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

1 erived from the oncogenic BCR/ABL protein in chronic myelogenous leukemia).

2 esults in a syndrome highly similar to human chronic myelogenous leukemia.

3 ing imatinib for the first-line treatment of chronic myelogenous leukemia.

4 cells in some hematopoietic cancers, such as chronic myelogenous leukemia.

5 f GVL against a mouse model of chronic-phase chronic myelogenous leukemia.

6 nown as a substrate of the BCR-ABL kinase in chronic myelogenous leukemia.

7 ntifies the current role of the procedure in chronic myelogenous leukemia.

8 plete cytogenetic remission in patients with chronic myelogenous leukemia.

9 gs, particularly imatinib mesylate, to treat chronic myelogenous leukemia.

10 t progress into a phenotype resembling human chronic myelogenous leukemia.

11 at thwart imatinib activity in patients with chronic myelogenous leukemia.

12 nism of imatinib resistance in patients with chronic myelogenous leukemia.

13 ntly in clinical trials for the treatment of chronic myelogenous leukemia.

14 s a constitutively active kinase that causes chronic myelogenous leukemia.

15 enic protein-tyrosine kinase responsible for chronic myelogenous leukemia.

16 fusion protein Bcr-Abl, the causal agent in chronic myelogenous leukemia.

17 ogy and in the development of both acute and chronic myelogenous leukemia.

18 yeloid leukemia and with the blast crisis of chronic myelogenous leukemia.

19 cal issue for patients in advanced phases of chronic myelogenous leukemia.

20 in therapy may have utility in patients with chronic myelogenous leukemia.

21 A 49-yr-old male with chronic myelogenous leukemia.

22 has clinical activity in imatinib refractory chronic myelogenous leukemia.

23 (GVL) against a mouse model of chronic-phase chronic myelogenous leukemia.

24 from the bone marrows of three patients with chronic myelogenous leukemia.

25 g 133 patients undergoing allogeneic HCT for chronic myelogenous leukemia.

26 the skin 6 years after HCT for treatment of chronic myelogenous leukemia.

27 mechanism, the disruption of which leads to chronic myelogenous leukemia.

28 ase inhibitor, effective in the treatment of chronic myelogenous leukemia.

29 e oncogenic fusion protein characteristic of chronic myelogenous leukemia.

30 ve not extended life to the degree seen with chronic myelogenous leukemia.

31 eptor tyrosine kinase inhibitor approved for chronic myelogenous leukemia.

32 efficacy in patients with imatinib-resistant chronic myelogenous leukemia.

33 onic myelomonocytic leukemia (CMML)/atypical chronic myelogenous leukemia (aCML), myelodysplastic syn

34 s with metastatic cancer and 9 patients with chronic myelogenous leukemia after allogeneic hematopoie

35 eloid leukemia, myelodysplastic syndrome and chronic myelogenous leukemia after umbilical cord blood

36 , growth, and potential relapse of acute and chronic myelogenous leukemia (AML and CML).

37 roduct of a t(3;21)(q26;q22) associated with chronic myelogenous leukemia and acute myelogenous leuke

38 reatment of Philadelphia chromosome-positive chronic myelogenous leukemia and B cell acute lymphoblas

39 ummarizes the history of transplantation for chronic myelogenous leukemia and defines the new natural

40 hogenesis of hematologic diseases other than chronic myelogenous leukemia and discusses the evidence

41 euticals, East Hanover, NJ) for treatment of chronic myelogenous leukemia and gastrointestinal stroma

42 The trail blazed by imatinib for chronic myelogenous leukemia and GIST has become a desir

43 ibitor that is currently being used to treat chronic myelogenous leukemia and other disorders.

44 is a deregulated tyrosine kinase that causes chronic myelogenous leukemia and Ph-positive acute lymph

45 or of therapeutic response for patients with chronic myelogenous leukemia and Philadelphia chromosome

46 t was recently approved for the treatment of chronic myelogenous leukemia and Philadelphia chromosome

47 emia vera patients, as well as patients with chronic myelogenous leukemia and prostate cancer, sugges

48 d bortezomib warrants further examination in chronic myelogenous leukemia and related hematologic mal

49 a tremendous impact on clinical outcomes in chronic myelogenous leukemia and revolutionized the fiel

50 BL oncogene is responsible for most cases of chronic myelogenous leukemia and some acute lymphoblasti

51 or overexpressed in breast cancer), BCR-ABL (chronic myelogenous leukemia and some cases of acute lym

52 ABL fusion kinase is the driving mutation of chronic myelogenous leukemias and is also expressed in a

53 noma), Jurkat (acute T-cell leukemia), K562 (chronic myelogenous leukemia) and MEC-2 (chronic lymphoc

54 ALK-positive anaplastic large cell lymphoma, chronic myelogenous leukemia, and acute leukemias.

55 loid leukemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndro

56 nous leukemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, and myelodysplastic syndro

57 ous against acute leukemias and blast-crisis chronic myelogenous leukemia (BC-CML).

58 The inability of myeloid chronic myelogenous leukemia blast crisis (CML-BC) proge

59 icular, its expression is highly elevated in chronic myelogenous leukemia blast crisis as compared wi

60 te lymphoblastic leukemia (ALL) and lymphoid chronic myelogenous leukemia blast crisis.

61 This procedure remains an option in chronic myelogenous leukemia but its use will become mor

62 e progression in patients with chronic phase chronic myelogenous leukemia, but the emergence of imati

63 e oncogenic BCR-ABL fusion protein kinase in chronic myelogenous leukemia, but which also potently in

64 ancers and broad H3K4me3 domains in the K562 chronic myelogenous leukemia cell line as well as the MC

65 Ectopic expression of PTPROt in the chronic myelogenous leukemia cell line K562 indeed resul

66 ens to identify essential genes in the human chronic myelogenous leukemia cell line K562.

67 ands, where cellular membrane fragments of a chronic myelogenous leukemia cell line, KU-812, were imm

68 ndogenous Crk was robustly phosphorylated in chronic myelogenous leukemia cell lines and in A431 and

69 lls, and they potently induced cell death in chronic myelogenous leukemia cell lines.

70 ase Lyn and Bcl-2 expression was examined in chronic myelogenous leukemia cells (K562 and LAMA84) dis

71 ite in vitro, was strongly phosphorylated in chronic myelogenous leukemia cells in a Src family kinas

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

73 Treatment of K562 chronic myelogenous leukemia cells with phorbol-12-myris

74 duces apoptosis in highly imatinib-resistant chronic myelogenous leukemia cells, most likely by inhib

75 appears to be effective in diseases such as chronic myelogenous leukemia, chronic lymphocytic leukem

76 raft versus tumor (GVT) effects for relapsed chronic myelogenous leukemia (CML) after allogeneic stem

77 fusion associated with dasatinib therapy for chronic myelogenous leukemia (CML) after failure of imat

78 inib 70 mg twice daily in chronic-phase (CP) chronic myelogenous leukemia (CML) after imatinib treatm

79 We reviewed 261 patients with chronicphase chronic myelogenous leukemia (CML) after interferon-alph

80 counterparts, leukemia stem cells (LSCs) in chronic myelogenous leukemia (CML) and acute myeloid leu

81 morigenesis in some human cancers, including chronic myelogenous leukemia (CML) and breast cancer.

82 ts with acute myelogenous leukemia (AML) and chronic myelogenous leukemia (CML) and demonstrated that

83 rs LSC self-renewal in p210(BCR-ABL)-induced chronic myelogenous leukemia (CML) and exhibits synergis

84 A) is being evaluated for imatinib-resistant chronic myelogenous leukemia (CML) and has multiple cell

85 PA) is low in the blast crisis (BC) stage of chronic myelogenous leukemia (CML) and is inversely corr

86 Cancer stem cells lie at the root of chronic myelogenous leukemia (CML) and mediate its conti

87 ne/paracrine fashion, their possible role in chronic myelogenous leukemia (CML) and resistance to ima

88 I) treatment, and prognostic significance in chronic myelogenous leukemia (CML) are largely unknown.

89 We use chronic myelogenous leukemia (CML) as a model of LIC-dep

90 g has had a major impact on the treatment of chronic myelogenous leukemia (CML) as well as other bloo

91 TA-2 was repressed in 32D-BCR/ABL, K562, and chronic myelogenous leukemia (CML) blast crisis (BC) pri

92 n ablation on the survival of drug-resistant chronic myelogenous leukemia (CML) blast crisis cells us

93 late is highly effective in the treatment of chronic myelogenous leukemia (CML) but fails to eliminat

94 HSCT) is effective therapy for patients with chronic myelogenous leukemia (CML) but is now mostly ind

95 oncogenic kinase Bcr-Abl is thought to cause chronic myelogenous leukemia (CML) by altering the trans

96 ectrochemical DNA biosensor for detection of chronic myelogenous leukemia (CML) by covalently immobil

97 inase has been targeted for the treatment of chronic myelogenous leukemia (CML) by imatinib mesylate.

98 ectrochemical DNA biosensor for detection of chronic myelogenous leukemia (CML) by immobilizing amine

99 Exposure to chronic myelogenous leukemia (CML) caused normal mouse h

100 Using the K562 chronic myelogenous leukemia (CML) cell line and the dox

101 The chronic myelogenous leukemia (CML) cell lines, KCL22 and

102 en was highly active against primary CD34(+) chronic myelogenous leukemia (CML) cells and Ba/F3 cells

103 Increased levels of Bcr-Abl expression in chronic myelogenous leukemia (CML) cells are associated

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

105 PKIs, were assessed in cell-free medium and chronic myelogenous leukemia (CML) cells overexpressing

106 ns as a regulator of imatinib sensitivity in chronic myelogenous leukemia (CML) cells through an unkn

107 or Bcr-Abl-mediated resistance of human K562 chronic myelogenous leukemia (CML) cells to Taxol-induce

108 In chronic myelogenous leukemia (CML) cells, Bcr-Abl phosph

109 46 and Ser65 as RI-mTORC1 signals in primary chronic myelogenous leukemia (CML) cells.

110 without affecting bcr/abl gene expression in chronic myelogenous leukemia (CML) cells.

111 562 and LAMA-84 cells, as well as in primary chronic myelogenous leukemia (CML) cells.

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

113 lphia chromosome (Ph)-positive chronic-phase chronic myelogenous leukemia (CML) due to the high rate

114 The imatinib paradigm in chronic myelogenous leukemia (CML) established continuou

115 Chronic myelogenous leukemia (CML) evolves from a chroni

116 Virtually all patients with chronic myelogenous leukemia (CML) express an aberrant p

117 ) have been implicated in the progression of chronic myelogenous leukemia (CML) from the indolent chr

118 Chronic myelogenous leukemia (CML) in children is relati

119 and provide insight into the progression of chronic myelogenous leukemia (CML) in humans.

120 Chronic myelogenous leukemia (CML) invariably progresses

121 Chronic phase-to-blast crisis transition in chronic myelogenous leukemia (CML) is associated with di

122 Chronic myelogenous leukemia (CML) is characterized by t

123 and activators of transcription 5 (STAT5) in chronic myelogenous leukemia (CML) is controversial.

124 Chronic myelogenous leukemia (CML) is driven by Bcr-Abl,

125 Although chronic myelogenous leukemia (CML) is effectively contro

126 ditional chromosomal abnormalities (ACAs) in chronic myelogenous leukemia (CML) is generally associat

127 Effective treatment of chronic myelogenous leukemia (CML) largely depends on th

128 ia chromosome in cells from individuals with chronic myelogenous leukemia (CML) led to the recognitio

129 he role of OBs in regulating normal HSCs and chronic myelogenous leukemia (CML) LSCs.

130 surveillance of minimal residual disease in chronic myelogenous leukemia (CML) may be relevant for l

131 such as donor lymphocyte infusion (DLI) for chronic myelogenous leukemia (CML) may result from immun

132 In patients with chronic myelogenous leukemia (CML) mutations of the BCR-

133 ssive leukemias in recipient mice resembling chronic myelogenous leukemia (CML) myeloid blast crisis.

134 esistant BCR-ABL mutations, in patients with chronic myelogenous leukemia (CML) or Ph-positive acute

135 TKI) are effective in inducing remissions in chronic myelogenous leukemia (CML) patients but do not e

136 Chronic myelogenous leukemia (CML) patients treated with

137 We previously demonstrated that chronic myelogenous leukemia (CML) patients treated with

138 pitulating events inferred to occur in human chronic myelogenous leukemia (CML) patients.

139 osine kinase is the causative factor in most chronic myelogenous leukemia (CML) patients.

140 netic response (CCR) in a high proportion of chronic myelogenous leukemia (CML) patients.

141 b response gene signatures in cell lines and chronic myelogenous leukemia (CML) patients.

142 including primitive leukemic precursors from chronic myelogenous leukemia (CML) patients.

143 s) have changed the therapeutic strategy for chronic myelogenous leukemia (CML) patients.

144 edly reduces the burden of leukemia cells in chronic myelogenous leukemia (CML) patients.

145 susceptibility to chromosomal aberrations in chronic myelogenous leukemia (CML) progenitors after exp

146 Therapeutic options for chronic myelogenous leukemia (CML) resistant to 400 to 6

147 Chronic myelogenous leukemia (CML) results from a chromo

148 Chronic myelogenous leukemia (CML) results from a t(9,22

149 Chronic myelogenous leukemia (CML) results from expressi

150 Chronic myelogenous leukemia (CML) results from malignan

151 Chronic myelogenous leukemia (CML) results from the tran

152 Chronic myelogenous leukemia (CML) results from transfor

153 Chronic myelogenous leukemia (CML) results from transfor

154 stitutively active mutant of Abl that causes chronic myelogenous leukemia (CML) stimulated the expres

155 Progression of chronic myelogenous leukemia (CML) to accelerated (AP) a

156 The progression of chronic myelogenous leukemia (CML) to blast crisis is su

157 d leukemia stem cells (LSC) in chronic phase chronic myelogenous leukemia (CML) using a transgenic mo

158 utrient selenium has been shown to alleviate chronic myelogenous leukemia (CML) via the elimination o

159 is found in Philadelphia chromosome-positive chronic myelogenous leukemia (CML) where all available k

160 Unlike in CLL, GRN was not upregulated in chronic myelogenous leukemia (CML) where miR-107 paralog

161 hain reaction (QPCR) levels in patients with chronic myelogenous leukemia (CML) who are in complete c

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

163 s with Philadelphia-chromosome (Ph)-negative chronic myelogenous leukemia (CML), 2 (18%) of 11 patien

164 propose and analyse a mathematical model for chronic myelogenous leukemia (CML), a cancer of the bloo

165 During blast crisis of chronic myelogenous leukemia (CML), abnormal granulocyte

166 plants for acute myelogenous leukemia (AML), chronic myelogenous leukemia (CML), acute lymphoblastic

167 ter F-->M HSCT was observed in patients with chronic myelogenous leukemia (CML), acute myelogenous le

168 nhibitor imatinib is remarkably effective in chronic myelogenous leukemia (CML), although drug resist

169 ation of megakaryocytes, the pathogenesis of chronic myelogenous leukemia (CML), and activation of pe

170 nducing complete remissions in patients with chronic myelogenous leukemia (CML), and evidence support

171 risis Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML), and imatinib-resista

172 bl plays a major role in the pathogenesis of chronic myelogenous leukemia (CML), and is the target of

173 inib is highly effective in the treatment of chronic myelogenous leukemia (CML), but primary and acqu

174 r remission in the majority of patients with chronic myelogenous leukemia (CML), but the persistence

175 -ABL1 inhibitors are effective therapies for chronic myelogenous leukemia (CML), but these inhibitors

176 translocation found in the vast majority of chronic myelogenous leukemia (CML), cooperates with AML1

177 s orally active in a K562 xenograft model of chronic myelogenous leukemia (CML), demonstrating comple

178 ine kinase inhibitors (TKIs), a treatment of chronic myelogenous leukemia (CML), has largely replaced

179 nosed with acute myelogenous leukemia (AML), chronic myelogenous leukemia (CML), or myelodysplastic s

180 ccessful therapies for the initial stages of chronic myelogenous leukemia (CML), refractory cases hig

181 lar targeted therapies, such as imatinib for chronic myelogenous leukemia (CML), represent the first

182 imatinib at inhibiting Bcr-Abl and treating chronic myelogenous leukemia (CML), resistance to the th

183 udied mutation frequency in 66 patients with chronic myelogenous leukemia (CML), using cDNA sequencin

184 (NK) cell-mediated antileukemic activity in chronic myelogenous leukemia (CML), we investigated the

185 For example, BCR/ABL causes chronic myelogenous leukemia (CML), whereas FLT3 mutatio

186 erm impact of this strategy in patients with chronic myelogenous leukemia (CML), which is driven by t

187 hown remarkable efficacy in the treatment of chronic myelogenous leukemia (CML), with a high proporti

188 NK) and subsequent induction of apoptosis of chronic myelogenous leukemia (CML)- or acute promyelocyt

189 ICSBP, since ICSBP-deficient mice develop a chronic myelogenous leukemia (CML)-like disease and a hi

190 viral oncogene homolog 1 (BCR-ABL1)-induced chronic myelogenous leukemia (CML)-like myeloproliferati

191 or, is a successful front-line treatment for chronic myelogenous leukemia (CML).

192 ling initiated by the BCR-ABL1 kinase causes chronic myelogenous leukemia (CML).

193 y the BCR-ABL inhibitor imatinib in treating chronic myelogenous leukemia (CML).

194 pathogenesis of many human cancers including chronic myelogenous leukemia (CML).

195 mic stem/progenitor cells from patients with chronic myelogenous leukemia (CML).

196 osine kinase inhibitor that is used to treat chronic myelogenous leukemia (CML).

197 small chromosome in cells from patients with chronic myelogenous leukemia (CML).

198 BL tyrosine kinase inhibitors and relapse of chronic myelogenous leukemia (CML).

199 Resistance to imatinib mesylate can occur in chronic myelogenous leukemia (CML).

200 ied example is the Bcr-Abl fusion protein in chronic myelogenous leukemia (CML).

201 atinib resistance constitutes a challenge in chronic myelogenous leukemia (CML).

202 s is a significant problem in advanced-stage chronic myelogenous leukemia (CML).

203 target and the initiating oncogene for human chronic myelogenous leukemia (CML).

204 ABL oncoprotein in the blast crisis phase of chronic myelogenous leukemia (CML).

205 a highly effective therapy for patients with chronic myelogenous leukemia (CML).

206 unit (CFU-GM) progenitors from patients with chronic myelogenous leukemia (CML).

207 s been highly successful in the treatment of chronic myelogenous leukemia (CML).

208 rative disorder (MPD) resembling early human chronic myelogenous leukemia (CML).

209 ylate (STI571) is effective in chronic phase chronic myelogenous leukemia (CML).

210 issions observed at lower doses than used in chronic myelogenous leukemia (CML).

211 1) is an effective therapy for all stages of chronic myelogenous leukemia (CML).

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

213 BL tyrosine kinase (BCR-ABL) oncogene causes chronic myelogenous leukemia (CML).

214 enome instability, leading to development of chronic myelogenous leukemia (CML).

215 gastrointestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

216 on of the chronic and blast crisis phases of chronic myelogenous leukemia (CML).

217 inate quiescent leukemia stem cells (LSC) in chronic myelogenous leukemia (CML).

218 gastrointestinal stromal tumors (GISTs) and chronic myelogenous leukemia (CML).

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

220 used for the treatment of imatinib-resistant chronic myelogenous leukemia (CML).

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

222 an essential mediator of the pathogenesis of chronic myelogenous leukemia (CML).

223 R-ABL is a causative tyrosine kinase (TK) of chronic myelogenous leukemia (CML).

224 inhibitors (TKI) have improved treatment of chronic myelogenous leukemia (CML); however, most patien

225 stration and revolutionized the treatment of chronic myelogenous leukemia (CML); in 2006 and 2007, ap

226 Blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia c

227 to induce long-term response in blast crisis chronic myelogenous leukemia (CML-BC) and Philadelphia c

228 that loss of miR-328 occurs in blast crisis chronic myelogenous leukemia (CML-BC) in a BCR/ABL dose-

229 st complete remission [CR] and chronic-phase chronic myelogenous leukemia [CML]) and 84 with poor ris

230 leukemia [AML]/myelodysplasia [MDS], 5 with chronic myelogenous leukemia [CML], and 1 with acute lym

231 sted that myeloid leukemia blasts (including chronic myelogenous leukemia [CML]-blast crisis cells) r

232 nt of Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemias (CMLs).

233 Leukemic stem cells in chronic phase chronic myelogenous leukemia (CP-CML) are responsible fo

234 ore than half of patients with chronic-phase chronic myelogenous leukemia (CP-CML) in complete molecu

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

236 on (alloSCT) is potent against chronic phase chronic myelogenous leukemia (CP-CML), but blast crisis

237 mia cell line, and they have homology to two chronic myelogenous leukemia-derived clones and a hepato

238 A 33-year-old woman with chronic myelogenous leukemia developed widespread alopec

239 26;q22) translocation found in patients with chronic myelogenous leukemia during blast phase, myelody

240 e, which was introduced for the treatment of chronic myelogenous leukemia, effectively controlled ano

241 ic stem cell transplantation was the goal in chronic myelogenous leukemia for over 20 years and remai

242 ib, a BCR-ABL inhibitor for the treatment of chronic myelogenous leukemia, has created a great impetu

243 the Philadelphia chromosome as a hallmark of chronic myelogenous leukemia in 1960 by Peter Nowell pro

244 eneic HCT for acute myelogenous leukemia and chronic myelogenous leukemia in 2719 patients who underw

245 PURPOSE Patients with chronic myelogenous leukemia in accelerated phase (CML-A

246 ressed and in CD34+ cells from patients with chronic myelogenous leukemia in blast crisis.

247 olated cases of AML M2, M5a, M3 relapse, and chronic myelogenous leukemia in blast phase.

248 advanced myelodysplastic syndromes (MDS), or chronic myelogenous leukemia in blastic phase (CML-BP) w

249 dysregulated tyrosine kinase BCR-ABL causes chronic myelogenous leukemia in humans and forms a large

250 an Abl family kinase inhibitor used to treat chronic myelogenous leukemia in humans.

251 an Abl-family kinase inhibitor used to treat chronic myelogenous leukemia in humans.

252 (acute myeloid leukemia in two patients, and chronic myelogenous leukemia in one patient).

253 differentiation of quiescent drug-resistant chronic myelogenous leukemia-initiating cells (CML LICs)

254 In human patients with chronic myelogenous leukemia, IRF8 transcript levels are

255 Successful treatment of chronic myelogenous leukemia is based on inhibitors bind

256 Chronic myelogenous leukemia is therefore classified as

257 Chronic myelogenous leukemia is typified by constitutive

258 clinical development for imatinib-resistant chronic myelogenous leukemia, is a dual SRC/ABL kinase i

259 evec, a well-known therapeutic agent against chronic myelogenous leukemia, is an effective inhibitor

260 Bcr-Abl, activated in chronic myelogenous leukemias, is a potent cell death in

261 hly effective treatment for BCR-ABL-positive chronic myelogenous leukemia, it has proven far less eff

262 e kinetics of DNA damage by 1 and 3 in human chronic myelogenous leukemia (K562) cells.

263 uman cell lines isolated from a patient with chronic myelogenous leukemia (KBM7 and HAP1), as well as

264 elop from a very early age a more aggressive chronic myelogenous leukemia-like disease than mice defi

265 tors (F/P(+) HSCs/Ps) into mice results in a chronic myelogenous leukemia-like disease, which does no

266 loss of IRF-8 in myeloid cells results in a chronic myelogenous leukemia-like syndrome, suggesting t

267 ped a GVL model against murine chronic-phase chronic myelogenous leukemia (mCP-CML) induced with retr

268 atients with myeloid malignancies (acute and chronic myelogenous leukemia, myelodysplastic syndrome,

269 rythroleukemia virus or those expressing the chronic myelogenous leukemia oncoprotein BCR-ABL in the

270 rtion of patients taking imatinib for either chronic myelogenous leukemia or gastrointestinal stromal

271 temia developed in some patients with either chronic myelogenous leukemia or gastrointestinal stromal

272 loid leukemia, acute lymphoblastic leukemia, chronic myelogenous leukemia, or myelodysplastic syndrom

273 potential, IM-resistant cells were found in chronic myelogenous leukemia patients with continuous BC

274 growth of primary leukemic progenitors from chronic myelogenous leukemia patients.

275 nancy, specifically in a subset of acute and chronic myelogenous leukemia patients.

276 ion oncogene give rise to drug resistance in chronic myelogenous leukemia patients.

277 c factor in Philadelphia chromosome-positive chronic myelogenous leukemia (Ph-positive CML).

278 ibited the colony formation of HLA-identical chronic myelogenous leukemia progenitor cells (73% inhib

279 geting the BCR-Abl translocation involved in chronic myelogenous leukemia, reportedly produces alopec

280 (ALL), acute myelogenous leukemia (AML), and chronic myelogenous leukemia (RR = 26.9, 66.5, and 93.1,

281 mias, including therapy-refractory B-ALL and chronic myelogenous leukemia samples, and inhibits growt

282 the formation of the BCR/ABL fusion gene in chronic myelogenous leukemia, seems to be essential for

283 , melanoma, colorectal and prostate cancers, chronic myelogenous leukemia, small cell lung cancer, an

284 In chronic myelogenous leukemia, the constitutive activatio

285 tablished role of STI571 in the treatment of chronic myelogenous leukemia, the precise mechanisms by

286 ive breast cancer, head and neck cancer, and chronic myelogenous leukemia; the FDA's approval of the

287 the Bcr-Abl tyrosine kinase associated with chronic myelogenous leukemia to small molecule inhibitor

288 ow doses (5-20 mg/m(2)/d), but patients with chronic myelogenous leukemia treated with high doses (10

289 y PH have been reported in patients who have chronic myelogenous leukemia treated with the tyrosine k

290 Chronic myelogenous leukemia was once the most common in

291 ose constitutive activity is responsible for chronic myelogenous leukemia, was covalently linked to t

292 L2Rgamma(-/-) mouse model of engrafted human chronic myelogenous leukemia, we now demonstrate the com

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

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

295 introduced by the Philadelphia chromosome in chronic myelogenous leukemia were unraveled, and these h

296 inhibitor Imatinib is currently standard for chronic myelogenous leukemia, which is also caused by Bc

297 is markedly activated in the blast crisis of chronic myelogenous leukemia, which represents the most

298 ons in the BCR-ABL oncogene in patients with chronic myelogenous leukemia who evolve resistance to AB

299 2 responders, 7 nonresponders) with relapsed chronic myelogenous leukemia who received CD4(+) DLI in

300 use models of chronic phase and blast crisis chronic myelogenous leukemia, without causing GVHD.