ライフサイエンスコーパス: blast crisis

1 me of transformation of CML to ALL (lymphoid blast crisis).

2 B-cell lymphoblastic disease, reminiscent of blast crisis.

3 ed a chronic MPD, but only one progressed to blast crisis.

4 ed as a single agent in patients with CML in blast crisis.

5 the disease progresses from chronic phase to blast crisis.

6 whom 229 had a confirmed diagnosis of CML in blast crisis.

7 Only one of 26 patients developed blast crisis.

8 ls affected with chronic myeloid leukemia in blast crisis.

9 id blast crisis and 20 had ALL or a lymphoid blast crisis.

10 f three with chronic myelogenous leukemia in blast crisis.

11 mouse model of chronic myelogenous leukemia blast crisis.

12 ents in stable phase, accelerated phase, and blast crisis.

13 s, a CML cell line derived from a patient in blast crisis.

14 opment of acute lymphoma/leukemia resembling blast crisis.

15 mission lost their response or progressed to blast crisis.

16 (25%), 19p (43%), and 20q (33%) in lymphoid blast crisis.

17 hase in a patient who subsequently developed blast crisis.

18 cific gene regulation in the shift of CML to blast crisis.

19 ty plays a role in the progression of CML to blast crisis.

20 loid leukemia, and chronic myeloid leukemia, blast crisis.

21 g chronic myelogenous leukemia (CML) myeloid blast crisis.

22 tually evolves into an accelerated stage and blast crisis.

23 atients with chronic myelogenous leukemia in blast crisis.

24 L) and lymphoid chronic myelogenous leukemia blast crisis.

25 reviously presented with lymphoid or myeloid blast crisis.

26 st of CD34+ progenitors from patients in CML blast crisis.

27 lent chronic phase to the aggressively fatal blast crisis.

28 with T315I mutant Bcr/Abl-expressing CML in blast crisis.

29 acute lymphoblastic leukemia (B-ALL) and CML blast crisis.

30 treatment and for CML transition to lymphoid blast crisis.

31 chronic phase CML (1.9 x 10(-4)) and CML in blast crisis (1.7 x 10(-4)).

32 disease transformed to accelerated phase or blast crisis (21 myeloid and 9 lymphoid cases).

33 ortality in CML are caused by progression to blast crisis, about which comparatively little is known

34 died of GVHD after DLI, and 1 relapsed into blast crisis after a transient cytogenetic remission.

35 ransplanted in second stable phase following blast crisis also relapsed.

36 eated with STI571; 38 patients had a myeloid blast crisis and 20 had ALL or a lymphoid blast crisis.

37 drug-resistance in chronic myeloid leukemia-blast crisis and acute myeloid leukemia cells.

38 ge progenitor pool from patients with CML in blast crisis and imatinib-resistant CML was expanded, ex

39 C/EBPalpha function) in murine models of CML blast crisis and in in vitro assays of BCR/ABL transform

40 tyrosine kinase, in patients who had CML in blast crisis and in patients with ALL who had the Ph chr

41 ic leukemia (CMML) and sAML, and also in CML blast crisis and juvenile myelomonocytic leukemia (JMML)

42 hronic myelogenous leukemia cells in myeloid blast crisis and myeloid precursors that ectopically exp

43 Nearly all patients with lymphoid blast crisis and Ph-positive ALL had a relapse within si

44 (1) acquired clinical resistance because of blast crisis and/or BCR-ABL1 mutations; and (2) document

45 es that cause progression to advanced stage (blast crisis) and increased expression of the Lyn tyrosi

46 p (29%), 18p (20%), and 20q (27%) in myeloid blast crisis, and on 1p (50%), 4p (25%), 7p (43%), 9p (2

47 ients progressed to accelerated-phase CML or blast crisis, and the estimated overall survival of pati

48 emia (CML) progression from chronic phase to blast crisis, and they can become BCR/ABL(+) late in the

49 espectively, progressed to accelerated phase/blast crisis (AP/BC) on treatment.

50 eight from patients in accelerated phase or blast crisis (AP/BC) were studied.

51 hly elevated in chronic myelogenous leukemia blast crisis as compared with the chronic phase.

52 l mRNA and protein in cells from patients in blast crisis (BC) are higher than in those chronic phase

53 ) that discriminated chronic phase (CP) from blast crisis (BC) CML.

54 Although the evolution from chronic phase to blast crisis (BC) in CML patients is an inevitable clini

55 from patients who had developed progressive blast crisis (BC) of chronic myelocytic leukemia (CML) w

56 K562, and chronic myelogenous leukemia (CML) blast crisis (BC) primary cells but only c-Myb levels de

57 Blast crisis (BC) remains the major challenge in the man

58 xpression of CEBPB (and CEBPA) is low in the blast crisis (BC) stage of chronic myelogenous leukemia

59 TKI-refractory CML, or after progression to blast crisis (BC), are lacking.

60 C) that harbor the BCR-ABL translocation, to blast crisis (BC), characterized by aberrant activation

61 ase inhibitors (TKIs) and its progression to blast crisis (BC), in part, through the alternative spli

62 esistant to treatment after it progresses to blast crisis (BC).

63 mia (CP-CML) evolves into an acute leukemia (blast crisis [BC]) that displays either myeloid or B-lym

64 t role in the transition of chronic phase to blast crisis, bone marrow cells from p53+/+ or p53-/- mi

65 ut hematologic remission, accelerated phase, blast crisis, bone marrow transplantation, and death).

66 detected in blood cells from CML patients in blast crisis but not in a normal marrow sample.

67 evidence suggests that the phenotype of CML blast crisis cells (enhanced proliferation and survival,

68 Interestingly, CML-blast crisis cells in peripheral blood differ from those

69 Thus, the differentiation arrest of CML blast crisis cells is a secondary consequence of these a

70 ite acquisition of additional mutations, CML blast crisis cells retain their dependence on BCR/ABL fo

71 resistant chronic myelogenous leukemia (CML) blast crisis cells using siRNA.

72 including chronic myelogenous leukemia [CML]-blast crisis cells) rely on c-Myb expression more than n

73 (TKIs) fail to induce long-term response in blast crisis chronic myelogenous leukemia (CML-BC) and P

74 Blast crisis chronic myelogenous leukemia (CML-BC) and P

75 re, we report that loss of miR-328 occurs in blast crisis chronic myelogenous leukemia (CML-BC) in a

76 c phase chronic myelogenous leukemia, 9 of 9 blast crisis chronic myelogenous leukemia and 5 of 8 lym

77 y relevant mouse models of chronic phase and blast crisis chronic myelogenous leukemia, without causi

78 hylated in 100% of recurrent ALL and 100% of blast crisis chronic myelogenous leukemia.

79 Further, in blast crisis chronic myeloid leukaemia, and a subset of

80 In blast crisis chronic myeloid leukemia (BC CML), we show

81 GVL against mouse chronic-phase (CP-CML) and blast crisis chronic myeloid leukemia (BC-CML).

82 , chronic phase, and serially transplantable blast crisis chronic myeloid leukemia (CML) progenitors

83 In a mouse model of blast crisis chronic myeloid leukemia (CML), adipose-res

84 tor, against both accelerated phase (AP) and blast crisis chronic myeloid leukemia (CML-BC) and again

85 rogramming of progenitors into self-renewing blast crisis chronic myeloid leukemia stem cells (BC LSC

86 less efficacious against acute leukemias and blast-crisis chronic myelogenous leukemia (BC-CML).

87 e chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (A

88 ust apoptosis in primary human AML cells and blast crisis CML (bcCML) cells while sparing normal hema

89 Analysis of primary AML, blast crisis CML (bcCML), ALL, and chronic lymphoblastic

90 ients with imatinib-resistant or -intolerant blast crisis CML (MBC, n = 74; LBC, n = 42).

91 CD36 also marks a fraction of human blast crisis CML and acute myeloid leukemia (AML) cells

92 T1 expression not only is activated in human blast crisis CML and de novo acute myeloid leukaemia, bu

93 n extremely effective for chronic phase CML, blast crisis CML and Ph+ acute lymphoblastic leukemia (A

94 reased apoptosis in LSC of chronic phase and blast crisis CML and reduced their growth in vitro and i

95 fferentiation and impairs the propagation of blast crisis CML both in vitro and in vivo.

96 ncogenic function through BCAA production in blast crisis CML cells.

97 y impairs the development and propagation of blast crisis CML in vitro and in vivo.

98 Blast crisis CML is difficult to treat due to resistance

99 lso decreased colony-forming units (CFUs) in blast crisis CML patient samples.

100 uclear cells obtained from chronic phase and blast crisis CML patients, K562/IMA-3 or LAMA4/IMA cells

101 4(+)/CD38(-) cells of both chronic phase and blast crisis CML patients, with levels increasing upon d

102 wn impaired in vivo self-renewal capacity of blast crisis CML progenitors.

103 hat NUP98-HOXA9, an oncogene associated with blast crisis CML, can trigger expression of the RNA-bind

104 FLT3 RNA was also observed in some cases of blast crisis CML.

105 L1 induced genomic instability, a feature of blast crisis CML.

106 nic RNA binding protein that is required for blast crisis CML.

107 Patients with CML in blast crisis (CML-BC) became rapidly resistant to therap

108 of Bcr-Abl in human chronic myeloid leukemia blast crisis (CML-BC) cells.

109 ptosis of the human chronic myeloid leukemia blast crisis (CML-BC) K562 cells and acute leukemia MV4-

110 To test this hypothesis, CML-blast crisis (CML-BC) primary cells were treated in vitr

111 lity of myeloid chronic myelogenous leukemia blast crisis (CML-BC) progenitors to undergo neutrophil

112 with chronic myelogenous leukemia during the blast crisis (CML-BC), and with de novo or therapy-relat

113 uman AML and chronic myeloid leukemia during blast crisis (CML-BC).

114 phase CML to advanced phase (accelerated and blast crisis) CML is a two-step rather than a three-step

115 xpression was significantly increased in CML blast crisis compared with chronic phase.

116 Seven patients with a myeloid blast crisis continue to receive treatment and remain in

117 tion result in progression of CML into fatal blast crisis, elevated leukemic potential of BCR-ABL-ind

118 rent stages of CML (chronic, aggressive, and blast crisis) express Hsp70.

119 CL22 cell line, derived from BCR-ABL+ CML in blast crisis, expressed wild-type C/EBPepsilon protein b

120 maintain durable responses; however, many in blast crisis fail to respond, or relapse quickly.

121 pressing cell line derived from a patient in blast crisis, failed to inhibit adhesion to fibronectin.

122 Most genetic abnormalities of CML blast crisis have a direct or indirect effect on p53 or

123 val; progression to accelerated-phase CML or blast crisis; hematologic, cytogenetic, and molecular re

124 ients, ET in 4, post-ET MMM in 1, and MMM in blast crisis in 3.

125 BCR/ABL cooperates with NUP98/HOXA9 to cause blast crisis in a murine model.

126 ivity are associated with poor prognosis and blast crisis in chronic myeloid leukemia (CML).

127 ion of chronic myelogenous leukemia (CML) to blast crisis in patients was correlated with down-modula

128 Progression of CML to acute leukemia (blast crisis) in humans has been associated with acquisi

129 iagnosis, in 10 of 10 (100%) CML patients in blast crisis, in 75 of 107 (70%) CML patients receiving

130 , and that the progression of the disease to blast crisis involves multiple genetic alterations.

131 m chronic phase through accelerated phase to blast crisis is poorly understood.

132 Pdelta in BCR-ABL-positive leukemic cells in blast crisis is sufficient for neutrophil differentiatio

133 pha expression in BCR-ABL+ leukemic cells in blast crisis is sufficient for rapid neutrophil differen

134 ion of chronic myelogenous leukemia (CML) to blast crisis is supported by self-renewing leukemic stem

135 Blast crisis is the most advanced stage of chronic myelo

136 e included chronic myelocytic leukemia (CML) blast crisis K562 and HL-60/Bcr-Abl cells, which contain

137 bl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl

138 d (2) the chronic myelogenous leukemia (CML)-blast crisis K562 cells, which have endogenous expressio

139 L) in myeloid blast crisis (MBC) or lymphoid blast crisis (LBC) remains poor.

140 Rho GEF (LARG), p115-RhoGEF (p115), lymphoid blast crisis (Lbc), and Dbl.

141 ted signaling upon interaction with lymphoid blast crisis (Lbc), the oncogenic form of A-kinase ancho

142 cDNAs included signaling molecules (lymphoid blast crisis [LBC], guanine nucleotide binding protein a

143 ritical in the transition of this disease to blast-crisis leukemia.

144 ative analysis of CML and its progression to blast crisis may help elucidate general mechanisms of ca

145 th chronic myeloid leukemia (CML) in myeloid blast crisis (MBC) or lymphoid blast crisis (LBC) remain

146 Short doubling times occurred with blast crisis (median, 9.0 days; range, 6.1-17.6 days; n

147 Using a model of CML-blast crisis, mice (n = 14) injected with p210(BCR/ABL)-

148 R/ABL+ cell lines and in patient-derived CML blast crisis mononuclear and CD34+ cells, p210(BCR/ABL)

149 In one case of chronic myeloid leukemia, at blast crisis, most of the cells at relapse were mismatch

150 yeloid leukemia, chronic myeloid leukemia in blast crisis, myelodysplastic syndrome, acute lymphoblas

151 During blast crisis of chronic myelogenous leukemia (CML), abno

152 hose expression is markedly activated in the blast crisis of chronic myelogenous leukemia, which repr

153 -related acute myeloid leukemia and with the blast crisis of chronic myelogenous leukemia.

154 reatment-related acute myeloid leukemia, and blast crisis of chronic myeloid leukemia results in the

155 such as going from the chronic phase to the blast crisis of chronic myeloid leukemia.

156 have an important role in the progression to blast crisis of CML.

157 tion did not prevent progression to lymphoid blast crisis or abolish established B-cell acute lymphob

158 individuals in both chronic phase and either blast crisis or accelerated phase were analyzed at 82 mi

159 All but one patient with a lymphoid blast crisis or ALL has relapsed.

160 Of 20 patients with a lymphoid blast crisis or ALL, 14 (70 percent) had a response, inc

161 larly sensitive to the costs associated with blast crisis or bone marrow transplantation.

162 not significantly affect either the time to blast crisis or overall survival.

163 onic phase but is much less effective in CML blast crisis or Ph(+) B-cell acute lymphoblastic leukemi

164 Patients in accelerated or blast crisis or who fail to reach landmarks on TKIs eith

165 None of the patients with AML, CML in blast crisis, or other diagnoses have survived.

166 atients with accelerated-phase CML, CML with blast crisis, or Ph-positive ALL.

167 cumulative incidences of accelerated phase, blast crisis, or remission rates were observed between p

168 erto, it has been widely postulated that CML blast crisis originates mainly via cell-autonomous mecha

169 investigate this possibility in the case of blast crisis origination in CML.

170 ined evidence that the driving mechanism for blast crisis origination is a cooperation between specif

171 for rational treatment of drug-resistant CML blast crisis, particularly when lymphoid in nature.

172 onogenic growth of CML-chronic phase and CML-blast crisis patient cells, while sparing normal bone ma

173 ion also induced apoptosis in CML cells from blast crisis patients but not in normal hematopoietic ce

174 positive cell lines and blood cells from CML blast crisis patients by tyrosine phosphorylation.

175 o detected in a subset of CML advanced phase/blast crisis patients with high levels of HOXA9 and HOXA

176 ells from chronic myelogenous leukemia (CML) blast crisis patients, and during disease progression.

177 ion is a consistent finding in 25-30% of CML blast crisis patients.

178 emia (CML) patients, but the majority of CML blast-crisis patients that respond to STI-571 relapse be

179 y high levels of Numb expression whereas the blast crisis phase has low levels of Numb expression, an

180 ts exerted by the BCR/ABL oncoprotein in the blast crisis phase of chronic myelogenous leukemia (CML)

181 In the blast crisis phase of chronic myelogenous leukemia (CML)

182 the treatment of CML; however, the terminal, blast crisis phase of the disease remains a clinical cha

183 slow growing chronic phase to an aggressive blast crisis phase, but the molecular basis of this tran

184 tion for the decreased levels of Numb in the blast crisis phase, we show that NUP98-HOXA9, an oncogen

185 blishment and propagation of the chronic and blast crisis phases of chronic myelogenous leukemia (CML

186 1 of 38 patients (55 percent) with a myeloid-blast-crisis phenotype; 4 of these 21 patients had a com

187 KBM5 cells, derived from a patient with blast crisis Philadelphia chromosome-positive (Ph+) chro

188 ry derived from chronic myelogenous leukemia-blast crisis primary cells.

189 Although the pathogenic effects of most CML blast crisis secondary changes are still poorly understo

190 rticular, when treated in THs, patients with blast crisis showed a superior outcome (2-year survival

191 progressive granulocytosis with evolution to blast crisis, similar to the course of human chronic mye

192 used this single-cell approach to identify a blast-crisis-specific SC population, which was also pres

193 e lymphoblastic leukemia (T-ALL), T-lymphoid blast crisis, T-lymphoma, and B-cell chronic lymphocytic

194 ble for the transition from chronic phase to blast crisis, the causes of genomic instability and faul

195 a (CML) progresses from the chronic phase to blast crisis, the levels of BCR-ABL increase.

196 (CML)-like disease manifesting in "lymphoid blast crisis." The biological heterogeneity of BCR-ABL1-

197 d myeloid cells that can progress to a fatal blast crisis, thereby resembling human chronic myelogene

198 phages that frequently progresses to a fatal blast crisis, thus resembling human chronic myelogenous

199 A major barrier to predicting and inhibiting blast crisis transformation has been the identification

200 tic syndrome, acute myeloid leukemia, and in blast crisis transformation of chronic myeloid leukemia.

201 genesis and, perhaps, it might contribute to blast crisis transformation.

202 long, and substantially decrease the risk of blast crisis transformation.

203 Chronic phase-to-blast crisis transition in chronic myelogenous leukemia

204 , Bcr-Abl(+) CML cell lines established from blast crisis were found to have low Erk MAP kinase activ

205 nced disease (three accelerated phase, three blast crisis), which was statistically highly significan

206 omosome as the sole genetic abnormality into blast crisis, which is often associated with additional

207 nous leukemia (CML) invariably progresses to blast crisis, which represents the most proliferative ph

208 ee patients with chronic myeloid leukemia in blast crisis who had progressive leukemia while receivin