukemia, chronic lymphocytic leukemia,

63 cute lymphoblastic leukemia (ALL) (n = 322), chronic myeloid leukemia (CML) (n = 646), lymphoma (n =

64 (TKIs) have revolutionized the treatment of chronic myeloid leukemia (CML) and are now widely accept

65 ral chemotherapeutic used primarily to treat chronic myeloid leukemia (CML) and gastrointestinal stro

66 BCR-ABL is the driving mutation in chronic myeloid leukemia (CML) and is uncommon to other

67 n several hematologic malignancies including chronic myeloid leukemia (CML) and myelodysplastic syndr

68 athways in leukemic cells from patients with chronic myeloid leukemia (CML) and Ph(+) B-cell acute ly

69 tyrosine kinase inhibitors in patients with chronic myeloid leukemia (CML) and Philadelphia chromoso

70 ding the myeloproliferative neoplasms (MPNs) chronic myeloid leukemia (CML) and polycythemia vera (PV

71 ays an essential role in the pathogenesis of chronic myeloid leukemia (CML) and some cases of acute l

72 imatinib mesylate (IM) induces autophagy in chronic myeloid leukemia (CML) and that this process is

73 kemic stem cells (LSCs) drive progression of chronic myeloid leukemia (CML) and tyrosine kinase inhib

74 oncogene homolog 1 (BCR-ABL) transcripts in chronic myeloid leukemia (CML) are e13a2 (b2a2) and e14a

75 more than 95% of all patients diagnosed with chronic myeloid leukemia (CML) are reported to the natio

76 vation contributes to imatinib resistance in chronic myeloid leukemia (CML) are unknown.

77 Using BCR-ABL-induced chronic myeloid leukemia (CML) as a disease model for CS

78 Using chronic myeloid leukemia (CML) as a paradigm for hierarc

79 (TKIs) are highly effective in treatment of chronic myeloid leukemia (CML) but do not eliminate leuk

80 esylate (imatinib) are effective in managing chronic myeloid leukemia (CML) but incapable of eliminat

81 yeloid leukemia of Down syndrome (ML-DS) and chronic myeloid leukemia (CML) by showing that these 2 l

82 es have demonstrated that some patients with chronic myeloid leukemia (CML) can maintain remission af

83 As chronic myeloid leukemia (CML) cell lines expressing BCR

84 ML), acute lymphoblastic leukemia (ALL), and chronic myeloid leukemia (CML) cell lines with commercia

85 gh sensitivity and specificity in live human chronic myeloid leukemia (CML) cell lines.

86 Mathematical models of chronic myeloid leukemia (CML) cell population dynamics

87 BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous

88 ixafor, an antagonist of CXCR4, may dislodge chronic myeloid leukemia (CML) cells from the niche, sen

89 ibitors (TKIs) in eliminating differentiated chronic myeloid leukemia (CML) cells, recent evidence su

90 nize folate receptor-beta-positive (FRbeta+) chronic myeloid leukemia (CML) cells, resulting in more

91 rk that maintains the survival and growth of chronic myeloid leukemia (CML) cells.

92 se activity by imatinib for the treatment of chronic myeloid leukemia (CML) currently serves as the p

93 Progression and disease relapse of chronic myeloid leukemia (CML) depends on leukemia-initi

94 yrosine kinase inhibitors (TKIs) in treating chronic myeloid leukemia (CML) depends on the requiremen

95 y interact with or depend on JAK2 or Lnk, in chronic myeloid leukemia (CML) development, suggesting t

96 he oncogene product BCR-ABL, has transformed chronic myeloid leukemia (CML) from a life-threatening d

97 e validated the platform with an established chronic myeloid leukemia (CML) fusion gene (BCR-ABL1) as

98 s) has led to the widespread perception that chronic myeloid leukemia (CML) has become another chroni

99 Chronic myeloid leukemia (CML) has been a model disease

100 cess of tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML) has given patients hope f

101 Tyrosine kinase inhibitor (TKI) treatment of chronic myeloid leukemia (CML) has limited efficacy agai

102 chromosome (causing the Bcr-Abl mutation) in chronic myeloid leukemia (CML) has provided a paradigm f

103 tions have been established for treatment of chronic myeloid leukemia (CML) in adults treated with ty

104 oven efficacy in adults with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CP) and

105 fficacy and safety outcomes of patients with chronic myeloid leukemia (CML) in chronic phase (CP) tre

106 ximately 5% of patients with newly diagnosed chronic myeloid leukemia (CML) in chronic phase (CP).

107 rogression-free survival among patients with chronic myeloid leukemia (CML) in the chronic phase, aft

108 udy enrolled 210 patients with chronic phase chronic myeloid leukemia (CML) in two equal, sequential

109 The acute myeloid leukemia (AML) and chronic myeloid leukemia (CML) incidences remained const

110 Chronic myeloid leukemia (CML) is a blood disease that d

111 Chronic myeloid leukemia (CML) is a chronic disease resu

112 Chronic myeloid leukemia (CML) is a clonal myeloprolifer

113 Chronic myeloid leukemia (CML) is a hematopoietic diseas

114 Chronic myeloid leukemia (CML) is a hematopoietic stem c

115 Chronic myeloid leukemia (CML) is a stem cell (SC) neopl

116 Chronic myeloid leukemia (CML) is a stem cell disease of

117 Molecular response to imatinib (IM) in chronic myeloid leukemia (CML) is associated with a biph

118 Chronic myeloid leukemia (CML) is caused by the acquisit

119 Chronic myeloid leukemia (CML) is characterized by a spe

120 Chronic myeloid leukemia (CML) is composed of 3% of pedi

121 Chronic myeloid leukemia (CML) is currently treated with

122 Chronic myeloid leukemia (CML) is derived from a stem ce

123 Chronic myeloid leukemia (CML) is effectively treated by

124 Among hematologic neoplasms, chronic myeloid leukemia (CML) is exquisitely sensitive

125 Chronic myeloid leukemia (CML) is induced by the oncogen

126 A major obstacle to curing chronic myeloid leukemia (CML) is the intrinsic resistan

127 Chronic myeloid leukemia (CML) is the model cancer, demo

128 ver, the role of lncRNAs in Bcr-Abl-mediated chronic myeloid leukemia (CML) is unknown.

129 kemia stem cells (LSCs) in a BCR-ABL-induced chronic myeloid leukemia (CML) mouse model, and we hypot

130 improvement in the survival of patients with chronic myeloid leukemia (CML) occurred after the introd

131 Patients with chronic myeloid leukemia (CML) often have comorbidities,

132 y in a phase 1/2 study in chronic-phase (CP) chronic myeloid leukemia (CML) or advanced Ph(+) leukemi

133 phase 2 trial of ponatinib in patients with chronic myeloid leukemia (CML) or Philadelphia chromosom

134 Chronic myeloid leukemia (CML) originates in a hematopoi

135 Recently, chronic myeloid leukemia (CML) patients already respondi

136 y within the LSC population in chronic phase chronic myeloid leukemia (CML) patients at diagnosis and

137 tyrosine kinase inhibitors, the treatment of chronic myeloid leukemia (CML) patients has migrated ext

138 vaccines were evaluated in 51 chronic phase chronic myeloid leukemia (CML) patients on imatinib, or

139 to achievement of deep molecular response in chronic myeloid leukemia (CML) patients on tyrosine kina

140 most common mechanism of drug resistance in chronic myeloid leukemia (CML) patients treated with ABL

141 Although the prognosis of chronic myeloid leukemia (CML) patients treated with ima

142 Chronic myeloid leukemia (CML) patients with the BCR-ABL

143 In chronic myeloid leukemia (CML) patients, a breakpoint cl

144 In chronic myeloid leukemia (CML) patients, tyrosine kinase

145 CD44v3 overexpression enhanced chronic phase chronic myeloid leukemia (CML) progenitor replating capa

146 se, and serially transplantable blast crisis chronic myeloid leukemia (CML) progenitors revealed incr

147 AMD1 was highly upregulated as chronic myeloid leukemia (CML) progressed from the chron

148 As chronic myeloid leukemia (CML) progresses from the chron

149 Targeted therapy with imatinib in chronic myeloid leukemia (CML) prompted a new treatment

150 A total of 1569 patients with chronic myeloid leukemia (CML) referred to our instituti

151 Chronic Myeloid Leukemia (CML) represents a paradigm for

152 introduction of imatinib in the treatment of chronic myeloid leukemia (CML) represents the most succe

153 fication of a population of highly quiescent chronic myeloid leukemia (CML) SCs that is enriched foll

154 The progress made in the understanding of chronic myeloid leukemia (CML) since the recognition of

155 tly demonstrate that CD26 is a new, specific chronic myeloid leukemia (CML) stem cell biomarker that

156 Chronic myeloid leukemia (CML) stem cell survival is not

157 Recent evidence suggests chronic myeloid leukemia (CML) stem cells are insensitiv

158 Chronic myeloid leukemia (CML) stem cells are not depend

159 l transcriptome profiling in treatment-naive chronic myeloid leukemia (CML) stem/progenitor cells and

160 Recent clinical findings in patients with chronic myeloid leukemia (CML) suggest that the risk of

161 alyze more than 2,000 SCs from patients with chronic myeloid leukemia (CML) throughout the disease co

162 Cs) play a pivotal role in the resistance of chronic myeloid leukemia (CML) to tyrosine kinase inhibi

163 Most patients with chronic myeloid leukemia (CML) treated with imatinib wil

164 safety is an emerging issue in patients with chronic myeloid leukemia (CML) treated with tyrosine kin

165 kinase inhibitors has significantly affected chronic myeloid leukemia (CML) treatment, transforming t

166 e report that loss of K3 in a mouse model of chronic myeloid leukemia (CML) triggers the release of L

167 hase 3 trial with ponatinib in patients with chronic myeloid leukemia (CML) was interrupted due to an

168 can safely be discontinued in patients with chronic myeloid leukemia (CML) who have had undetectable

169 MR(4.5)) defines a subgroup of patients with chronic myeloid leukemia (CML) who may stay in unmaintai

170 ors (TKIs) among Medicare beneficiaries with chronic myeloid leukemia (CML) with and without cost-sha

171 In the treatment of chronic myeloid leukemia (CML) with BCR-ABL kinase inhib

172 sults have been obtained in the treatment of chronic myeloid leukemia (CML) with first-line imatinib

173 Treatment of chronic myeloid leukemia (CML) with imatinib mesylate an

174 Treatment of chronic myeloid leukemia (CML) with the tyrosine kinase

175 matopoietic stem cell (HSC) self-renewal and chronic myeloid leukemia (CML), a prototypical stem cell

176 nuclear and cytoplasmic functions of p27 in chronic myeloid leukemia (CML), a well-characterized mal

177 In a mouse model of blast crisis chronic myeloid leukemia (CML), adipose-resident LSCs ex

178 kemia (CNL) and atypical (BCR-ABL1-negative) chronic myeloid leukemia (CML), both of which are diagno

179 ased survival dramatically for patients with chronic myeloid leukemia (CML), but continuous administr

180 Chronic myeloid leukemia (CML), caused by constitutively

181 s enabled durable responses in patients with chronic myeloid leukemia (CML), issues of drug resistanc

182 (TKIs) in 1998 transformed the management of chronic myeloid leukemia (CML), leading to significantly

183 The treatment policy of chronic myeloid leukemia (CML), particularly with tyrosi

184 nase inhibitors (TKI) changed the outcome of chronic myeloid leukemia (CML), turning a life-threateni

185 of the oncogenic tyrosine kinase BCR-ABL in chronic myeloid leukemia (CML), using highly enriched CM

186 As a group of more than 100 experts in chronic myeloid leukemia (CML), we draw attention to the

187 ause treatment outcomes are poor in advanced chronic myeloid leukemia (CML), we hypothesized that exp

188 l human hematopoietic malignancies including chronic myeloid leukemia (CML), where BCL6 expression wa

189 demonstrate proof of concept in the case of chronic myeloid leukemia (CML), wherein our model recapi

190 ions are a common mechanism of resistance in chronic myeloid leukemia (CML), yet the mechanism of res

191 -Abl1(-/-) cells generated highly aggressive chronic myeloid leukemia (CML)-blast phase-like disease

192 nses to tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML)-chronic phase (CP) are as

193 enic tyrosine (Y) kinase, does not eradicate chronic myeloid leukemia (CML)-initiating cells.

194 1-positive clonal hematopoiesis resembling a chronic myeloid leukemia (CML)-like disease manifesting

195 tes disease progression in a murine model of chronic myeloid leukemia (CML)-like myeloproliferative n

196 ition between normal and cancerous states in chronic myeloid leukemia (CML).

197 ge of Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML).

198 bitors (TKIs) has revolutionized therapy for chronic myeloid leukemia (CML).

199 (LSCs) in a murine model of BCR-ABL-induced chronic myeloid leukemia (CML).

200 patients with imatinib-resistant/-intolerant chronic myeloid leukemia (CML).

201 L oncoprotein in a majority of patients with chronic myeloid leukemia (CML).

202 greatly increased survival for patients with chronic myeloid leukemia (CML).

203 nse to imatinib predicts clinical outcome in chronic myeloid leukemia (CML).

204 ative treatment schedule of imatinib (IM) in chronic myeloid leukemia (CML).

205 to ABL tyrosine kinase inhibitors (TKIs) in chronic myeloid leukemia (CML).

206 sed in the leukemic stem/progenitor cells of chronic myeloid leukemia (CML).

207 ine kinase inhibitor (TKI)-free remission in chronic myeloid leukemia (CML).

208 Symptom Inventory (MDASI) for patients with chronic myeloid leukemia (CML).

209 ling pathways, resulting in the induction of chronic myeloid leukemia (CML).

210 em cell expansion and disease progression in chronic myeloid leukemia (CML).

211 imatinib-resistant/-intolerant patients with chronic myeloid leukemia (CML).

212 ins the major challenge in the management of chronic myeloid leukemia (CML).

213 regulation of leukemia stem cells (LSCs) in chronic myeloid leukemia (CML).

214 tor (TKI), has shown potent activity against chronic myeloid leukemia (CML).

215 h imatinib in newly diagnosed, chronic-phase chronic myeloid leukemia (CML).

216 ilure of imatinib mesylate (IM) to eradicate chronic myeloid leukemia (CML).

217 inhibitor, has shown potent activity against chronic myeloid leukemia (CML).

218 ce to ABL inhibitor therapy in patients with chronic myeloid leukemia (CML).

219 vity of Bcr-abl fusion protein kinase causes chronic myeloid leukemia (CML).

220 ls and is responsible for the development of chronic myeloid leukemia (CML).

221 n correlated with remission in patients with chronic myeloid leukemia (CML).

222 ene-free iPSCs from the BM of a patient with chronic myeloid leukemia (CML).

223 l transplantation as a curative treatment of chronic myeloid leukemia (CML).

224 ated with poor prognosis and blast crisis in chronic myeloid leukemia (CML).

225 ieved with imatinib therapy in patients with chronic myeloid leukemia (CML).

226 in transforms pluripotent HSCs and initiates chronic myeloid leukemia (CML).

227 fusion protein kinase-induced mouse model of chronic myeloid leukemia (CML).

228 or, improved the prognosis for patients with chronic myeloid leukemia (CML).

229 signed to evaluate 2G-TKI discontinuation in chronic myeloid leukemia (CML).

230 ree models: melanoma, pancreatic cancer, and chronic myeloid leukemia (CML).

231 ve revolutionized treatment of patients with chronic myeloid leukemia (CML).

232 resistant to current therapies used to treat chronic myeloid leukemia (CML).

233 nib, nilotinib) have been developed to treat Chronic Myeloid Leukemia (CML).

234 proving outcome for patients with refractory chronic myeloid leukemia (CML).

235 e and overall survival (OS) in patients with chronic myeloid leukemia (CML).

236 cute lymphoblastic leukemia (ALL, n = 1883); chronic myeloid leukemia (CML, n = 1079); and myelodyspl

237 both accelerated phase (AP) and blast crisis chronic myeloid leukemia (CML-BC) and against Philadelph

238 io, 1.79; 95% CI, 1.13 to 2.82; P = .01) and chronic myeloid leukemia (CML; hazard ratio, 3.44; 95% C

239 total of 39 patients (solid tumors, n = 28; chronic myeloid leukemia [CML], n = 9; acute lymphoblast

240 oncoprotein associated with the majority of chronic myeloid leukemias (CMLs), induces accumulation o

241 phases emerge as patients with chronic phase chronic myeloid leukemia (CP-CML) are treated with tyros

242 Without effective therapy, chronic-phase chronic myeloid leukemia (CP-CML) evolves into an acute

243 own to predict for response in chronic phase-chronic myeloid leukemia (CP-CML) patients treated with

244 sed BCR-ABL1 inhibitors for the treatment of chronic myeloid leukemia do not eliminate leukemic stem

245 e Evaluation of Ponatinib versus Imatinib in Chronic Myeloid Leukemia (EPIC) study was a randomised,

246 stant patients enrolled in the PONATINIB for Chronic Myeloid Leukemia Evaluation and Ph(+)Acute Lymph

247 creased risk of bleeding among patients with chronic myeloid leukemia, even in the absence of thrombo

248 detection of the BCR-ABL1 fusion delineates chronic myeloid leukemia from classic BCR-ABL1(-) MPNs,

249 n associated with various cancers, including chronic myeloid leukemia, head and neck squamous cell ca

250 We suggest that chronic myeloid leukemia heralds a fundamental shift in

251 otinib or dasatinib therapy in patients with chronic myeloid leukemia; however, such therapy also fai

252 ignancies, including acute myeloid leukemia, chronic myeloid leukemia in blast crisis, myelodysplasti

253 nt efficacy in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP) and i

254 BCR-ABL1 transcript levels in patients with chronic myeloid leukemia in chronic phase (CML-CP) at 3,

255 r responses on the outcomes of patients with chronic myeloid leukemia in chronic phase (CML-CP) in th

256 Chronic myeloid leukemia in chronic phase (CML-CP) is in

257 Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resul

258 hing to nilotinib enabled more patients with chronic myeloid leukemia in chronic phase (CML-CP) to su

259 ved for use in patients with newly diagnosed chronic myeloid leukemia in chronic phase (CML-CP), and

260 ients with imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase from the phase

261 rvival (OS) in patients with newly diagnosed chronic myeloid leukemia in chronic phase treated with i

262 on outcomes in patients with newly diagnosed chronic myeloid leukemia in chronic phase treated with n

263 or outcome and response in 123 patients with chronic myeloid leukemia in chronic phase treated with s

264 a in first complete remission (N = 1742) and chronic myeloid leukemia in first chronic phase (N = 257

265 investigation using CAPRI to study atypical Chronic Myeloid Leukemia, in which we uncovered non triv

266 in tyrosine kinase inhibitor (TKI)-resistant chronic myeloid leukemia, irrespective of BCR-ABL KD mut

267 Chronic myeloid leukemia is effectively treated with ima

268 disorders, unlike bcr/abl tyrosine kinase in chronic myeloid leukemia, is not a causative but rather

269 inhibitors results in potent suppression of chronic myeloid leukemia leukemic precursors and Ph(+) a

270 ng chronic myelomonocytic leukemia, atypical chronic myeloid leukemia, MDS/MPN-Unclassifiable, ring s

271 Increased serum OPN concentrations occur in chronic myeloid leukemia, multiple myeloma, and acute my

272 leagues show that, during the development of chronic myeloid leukemia, mutated cells transform normal

273 Frequently linked to polycythemia vera and chronic myeloid leukemia, myelofibrosis displays high pa

274 hematopoietic progenitors from patients with chronic myeloid leukemia or myeloproliferative neoplasms

275 of early CCyR remains a major determinant of chronic myeloid leukemia outcome regardless of whether M

276 ells with high pCRKL and pSTAT5 signaling in chronic myeloid leukemia patient blood samples.

277 f 6 acute lymphoblastic leukemia, and 3 of 6 chronic myeloid leukemia patient samples exposed to SB,

278 nib Versus Imatinib Study in Treatment-Naive Chronic Myeloid Leukemia Patients (DASISION) trial, eval

279 ne the frequency of compound mutations among chronic myeloid leukemia patients on ABL1 TKI therapy, i

280 c responses (CCyRs) in approximately half of chronic myeloid leukemia patients treated while still in

281 explain resistance in clinical samples from chronic myeloid leukemia patients.

282 ute myeloid leukemia and 0.9% and 2.4% among chronic myeloid leukemia patients.

283 its inability to fully eradicate disease in chronic myeloid leukemia patients.

284 ression and transit times between normal and chronic myeloid leukemia progenitors that may inform can

285 development, and targeting SIRT1 sensitized chronic myeloid leukemia progenitors to tyrosine kinase

286 However, in blast crisis chronic myeloid leukemia progenitors, loss of EZH2 expre

287 Patients with chronic myeloid leukemia receiving inhibitors of c-Abl t

288 Chronic myeloid leukemia responds well to therapy target

289 In chronic myeloid leukemia, SIRT1 promoted leukemia develo

290 progenitors into self-renewing blast crisis chronic myeloid leukemia stem cells (BC LSCs) was partia

291 found to be highly upregulated on candidate chronic myeloid leukemia stem cells, allowing for leukem

292 In chronic myeloid leukemia, the emergence of tyrosine kina

293 onclusion, 8% of patients with chronic phase chronic myeloid leukemia treated at our institution are

294 it to 465 patients with early chronic phase chronic myeloid leukemia treated with standard-dose imat

295 Advances in chronic myeloid leukemia treatment, particularly regardi

296 For most patients with chronic myeloid leukemia, tyrosine kinase inhibitors (TK

297 patients with newly diagnosed chronic-phase chronic myeloid leukemia were randomized to IM 400 mg/da

298 to inhibit the dysregulated proliferation of chronic myeloid leukemia, which is associated with the B

299 We analyzed a cohort of 26 patients with chronic myeloid leukemia who had failed imatinib and a s

300 strikingly effective in the initial stage of chronic myeloid leukemia with more than 90% of the patie