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 s a constitutively active kinase that causes chronic myelogenous leukemia.

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

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

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

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

17 fusion protein Bcr-Abl, the causal agent in 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 the skin 6 years after HCT for treatment of chronic myelogenous leukemia.

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

26 g 133 patients undergoing allogeneic HCT for 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 This agent has shown striking activity in chronic myelogenous leukemia.

30 e oncogenic fusion protein characteristic of chronic myelogenous leukemia.

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

32 eptor tyrosine kinase inhibitor approved for chronic myelogenous leukemia.

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

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

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

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

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

38 BCR-ABL is critical to the pathogenesis of chronic myelogenous leukemia and a subset of acute leuke

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 Chronic myelogenous leukemia (CML) evolves from a chroni

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

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

119 Chronic myelogenous leukemia (CML) in children is relati

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

121 Chronic myelogenous leukemia (CML) invariably progresses

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

123 Chronic myelogenous leukemia (CML) is characterized by t

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

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

126 Although chronic myelogenous leukemia (CML) is effectively contro

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

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

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

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

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

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

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

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

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

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

137 Chronic myelogenous leukemia (CML) patients treated with

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

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

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

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

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

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

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

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

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

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

148 Chronic myelogenous leukemia (CML) results from a chromo

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

150 Chronic myelogenous leukemia (CML) results from expressi

151 Chronic myelogenous leukemia (CML) results from malignan

152 Chronic myelogenous leukemia (CML) results from the tran

153 Chronic myelogenous leukemia (CML) results from transfor

154 Chronic myelogenous leukemia (CML) results from transfor

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 gastrointestinal stromal tumors (GISTs) and 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 egulated in patients with advanced stages of chronic myelogenous leukemia (CML).

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

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

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

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

223 or, is a successful front-line treatment for 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.