ライフサイエンスコーパス: Philadelphia chromosome-positive

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

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

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

4 In Philadelphia chromosome-positive acute lymphoblastic leu

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

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

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

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

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

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

11 Philadelphia chromosome-positive acute lymphoblastic leu

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

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

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

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

16 1 to 2011, 122 patients with newly diagnosed Philadelphia chromosome-positive acute lymphoblastic leu

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

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

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

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

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

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

23 Philadelphia chromosome-positive acute lymphoblastic leu

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

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

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

27 In Philadelphia chromosome-positive acute lymphocytic leuka

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

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

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

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

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

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

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

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

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

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

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

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

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

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

42 The Philadelphia chromosome positive arm of the UKALLXII/ECO

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Advanced phase Philadelphia chromosome-positive myeloid disease-consist

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

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

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

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

78 3 studies including 2962 patients, excluding Philadelphia chromosome-positive patients, showed a surv

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

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

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

82 25 metaphases for monitoring the presence of Philadelphia chromosome positive (Ph+) cells in chronic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 Philadelphia chromosome-positive (Ph+) acute lymphoblast

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 13 cases with t(9;22)(q34;q11) Philadelphia chromosome-positive [Ph+]) and IGH rearrang

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

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

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

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

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