ライフサイエンスコーパス: Philadelphia chromosome

1 f this chromosome, which became known as the Philadelphia chromosome.

2 BCR-ABL tyrosine kinase, the product of the Philadelphia chromosome.

3 B-cell ALL and B-lineage ALL patients with a Philadelphia chromosome.

4 vated tyrosine kinase, is the product of the Philadelphia chromosome.

5 ads to a shortened chromosome 22, called the Philadelphia chromosome.

6 rcent of cells in metaphase positive for the Philadelphia chromosome); 7 of these patients had comple

7 The Philadelphia chromosome, a chromosomal abnormality that

8 Notably, all six cases with the Philadelphia chromosome, a known high-risk feature, had

9 the bone marrow that is precipitated by the Philadelphia chromosome, a t(9;22) balanced translocatio

10 ated with adverse genetic abnormalities--the Philadelphia chromosome and MLL gene rearrangements--but

11 etic stem cell disorder characterized by the Philadelphia chromosome and resultant production of the

12 c change associated with a human cancer (the Philadelphia chromosome) and the clonal nature of these

13 method, phenotype/genotype (B cell, T cell, Philadelphia chromosome), and EFS and OS.

14 count, leukemia with a T-cell phenotype, the Philadelphia chromosome, and 11q23 rearrangement.

15 The CR rate (assessed in Philadelphia chromosome- and BCR-ABL-negative ALL withou

16 ncluding trisomy 8, -Y, and an extra copy of Philadelphia chromosome; and group 2 with a relatively p

17 The discovery of the Philadelphia chromosome as a hallmark of chronic myeloge

18 es from a chronic phase characterized by the Philadelphia chromosome as the sole genetic abnormality

19 ated tyrosine kinase oncogene encoded by the Philadelphia chromosome associated with human chronic my

20 Philadelphia chromosome-associated leukemias are among t

21 coprotein is the primary causative factor in Philadelphia chromosome-associated leukemias.

22 emotherapy-blinatumomab combination in adult Philadelphia chromosome/BCR::ABL1 rearrangement-negative

23 sruption of Abl kinase signaling through the Philadelphia chromosome (causing the Bcr-Abl mutation) i

24 chromosomal abnormalities in addition to the Philadelphia chromosome (clonal evolution) is considered

25 The Philadelphia chromosome, detected in virtually all cases

26 Disappearance of the Philadelphia chromosome during treatment for chronic mye

27 well and David Hungerford's discovery of the Philadelphia chromosome facilitated many critical studie

28 The Philadelphia chromosome found in virtually all cases of

29 decades, the translocation resulting in the Philadelphia chromosome has been identified, its role in

30 count higher than 30 x 10(9)/L, presence of Philadelphia chromosome, high systemic risk classificati

31 The sighting of the Philadelphia chromosome in 1960, later shown to harbor t

32 linked to distinct malignancies, such as the Philadelphia chromosome in acute lymphoblastic leukemia,

33 The identification of the Philadelphia chromosome in cells from individuals with c

34 ecular and genetic changes introduced by the Philadelphia chromosome in chronic myelogenous leukemia

35 The Philadelphia chromosome in chronic myeloid leukaemia (CM

36 The presence of the Philadelphia chromosome in patients with acute lymphobla

37 ransformed by the BCR/ABL oncoprotein of the Philadelphia chromosome is characterized by growth facto

38 The Philadelphia chromosome is present in approximately 20%

39 that the Bcr-Abl oncoprotein encoded by the Philadelphia chromosome is responsible for causing chron

40 Philadelphia chromosome-like (Ph-like) acute lymphoblast

41 Philadelphia chromosome-like (Ph-like) acute lymphoblast

42 of the erythropoietin receptor gene EPOR in Philadelphia chromosome-like (Ph-like) ALL.

43 Philadelphia chromosome-like acute lymphoblastic leukemi

44 Philadelphia chromosome-like acute lymphoblastic leukemi

45 Philadelphia chromosome-like acute lymphoblastic leukemi

46 ry germline variant in GATA3 associated with Philadelphia chromosome-like ALL (Ph-like ALL).

47 as Philadelphia chromosome-positive and some Philadelphia chromosome-like ALL cases to ABL-class tyro

48 Children and adults with Philadelphia chromosome-like B cell acute lymphoblastic

49 Philadelphia chromosome-like B-cell acute lymphoblastic

50 are tyrosine kinase inhibitors targeting the Philadelphia Chromosome mutation product, which have bee

51 f activated tyrosine kinase signaling in the Philadelphia chromosome negative myeloproliferative diso

52 patients with B-cell precursor ALL who were Philadelphia chromosome negative, those with an IGH@ tra

53 nce of the JAK2V617F mutation in the classic Philadelphia-chromosome negative myeloproliferative diso

54 However, JAK2V617F in the Philadelphia-chromosome negative myeloproliferative diso

55 The pathophysiology of Philadelphia-chromosome negative myeloproliferative diso

56 aged 60 years or older with newly diagnosed, Philadelphia-chromosome negative, B-cell acute lymphocyt

57 Clonal chromosomal abnormalities in Philadelphia chromosome-negative (CCA/Ph(-)) metaphases

58 bitor belonging to the hydroxamate class, in Philadelphia chromosome-negative (Ph(-)) acute lymphobla

59 l transplantation (allo-HSCT) in adults with Philadelphia chromosome-negative (Ph-) acute lymphoblast

60 years and older with newly diagnosed CD22(+) Philadelphia chromosome-negative (Ph-) B-cell precursor

61 of in vivo priming on the ability to select Philadelphia chromosome-negative (Ph-negative) CD34(+)HL

62 ger) antibody construct for the treatment of Philadelphia chromosome-negative acute B-lymphoblastic l

63 ensive chemotherapy regimen for treatment of Philadelphia chromosome-negative acute lymphoblastic leu

64 rm prognosis of adult patients with relapsed Philadelphia chromosome-negative acute lymphoblastic lym

65 udy was performed in 423 younger adults with Philadelphia chromosome-negative ALL in first remission

66 d a markedly improved outcome in adults with Philadelphia chromosome-negative ALL, we aimed to reasse

67 zed methods and terminology in patients with Philadelphia chromosome-negative ALL.

68 me of initial remission in 199 patients with Philadelphia chromosome-negative and MLL(-) ALL.

69 rs) with Philadelphia chromosome-positive or Philadelphia chromosome-negative B-ALL who received Blin

70 abnormalities have also been reported in the Philadelphia chromosome-negative cells present in comple

71 Of the subgroup of 6 Philadelphia chromosome-negative MRD responders with no

72 ruritus is a common symptom in patients with Philadelphia chromosome-negative myeloproliferative diso

73 Philadelphia chromosome-negative myeloproliferative neop

74 Polycythemia vera (PV) is a Philadelphia chromosome-negative myeloproliferative neop

75 novel predisposition alleles associated with Philadelphia chromosome-negative myeloproliferative neop

76 mon causes of morbidity and mortality in the Philadelphia chromosome-negative myeloproliferative neop

77 a rare phenomenon observed in patients with Philadelphia chromosome-negative myeloproliferative neop

78 The most frequent contributing factor in Philadelphia chromosome-negative myeloproliferative neop

79 primary pathogenic mutation in patients with Philadelphia chromosome-negative myeloproliferative neop

80 Philadelphia chromosome-negative myeloproliferative neop

81 Philadelphia chromosome-negative myeloproliferative neop

82 Myelofibrosis is a Philadelphia chromosome-negative myeloproliferative neop

83 A donor versus no-donor analysis showed that Philadelphia chromosome-negative patients with a donor h

84 ase 2 study, we enrolled adult patients with Philadelphia-chromosome-negative, primary refractory or

85 The legacy of the Philadelphia chromosome now serves as a paradigm for how

86 n as part of the fusion gene BCR-ABL1 in the Philadelphia chromosome of leukemia cancer cells.

87 ses with unfavorable genetic features (e.g., Philadelphia-chromosome or MLL gene rearrangements); thr

88 five ALL samples with the t(9;22)(q34;q11) (Philadelphia chromosome) or 11q23 abnormalities, karyoty

89 on the abnormal chromosome 9 and one on the Philadelphia chromosome (Ph chromosome).

90 The response of Philadelphia chromosome (Ph(+)) acute lymphoblastic leuk

91 le for the initiation and maintenance of the Philadelphia chromosome (Ph(1))-positive chronic myeloge

92 Purpose Philadelphia chromosome (Ph) -like acute lymphoblastic l

93 ed high-dose VSLI monotherapy in adults with Philadelphia chromosome (Ph) -negative ALL that was mult

94 The Philadelphia chromosome (Ph) encoding the oncogenic BCR-

95 pically characterized by the presence of the Philadelphia chromosome (Ph) in which 5' portions of the

96 ng single-cell RNA sequencing (scRNA-seq) of Philadelphia chromosome (Ph) negative macrophages we rev

97 s in hematologic remission had a decrease in Philadelphia chromosome (Ph) percentage (3 concurrently

98 Nine patients were Philadelphia chromosome (Ph) positive (4 cases: 44 chrom

99 The Philadelphia chromosome (Ph) translocation generates a c

100 The product of the Philadelphia chromosome (Ph) translocation, the BCR/ABL

101 ), in models of acute leukemia harboring the Philadelphia chromosome (Ph) translocation.

102 L genes, resulting from the formation of the Philadelphia chromosome (Ph), is the hallmark of Ph-posi

103 otype (34+DR-) may result in the recovery of Philadelphia chromosome (Ph)- and BCR/ABL-negative long-

104 Philadelphia chromosome (Ph)-like acute lymphoblastic le

105 Philadelphia chromosome (Ph)-like acute lymphoblastic le

106 nd JAK2 fusion genes have been identified in Philadelphia chromosome (Ph)-like acute lymphoblastic le

107 Philadelphia chromosome (Ph)-like B-cell acute lymphobla

108 (18 to 59 years of age) with CD20-positive, Philadelphia chromosome (Ph)-negative ALL to receive che

109 ars or older with confirmed, newly diagnosed Philadelphia chromosome (Ph)-negative B-cell acute lymph

110 netic subgroups have been described in adult Philadelphia chromosome (Ph)-negative B-cell precursor (

111 mbination with chemotherapy in patients with Philadelphia chromosome (Ph)-negative CD20-positive B-ce

112 a (CML) develop chromosomal abnormalities in Philadelphia chromosome (Ph)-negative cells.

113 nt of chromosomal abnormalities (CAs) in the Philadelphia chromosome (Ph)-negative metaphases during

114 of p73, p15, and p57KIP2 occurred in 22% of Philadelphia chromosome (Ph)-negative patients.

115 ghty-two adolescents and adults with de novo Philadelphia chromosome (Ph)-negative precursor B-lineag

116 umomab has demonstrated clinical activity in Philadelphia chromosome (Ph)-negative relapsed or refrac

117 were age 60 years and older with untreated, Philadelphia chromosome (Ph)-negative, CD22-positive, B-

118 (n = 58) with (i) imatinib-pretreated CML or Philadelphia chromosome (Ph)-positive acute lymhoblastic

119 Outcomes in patients with Philadelphia chromosome (Ph)-positive acute lymphoblasti

120 bl-mutated chronic myeloid leukemia (CML) or Philadelphia chromosome (Ph)-positive acute lymphocytic

121 , has modest activity in refractory/relapsed Philadelphia chromosome (Ph)-positive acute lymphocytic

122 onatinib in 60 patients with newly diagnosed Philadelphia chromosome (Ph)-positive ALL.

123 Unexpectedly, all cells in the primary Philadelphia chromosome (Ph)-positive and Ph-negative AL

124 CR/ABL-transformed hematopoietic cell lines, Philadelphia chromosome (Ph)-positive cell lines, and pr

125 ha (IFN-alpha) therapy improves prognosis in Philadelphia chromosome (Ph)-positive chronic myelogenou

126 low-dose cytarabine (ara-C) in patients with Philadelphia chromosome (Ph)-positive chronic myelogenou

127 opoietic progenitors from some patients with Philadelphia chromosome (Ph)-positive chronic myeloid le

128 d in the randomized study in newly diagnosed Philadelphia chromosome (Ph)-positive chronic-phase chro

129 ic and cytogenetic response in patients with Philadelphia chromosome (Ph)-positive CML may improve pr

130 Patients with Philadelphia chromosome (Ph)-positive CML receiving tyro

131 ity and is implicated in the pathogenesis of Philadelphia chromosome (Ph)-positive human leukemias, s

132 Philadelphia chromosome (Ph)-positive leukaemia cells ex

133 ne kinase induces constitutive DNA damage in Philadelphia chromosome (Ph)-positive leukemia cells.

134 with relapsed or refractory, CD22-positive, Philadelphia chromosome (Ph)-positive or Ph-negative B-c

135 Philadelphia chromosome (Ph)-positive patients were offe

136 erately intensive chemotherapy protocols for Philadelphia chromosome (Ph)/BCR::ABL-negative ALL in ol

137 t in chronic myelogenous leukemia (CML), the Philadelphia chromosome (Ph+) clone has a growth advanta

138 were defined as KMT2A (MLL) rearrangements, Philadelphia chromosome (Ph+), Ph-like, hypodiploidy, or

139 ical use, and remains first-line therapy for Philadelphia chromosome (Ph+)-positive chronic myelogeno

140 gements associated with the formation of the Philadelphia chromosome (Ph-associated rearrangements) a

141 also detected in 3 (19%) of 16 patients with Philadelphia-chromosome (Ph)-negative chronic myelogenou

142 ents (96%) had a major cytogenetic response (Philadelphia chromosome [Ph] < 35%), and 103 (90%) had a

143 gulated tyrosine kinase that is expressed in Philadelphia chromosome (Ph1) positive human leukemias.

144 In Philadelphia chromosome (Ph1)-positive human leukemia, t

145 active tyrosine kinase that is expressed in Philadelphia chromosome (Ph1)-positive human leukemias.

146 entific observations, the description of the Philadelphia chromosome posed many more questions than w

147 romising agent for the treatment of advanced Philadelphia chromosome positive (Ph(+)) acute lymphobla

148 The characterization and targeting of Philadelphia chromosome positive (Ph(+)) acute lymphobla

149 al blood and 55 bone marrow samples with 127 Philadelphia chromosome positive (Ph+) and 6 Ph-/BCR-ABL

150 25 metaphases for monitoring the presence of Philadelphia chromosome positive (Ph+) cells in chronic

151 ) kinase inhibitors used in the treatment of Philadelphia chromosome positive (Ph+) leukemias.

152 tients with acute lymphoblastic leukemia are Philadelphia chromosome positive (Ph-positive acute lymp

153 focusing on recent advances in treatment of Philadelphia chromosome positive acute lymphoblastic leu

154 The Philadelphia chromosome positive arm of the UKALLXII/ECO

155 Abl oncoprotein observed in several types of Philadelphia chromosome positive leukemia patients.

156 Kinase inhibitor therapy options for Philadelphia chromosome positive leukemias have rapidly

157 ple options exist today for the treatment of Philadelphia chromosome positive leukemias.

158 the fusion partner for Abl (p210 Bcr-Abl) in Philadelphia chromosome positive leukemias.

159 arry the oncogenic BCR-ABL1 tyrosine kinase (Philadelphia chromosome positive), which mimics constitu

160 tyrosine kinase activity of abl oncogene in Philadelphia chromosome positive-leukemic cells leads to

161 ctly causes chronic myelogenous leukemia and Philadelphia-chromosome positive acute lymphoblastic leu

162 commonly observed in patients with advanced Philadelphia chromosome- positive (Ph(+)) leukemias.

163 etic stem cell transplantation (alloHSCT) in Philadelphia chromosome-positive (Ph(+)) acute lymphobla

164 tyrosine kinase inhibitors are effective in Philadelphia chromosome-positive (Ph(+)) acute lymphobla

165 udy, we identified a unique subpopulation of Philadelphia chromosome-positive (Ph(+)) acute lymphobla

166 development testing in patients with CML and Philadelphia chromosome-positive (Ph(+)) acute lymphobla

167 hieving complete molecular response (CMR) in Philadelphia chromosome-positive (Ph(+)) acute lymphobla

168 is chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph(+)) acute lymphobla

169 b has improved the outcome for patients with Philadelphia chromosome-positive (Ph(+)) acute lymphobla

170 We adapted this high-throughput Philadelphia chromosome-positive (Ph(+)) ALL animal mode

171 Philadelphia chromosome-positive (Ph(+)) B-acute lymphob

172 utic options are available for patients with Philadelphia chromosome-positive (Ph(+)) B-precursor acu

173 Whereas all patients were approximately 100% Philadelphia chromosome-positive (Ph(+)) before transpla

174 ients, despite major responses, still harbor Philadelphia chromosome-positive (Ph(+)) cells.

175 ht overcome drug resistance in patients with Philadelphia chromosome-positive (Ph(+)) chronic myeloge

176 ated with the development and progression of Philadelphia chromosome-positive (Ph(+)) chronic myeloge

177 Fifty patients with Philadelphia chromosome-positive (Ph(+)) chronic myeloge

178 ered orally twice daily to 280 patients with Philadelphia chromosome-positive (Ph(+)) chronic myeloid

179 atinib is highly effective at treating human Philadelphia chromosome-positive (Ph(+)) chronic myeloid

180 inib mesylate is the preferred treatment for Philadelphia chromosome-positive (Ph(+)) chronic myeloid

181 o tyrosine kinase inhibitor (TKI) therapy in Philadelphia chromosome-positive (Ph(+)) leukemia is eff

182 at suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph(+)) leukemia, inclu

183 se inhibitor (TKI) with clinical activity in Philadelphia chromosome-positive (Ph(+)) leukemia.

184 drive lymphoid and myeloid proliferation in Philadelphia chromosome-positive (Ph(+)) leukemias.

185 disorders can be broadly characterized into Philadelphia chromosome-positive (Ph(+)) or negative (Ph

186 The Philadelphia chromosome-positive (Ph(+)) subtype of ALL

187 Dasatinib is an effective treatment for Philadelphia chromosome-positive (Ph+) acute leukemia, b

188 Philadelphia chromosome-positive (Ph+) acute lymphoblast

189 Historically, Philadelphia chromosome-positive (Ph+) acute lymphoblast

190 B) in 268 adults (median age, 47 years) with Philadelphia chromosome-positive (Ph+) acute lymphoblast

191 prevention of resistance in a mouse model of Philadelphia chromosome-positive (Ph+) acute lymphoblast

192 imatinib, for patients with newly diagnosed Philadelphia chromosome-positive (Ph+) acute lymphoblast

193 Four patients with Philadelphia chromosome-positive (Ph+) ALL achieved hema

194 itoring measurable residual disease (MRD) in Philadelphia chromosome-positive (Ph+) ALL.

195 In cellular models of Philadelphia Chromosome-positive (Ph+) B-ALL, mTOR kinas

196 A2 induced alpha5Beta1-dependent adhesion of Philadelphia chromosome-positive (Ph+) CD34+/HLA-DR+ cel

197 en a remarkable success for the treatment of Philadelphia chromosome-positive (Ph+) chronic myelogeno

198 ls, derived from a patient with blast crisis Philadelphia chromosome-positive (Ph+) chronic myelogeno

199 he outcomes for patients with every stage of Philadelphia chromosome-positive (Ph+) chronic myeloid l

200 nd dasatinib are the preferred treatment for Philadelphia chromosome-positive (Ph+) leukemias, and th

201 mab are effective therapies in patients with Philadelphia chromosome-positive (Ph-positive) acute lym

202 The outcome of children with Philadelphia chromosome-positive (Ph-positive) acute lym

203 BCR::ABL1 tyrosine kinase inhibitors (TKIs), Philadelphia chromosome-positive (Ph-positive) acute lym

204 el selective BCR::ABL1 TKI, in patients with Philadelphia chromosome-positive (Ph-positive) chronic m

205 ne kinase inhibitor imatinib is effective in Philadelphia chromosome-positive (Ph-positive) leukemias

206 hronic myeloid leukemia (CML-BC) and against Philadelphia chromosome-positive (Ph1) acute lymphoblast

207 ted donors was investigated in patients with Philadelphia chromosome-positive (Ph1+) acute lymphoblas

208 is chronic myelogenous leukemia (CML-BC) and Philadelphia chromosome-positive (Ph1-positive) acute ly

209 ard define optimal response, whereas no CyR (Philadelphia chromosome-positive [Ph+] >95%) at 3 months

210 13 cases with t(9;22)(q34;q11) Philadelphia chromosome-positive [Ph+]) and IGH rearrang

211 h tyrosine kinase inhibitors (TKIs), against Philadelphia chromosome-positive acute leukemia in murin

212 s, we studied blast cells from patients with Philadelphia chromosome-positive acute leukemic transfor

213 ly known curative modality for patients with Philadelphia chromosome-positive acute lymphoblastic leu

214 reatment of chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphoblastic leu

215 and cytogenetic remissions in patients with Philadelphia chromosome-positive acute lymphoblastic leu

216 val for high-risk groups, such as those with Philadelphia chromosome-positive acute lymphoblastic leu

217 inib mesylate into the treatment regimen for Philadelphia chromosome-positive acute lymphoblastic leu

218 Philadelphia chromosome-positive acute lymphoblastic leu

219 have previously developed a murine model of Philadelphia chromosome-positive acute lymphoblastic leu

220 Thirty-six patients with Philadelphia chromosome-positive acute lymphoblastic leu

221 Chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphoblastic leu

222 such as acute promyelocytic leukemia (APL), Philadelphia chromosome-positive acute lymphoblastic leu

223 rosine kinase inhibitors in the treatment of Philadelphia chromosome-positive acute lymphoblastic leu

224 In Philadelphia chromosome-positive acute lymphoblastic leu

225 remissions in patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leu

226 hemotherapy with ponatinib for patients with Philadelphia chromosome-positive acute lymphoblastic leu

227 Philadelphia chromosome-positive acute lymphoblastic leu

228 e inhibitor is effective in the treatment of Philadelphia chromosome-positive acute lymphoblastic leu

229 al, adult patients with previously untreated Philadelphia chromosome-positive acute lymphoblastic leu

230 In chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leu

231 ients with chronic myeloid leukemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leu

232 1 to 2011, 122 patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leu

233 tinib-resistant chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leu

234 ents with chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leu

235 tients with chronic myelogenous leukemia and Philadelphia chromosome-positive acute lymphoblastic leu

236 In Philadelphia chromosome-positive acute lymphocytic leuka

237 last phase and in the accelerated phase, and Philadelphia chromosome-positive acute myeloid leukaemia

238 celerated phase, and two with advanced phase Philadelphia chromosome-positive acute myeloid leukaemia

239 ukaemia-accelerated phase, or advanced phase Philadelphia chromosome-positive acute myeloid leukaemia

240 mab with targeted therapies, particularly in Philadelphia chromosome-positive ALL (Ph+ ALL).

241 h an expression signature resembling that of Philadelphia chromosome-positive ALL and poor prognosis

242 ic leukemia (ALL) cell line generated from a Philadelphia chromosome-positive ALL patient.

243 relapse, excluding those with Down syndrome, Philadelphia chromosome-positive ALL, prior hematopoieti

244 es is uncommon in ALL, with the exception of Philadelphia chromosome-positive ALL, where the t(9,22)(

245 in CR1 and seven (27%) in CR2+; 16 (62%) had Philadelphia chromosome-positive ALL.

246 table population of quiescent (G0) leukemic (Philadelphia chromosome-positive and BCR-ABL-positive [B

247 ble to available targeted therapies, such as Philadelphia chromosome-positive and some Philadelphia c

248 rs of age, within 6 months of diagnosis, and Philadelphia chromosome-positive by cytogenetic assessme

249 particularly challenging example is found in Philadelphia chromosome-positive chronic myelogenous leu

250 mesylate has been useful in the treatment of Philadelphia chromosome-positive chronic myelogenous leu

251 on (CE) is a known poor prognostic factor in Philadelphia chromosome-positive chronic myelogenous leu

252 le patients were aged 18 years or older with Philadelphia chromosome-positive chronic myeloid leukaem

253 an imatinib in patients with newly diagnosed Philadelphia chromosome-positive chronic myeloid leukaem

254 ay 1985 and December 1994, 196 patients with Philadelphia chromosome-positive chronic myeloid leukemi

255 they had been diagnosed with chronic phase, Philadelphia chromosome-positive CML within the previous

256 of more than 30 x 10(9)/L was found in 26%, Philadelphia chromosome-positive disease in 16% (20% of

257 ALL.Significance: MYB blockade can suppress Philadelphia chromosome-positive leukemia in mice, sugge

258 TEN functions as a tumor suppressor in human Philadelphia chromosome-positive leukemia that includes

259 ractory solid tumors or imatinib-refractory, Philadelphia chromosome-positive leukemia was performed.

260 ylate (Gleevec) is effective therapy against Philadelphia chromosome-positive leukemia, but resistanc

261 st a potential strategy for the treatment of Philadelphia chromosome-positive leukemia.

262 e useful for reduction of Bcr-Abl mutants in Philadelphia chromosome-positive leukemia.

263 cquired imatinib resistance in patients with Philadelphia chromosome-positive leukemia.

264 plays a critical role in the pathogenesis of Philadelphia chromosome-positive leukemia.

265 onsidered responsible for the development of Philadelphia chromosome-positive leukemia.

266 s been effectively used for the treatment of Philadelphia chromosome-positive leukemias and gastroint

267 I trial that included 64 adult patients with Philadelphia chromosome-positive leukemias.

268 I571 has been successful in the treatment of Philadelphia chromosome-positive leukemias.

269 rrangement, yet demonstrated from 12% to 20% Philadelphia chromosome-positive metaphase cells in the

270 lost CHR, and six experienced an increase in Philadelphia chromosome-positive metaphases.

271 The Bcr-Abl oncogene, found in Philadelphia chromosome-positive myelogenous leukemia (C

272 Advanced phase Philadelphia chromosome-positive myeloid disease-consist

273 kinase inhibitor ponatinib in advanced phase Philadelphia chromosome-positive myeloid diseases.

274 articipants were adults (aged 16 years) with Philadelphia chromosome-positive or BCR-ABL1-positive bl

275 ticipants were adults (aged >=16 years) with Philadelphia chromosome-positive or BCR-ABL1-positive bl

276 ed for consecutive CYP (age 1-24 years) with Philadelphia chromosome-positive or Philadelphia chromos

277 3 studies including 2962 patients, excluding Philadelphia chromosome-positive patients, showed a surv

278 From a prospective cohort of 91 Philadelphia chromosome-positive, previously untreated,

279 a promising agent for treatment of advanced Philadelphia-chromosome-positive (Ph+) acute lymphoblast

280 ) therapy allows a much higher proportion of Philadelphia-chromosome-positive ALL patients to attain

281 have improved the outcomes for patients with Philadelphia-chromosome-positive ALL.

282 ft-versus-host disease, in 109 patients with Philadelphia-chromosome-positive malignancies.

283 variate analysis of EFS after adjustment for Philadelphia chromosome status, age, white blood cell (W

284 s including age, white blood cell count, and Philadelphia chromosome status.

285 ukemias driven by the BCR-ABL translocation (Philadelphia chromosome), suggesting that BCL6 is a nove

286 g myeloid cells driven by the product of the Philadelphia chromosome, the BCR-ABL1 tyrosine kinase.

287 The Philadelphia chromosome translocation (t(9;22)) results

288 of its fusion to Abl as a consequence of the Philadelphia chromosome translocation found in chronic m

289 The Philadelphia chromosome translocation generates a chimer

290 enetic analysis revealed the presence of the Philadelphia chromosome translocation in 17 out of 20 me

291 The pathophysiologic role of the Philadelphia chromosome translocation in chronic myeloge

292 The products of the Philadelphia chromosome translocation, P210 and P190(BCR

293 The presence of the Philadelphia chromosome was significantly associated wit

294 yeloid leukemia (CML) is associated with the Philadelphia chromosome, which arises by a reciprocal tr

295 eoplasm characterized by the presence of the Philadelphia chromosome, which is defined by the BCR::AB