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

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

24 The Philadelphia chromosome, detected in virtually all cases

25 Disappearance of the Philadelphia chromosome during treatment for chronic mye

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

27 The Philadelphia chromosome found in virtually all cases of

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

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

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

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

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

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

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

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

36 The Philadelphia chromosome is present in approximately 20%

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

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

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

40 Philadelphia chromosome-like acute lymphoblastic leukemi

41 Philadelphia chromosome-like acute lymphoblastic leukemi

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

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

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

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

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

47 The pathophysiology of Philadelphia-chromosome negative myeloproliferative diso

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

65 Philadelphia chromosome-negative myeloproliferative neop

66 Philadelphia chromosome-negative myeloproliferative neop

67 Myelofibrosis is a Philadelphia chromosome-negative myeloproliferative neop

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 The Philadelphia chromosome (Ph) translocation generates a c

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

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

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

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

88 Philadelphia chromosome (Ph)-like acute lymphoblastic le

89 Philadelphia chromosome (Ph)-like acute lymphoblastic le

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

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

92 (18 to 59 years of age) with CD20-positive, Philadelphia chromosome (Ph)-negative ALL to receive che

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 Philadelphia chromosome (Ph)-positive leukaemia cells ex

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

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

114 Philadelphia chromosome (Ph)-positive patients were offe

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

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

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

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

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

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

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

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

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

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

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

126 25 metaphases for monitoring the presence of Philadelphia chromosome positive (Ph+) cells in chronic

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

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

129 The Philadelphia chromosome positive arm of the UKALLXII/ECO

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

161 Philadelphia chromosome-positive (Ph+) acute lymphoblast

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 13 cases with t(9;22)(q34;q11) Philadelphia chromosome-positive [Ph+]) and IGH rearrang

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

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

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

180 Philadelphia chromosome-positive acute lymphoblastic leu

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

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

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

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

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

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

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

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

189 Philadelphia chromosome-positive acute lymphoblastic leu

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

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

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

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

194 1 to 2011, 122 patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

227 3 studies including 2962 patients, excluding Philadelphia chromosome-positive patients, showed a surv

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

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

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

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

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

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

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

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

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

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

238 The Philadelphia chromosome translocation generates a chimer

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

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

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

242 The presence of the Philadelphia chromosome was significantly associated wit

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