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

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

2 60% to 78% (P < .001) for AML, ALL, MDS, and chronic myeloid leukemia.

3 kemia, and in blast crisis transformation of 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 monocytes of patients receiving imatinib for chronic myeloid leukemia.

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

15 of a targeted molecular therapy for treating chronic myeloid leukemia.

16 tant to all currently marketed therapies 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 as the clinically related diagnosis atypical chronic myeloid leukemia.

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

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

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

26 ificantly in their management strategies for chronic myeloid leukemia, acute and chronic graft-versus

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

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

29 01 for treatment of many different stages of chronic myeloid leukemia and in 2002 for treatment of ga

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

31 In chronic myeloid leukemia and Philadelphia chromosome-pos

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 17f inhibited the growth of acute and chronic myeloid leukemia cells and the phosphorylation a

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

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

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

54 mutations conferring imatinib resistance in chronic myeloid leukemia cells.

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

56 Unlike chronic myeloid leukemia, chronic lymphocytic leukemia (

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

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

59 Dasatinib is effective therapy for chronic myeloid leukemia (CML) after imatinib failure.

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

61 a chromosome-positive leukemia that includes chronic myeloid leukemia (CML) and B-cell acute lymphobl

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

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

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

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

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

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

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

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

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

71 The most common BCR-ABL transcripts in chronic myeloid leukemia (CML) are e13a2(b2a2) and e14a2

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 PRAME mRNA expression increased with chronic myeloid leukemia (CML) disease progression and i

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

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

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

96 Chronic myeloid leukemia (CML) has been regarded as the

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

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

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

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

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

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

103 Although most patients with chronic myeloid leukemia (CML) in chronic phase respond

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

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

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

107 Chronic myeloid leukemia (CML) is a clonal myeloprolifer

108 Chronic myeloid leukemia (CML) is a hematopoietic diseas

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

110 Chronic myeloid leukemia (CML) is a Ph(+) MPD that is de

111 Molecular monitoring in chronic myeloid leukemia (CML) is a powerful tool to doc

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

113 Secondary imatinib resistance in chronic myeloid leukemia (CML) is associated in approxim

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

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

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

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

118 Chronic myeloid leukemia (CML) is currently treated with

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

120 Chronic myeloid leukemia (CML) is effectively treated by

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 In chronic-phase chronic myeloid leukemia (CML) patients, the lack of a m

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

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

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

141 that can determine where in the spectrum of chronic myeloid leukemia (CML) progression an individual

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

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

144 Chronic Myeloid Leukemia (CML) represents a paradigm for

145 Chronic myeloid leukemia (CML) represents an important p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 During therapy for chronic myeloid leukemia (CML), decline of the number of

172 ieve maximal therapeutic benefit in treating chronic myeloid leukemia (CML), establishing a paradigm

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

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

175 In imatinib-treated chronic myeloid leukemia (CML), secondary drug resistanc

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

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

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

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

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

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

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

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

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

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

186 1-positive clonal hematopoiesis resembling a chronic myeloid leukemia (CML)-like disease manifesting

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

215 eukemia stem cells (LSCs) in BCR-ABL-induced chronic myeloid leukemia (CML).

216 treatment for newly diagnosed patients with chronic myeloid leukemia (CML).

217 h(+)) acute lymphoblastic leukemia (ALL) and chronic myeloid leukemia (CML).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 d ICSBP expression is found in human AML and chronic myeloid leukemia during blast crisis (CML-BC).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

253 ted platelet aggregation in 91 patients with chronic myeloid leukemia in chronic phase either off-the

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

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

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

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

258 imatinib dose escalation in 84 patients with chronic myeloid leukemia in chronic phase who met the cr

259 sponse, and progression in 258 patients with chronic myeloid leukemia in early chronic phase at 3, 6,

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

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

262 ice daily in patients with accelerated-phase chronic myeloid leukemia intolerant or resistant to imat

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

264 yrosine kinase inhibitor (TKI) resistance in chronic myeloid leukemia is associated with characterist

265 Chronic myeloid leukemia is effectively treated with ima

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

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

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

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

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

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

272 lts from the subgroup with accelerated-phase chronic myeloid leukemia (n = 317) with a median follow-

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

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

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

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

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

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

279 We report on 48 chronic myeloid leukemia patients sequentially treated w

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

281 e analyzed DNA samples from 45 TKI-resistant chronic myeloid leukemia patients with 250K single nucle

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

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

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

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

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

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