ライフサイエンスコーパス: childhood acute lymphoblastic leukemia

1 d with resistance to asparaginase therapy in childhood acute lymphoblastic leukemia.

2 common tumor suppressor and fusion genes in childhood acute lymphoblastic leukemia.

3 nt types of therapies directed at the CNS in childhood acute lymphoblastic leukemia.

4 of the most common genetic abnormalities in childhood acute lymphoblastic leukemia.

5 hildren's Cancer Group case-control study of childhood acute lymphoblastic leukemia (1989-1993), livi

6 Neurotoxic intrathecal chemotherapy for childhood acute lymphoblastic leukemia (ALL) affects dev

7 494del6, and TS 28bp repeat) in 939 cases of childhood acute lymphoblastic leukemia (ALL) and 89 case

8 the biologic understanding and treatment of childhood acute lymphoblastic leukemia (ALL) and acute m

9 hildhood is a suspected risk factor for both childhood acute lymphoblastic leukemia (ALL) and allergi

10 himeric fusion genes are highly prevalent in childhood acute lymphoblastic leukemia (ALL) and are mos

11 sessed the principal mode of inactivation in childhood acute lymphoblastic leukemia (ALL) and frequen

12 is the most common genetic rearrangement in childhood acute lymphoblastic leukemia (ALL) and gives r

13 tice in frontline treatment of virtually all childhood acute lymphoblastic leukemia (ALL) and in many

14 most widely used drugs for the treatment of childhood acute lymphoblastic leukemia (ALL) and is comm

15 (SMN) are devastating late complications of childhood acute lymphoblastic leukemia (ALL) and its tre

16 oids are integral to successful treatment of childhood acute lymphoblastic leukemia (ALL) and other l

17 The associations between childhood acute lymphoblastic leukemia (ALL) and several

18 ment regimens, event-free survival rates for childhood acute lymphoblastic leukemia (ALL) approach or

19 Survivors of childhood acute lymphoblastic leukemia (ALL) are at incr

20 Purpose Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk

21 Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk

22 Survivors of childhood acute lymphoblastic leukemia (ALL) are at risk

23 Although five-year survival rates for childhood acute lymphoblastic leukemia (ALL) are now ove

24 alignant neoplasms (SMNs) after diagnosis of childhood acute lymphoblastic leukemia (ALL) are rare ev

25 underlying pathways that lead to relapse in childhood acute lymphoblastic leukemia (ALL) are unknown

26 Most childhood acute lymphoblastic leukemia (ALL) arises from

27 Childhood acute lymphoblastic leukemia (ALL) can often b

28 Relapsed childhood acute lymphoblastic leukemia (ALL) carries a p

29 The ETV6-RUNX1 fusion gene, found in 25% of childhood acute lymphoblastic leukemia (ALL) cases, is a

30 romosomal translocation is detected in 5% of childhood acute lymphoblastic leukemia (ALL) cases.

31 EFS) and treatment-related toxicity (TRT) in childhood acute lymphoblastic leukemia (ALL) considered

32 Modern clinical treatments of childhood acute lymphoblastic leukemia (ALL) employ enzy

33 With cure rates of childhood acute lymphoblastic leukemia (ALL) exceeding 8

34 Survivors of childhood acute lymphoblastic leukemia (ALL) exhibit inc

35 bstacle to uniformly successful treatment of childhood acute lymphoblastic leukemia (ALL) for many ye

36 An infectious etiology for childhood acute lymphoblastic leukemia (ALL) has been su

37 A role for HLA class I polymorphism in childhood acute lymphoblastic leukemia (ALL) has been su

38 the level of expression of these proteins in childhood acute lymphoblastic leukemia (ALL) has not bee

39 Although cure rate of childhood acute lymphoblastic leukemia (ALL) has surpass

40 tions that contribute to the pathogenesis of childhood acute lymphoblastic leukemia (ALL) have been i

41 ther recent improvements in the treatment of childhood acute lymphoblastic leukemia (ALL) have nullif

42 Cytogenetic analysis of childhood acute lymphoblastic leukemia (ALL) identified

43 Cytogenetic analysis of childhood acute lymphoblastic leukemia (ALL) identified

44 Recent genomic profiling of childhood acute lymphoblastic leukemia (ALL) identified

45 Outcome of childhood acute lymphoblastic leukemia (ALL) improved gr

46 defines a particular relapse-prone subset of childhood acute lymphoblastic leukemia (ALL) in Italian

47 e identified several susceptibility loci for childhood acute lymphoblastic leukemia (ALL) in populati

48 A retrospective analysis of the treatment of childhood acute lymphoblastic leukemia (ALL) in second r

49 Conventional therapy for childhood acute lymphoblastic leukemia (ALL) includes pr

50 St Jude Total Therapy Study XIIIB for childhood acute lymphoblastic leukemia (ALL) incorporate

51 The relapse rate in childhood acute lymphoblastic leukemia (ALL) is approxim

52 Therapy for childhood acute lymphoblastic leukemia (ALL) is associat

53 opurine (6MP) during maintenance therapy for childhood acute lymphoblastic leukemia (ALL) is critical

54 relationship of mode of delivery to risk of childhood acute lymphoblastic leukemia (ALL) is uncertai

55 n and methylation status of MTS1 and MTS2 in childhood acute lymphoblastic leukemia (ALL) of both T-c

56 A total of 68 survivors of childhood acute lymphoblastic leukemia (ALL) or brain tu

57 Previous, smaller studies of childhood acute lymphoblastic leukemia (ALL) provided co

58 Treatment for childhood acute lymphoblastic leukemia (ALL) regularly i

59 he most common cause of treatment failure in childhood acute lymphoblastic leukemia (ALL) remains rel

60 topoietic stem cell (HSC) transplantation in childhood acute lymphoblastic leukemia (ALL) requires th

61 Polymerase chain reaction-based screening of childhood acute lymphoblastic leukemia (ALL) samples sho

62 tors for these MTX-related toxicities during childhood acute lymphoblastic leukemia (ALL) therapy and

63 Induction therapy for childhood acute lymphoblastic leukemia (ALL) traditional

64 Survivors of childhood acute lymphoblastic leukemia (ALL) treated wit

65 eurocognitive outcomes in adult survivors of childhood acute lymphoblastic leukemia (ALL) treated wit

66 Survivors of childhood acute lymphoblastic leukemia (ALL) treated wit

67 ciation between parental smoking and risk of childhood acute lymphoblastic leukemia (ALL) was investi

68 een socioeconomic position (SEP) and risk of childhood acute lymphoblastic leukemia (ALL) were invest

69 one (GH) replacement therapy in survivors of childhood acute lymphoblastic leukemia (ALL) who have GH

70 Outcome for children with childhood acute lymphoblastic leukemia (ALL) who relapse

71 , and hay fever investigated separately, and childhood acute lymphoblastic leukemia (ALL) with some c

72 ted the potent sensitivity of many high-risk childhood acute lymphoblastic leukemia (ALL) xenografts

73 In childhood acute lymphoblastic leukemia (ALL), a rapid de

74 t common molecular abnormality identified in childhood acute lymphoblastic leukemia (ALL), and it gen

75 administration, is critical in treatment of childhood acute lymphoblastic leukemia (ALL), but elicit

76 ion (DI) is an integral part of treatment of childhood acute lymphoblastic leukemia (ALL), but it is

77 In previous clinical trials of childhood acute lymphoblastic leukemia (ALL), dexamethas

78 In childhood acute lymphoblastic leukemia (ALL), early resp

79 ergy balance, and fitness among survivors of childhood acute lymphoblastic leukemia (ALL), especially

80 most common molecular genetic abnormality in childhood acute lymphoblastic leukemia (ALL), occurring

81 With the use of risk-directed therapy for childhood acute lymphoblastic leukemia (ALL), outcome ha

82 In childhood acute lymphoblastic leukemia (ALL), persistenc

83 To identify novel predictors of outcome in childhood acute lymphoblastic leukemia (ALL), we analyze

84 To identify risk variants for childhood acute lymphoblastic leukemia (ALL), we conduct

85 g recent reports of KIR gene associations in childhood acute lymphoblastic leukemia (ALL), we present

86 are the backbone of continuation therapy for childhood acute lymphoblastic leukemia (ALL).

87 ay an interactive role in the development of childhood acute lymphoblastic leukemia (ALL).

88 The CNS is an important sanctuary site in childhood acute lymphoblastic leukemia (ALL).

89 nces in the incidence and characteristics of childhood acute lymphoblastic leukemia (ALL).

90 d SNPs in six genes that are associated with childhood acute lymphoblastic leukemia (ALL).

91 ke exposure has been associated with risk of childhood acute lymphoblastic leukemia (ALL).

92 re candidate genetic susceptibility loci for childhood acute lymphoblastic leukemia (ALL).

93 osteoporosis are a potential complication of childhood acute lymphoblastic leukemia (ALL).

94 in ARID5B associated with susceptibility to childhood acute lymphoblastic leukemia (ALL).

95 usion is usually an early, prenatal event in childhood acute lymphoblastic leukemia (ALL).

96 l residual disease (MRD) in 48 patients with childhood acute lymphoblastic leukemia (ALL).

97 is a key therapeutic agent for treatment of childhood acute lymphoblastic leukemia (ALL).

98 almost universally expressed in B-precursor childhood acute lymphoblastic leukemia (ALL).

99 = 30 kg/m2) frequently follow treatment for childhood acute lymphoblastic leukemia (ALL).

100 s for 10% to 15% of newly diagnosed cases of childhood acute lymphoblastic leukemia (ALL).

101 s complication after successful treatment of childhood acute lymphoblastic leukemia (ALL).

102 cells is a favorable prognostic indicator in childhood acute lymphoblastic leukemia (ALL).

103 and days 22 to 25 of remission induction in childhood acute lymphoblastic leukemia (ALL).

104 lationship for the use of corticosteroids in childhood acute lymphoblastic leukemia (ALL).

105 nd often protracted latency and the need, in childhood acute lymphoblastic leukemia (ALL)/acute myelo

106 g a large sample of young adult survivors of childhood acute lymphoblastic leukemia (ALL; N = 555).

107 ected cytogenetically in approximately 5% of childhood acute lymphoblastic leukemias (ALLs) and its p

108 ce nor exposure index was related to risk of childhood acute lymphoblastic leukemia, although both we

109 s, has been implicated in the development of childhood acute lymphoblastic leukemia (C-ALL).

110 rated over-transmission of this allele among childhood acute lymphoblastic leukemia cases, the meta-a

111 de association study of 907 individuals with childhood acute lymphoblastic leukemia (cases) and 2,398

112 ylation by CDK4 also occurred in extracts of childhood acute lymphoblastic leukemia cells but not in

113 As cure rates in childhood acute lymphoblastic leukemia edge toward 80%,

114 ause of treatment-related mortality (TRM) in childhood acute lymphoblastic leukemia, factors associat

115 Overall, childhood acute lymphoblastic leukemia is associated wit

116 5 doxorubicin-treated long-term survivors of childhood acute lymphoblastic leukemia (median age at di

117 In childhood acute lymphoblastic leukemia, NG2 expression c

118 ary brain tumors, in particular survivors of childhood acute lymphoblastic leukemia or childhood brai

119 rapy (CT) and cranial radiotherapy (CRT) for childhood acute lymphoblastic leukemia or lymphoma have

120 Group or German Cooperative Study Group for Childhood Acute Lymphoblastic Leukemia protocols.

121 ite significant progress in the treatment of childhood acute lymphoblastic leukemia, therapy is still

122 armacogenetics) have pushed the cure rate of childhood acute lymphoblastic leukemia to near 90%.

123 Survivors of childhood acute lymphoblastic leukemia treated on contem

124 Fifty years ago, childhood acute lymphoblastic leukemia was universally f

125 sion, the most common genetic abnormality in childhood acute lymphoblastic leukemia, was recently sho

126 B-cell precursor childhood acute lymphoblastic leukemia with ETV6-RUNX1 (

127 nic and racial differences in survival after childhood acute lymphoblastic leukemia, with poorer outc