ライフサイエンスコーパス: childhood ALL

1 We treated 10 childhood ALL patient-derived xenograft models harboring

2 ion, we performed a three-stage GWAS of 1184 childhood ALL cases and 3219 non-ALL controls.

3 w4 supertype ligands, was carried out in 212 childhood ALL cases and 231 healthy controls.

4 ed mutational analysis of TEL and KIP1 in 33 childhood ALL patients known to have loss of heterozygos

5 esequencing the CDKN2A-CDKN2B locus in 2,407 childhood ALL cases reveals 19 additional putative funct

6 bsequent targeted sequencing of ETV6 in 4405 childhood ALL cases identified 31 exonic variants (four

7 Ethnic differences in survival after childhood ALL have been reported in many clinical studie

8 n was observed between C-section overall and childhood ALL risk (<15 years of age), but elective C-se

9 in the development of both T and precursor-B childhood ALLs.

10 performed to assess the association between childhood ALL and allergies.

11 nfant leukemia samples (n = 5), other common childhood ALLs (n = 5), and normals (n = 5).

12 alleles contribute to the risk of developing childhood ALL and provide new insight into disease causa

13 lasts from 270 patients with newly diagnosed childhood ALL to that of normal CD19(+)CD10(+) B-cell pr

14 free survival rates of approximately 80% for childhood ALL and almost 60% for pediatric AML.

15 geneic bone marrow transplantation (BMT) for childhood ALL.

16 s associated with the use of doxorubicin for childhood ALL without compromising the antileukemic effi

17 ongenital CMV infection is a risk factor for childhood ALL and is more prominent in Hispanic children

18 ion was not an adverse prognostic factor for childhood ALL.

19 the time of conception is a risk factor for childhood ALL.

20 1 may be one of the genetic risk factors for childhood ALL.

21 c criteria for use in treatment planning for childhood ALL.

22 ades; currently the 5-year survival rate for childhood ALL is more than 80%.

23 s are associated with treatment response for childhood ALL, with polymorphisms related to leukemia ce

24 poor responders is an effective strategy for childhood ALL.

25 Although modern therapy for childhood ALL has eliminated the use of cranial radiatio

26 s presented in which maintenance therapy for childhood ALL is personalized using routine patient meas

27 been shown that individualizing therapy for childhood ALL patients by adjusting doses based on the b

28 g 6-MP intake during maintenance therapy for childhood ALL should aim to simplify administration.

29 ndary malignant neoplasm after treatment for childhood ALL, according to Berlin-Frankfurt-Munster str

30 ts in 1 of 2 prospective clinical trials for childhood ALL that included treatment with 36 to 39 dose

31 report 15 EBF1-PDGFRB-positive patients from childhood ALL treatment trials (ALL 97/99, UKALL 2003, U

32 Importantly, childhood ALL patients with low TPMT activity have been

33 s a common class of genomic abnormalities in childhood ALL and that recurrent translocations involvin

34 on is a significant secondary abnormality in childhood ALL strongly correlated with phenotype and gen

35 We reconsidered the HLA-DR association in childhood ALL in 114 patients from a single center and 3

36 omegalovirus (CMV) infection at diagnosis in childhood ALL, demonstrating active viral transcription

37 MDM2 overexpression and resistant disease in childhood ALL.

38 x, here we have investigated its efficacy in childhood ALL.

39 In conclusion, increased BCL-2 expression in childhood ALL appears to enhance the ability of lymphobl

40 last cells, a favorable prognostic factor in childhood ALL.

41 ese potential causes of treatment failure in childhood ALL.

42 l gene rearrangements is a common feature in childhood ALL.

43 of MTS2, in contrast to MTS1, is frequent in childhood ALL.

44 that potential alteration in p53 function in childhood ALL is more common (P = .036) in cases of earl

45 is the critical 12p tumor suppressor gene in childhood ALL.

46 Self-report of 6MP intake in childhood ALL overestimates true intake, particularly in

47 5 strongly associated with MP intolerance in childhood ALL, which may have implications for treatment

48 testing for the major cytogenetic lesions in childhood ALL: ETV6-RUNX1, TCF3-PBX1, BCR-ABL1, and MLL

49 role for KIR genes and their HLA ligands in childhood ALL etiology that may vary among ethnic groups

50 ures predictive of poor treatment outcome in childhood ALL, such as older age, high white blood cell

51 he potential of further improving outcome in childhood ALL.

52 n therapy and subsequent clinical outcome in childhood ALL.

53 sed the effects of PTL on LIC populations in childhood ALL.

54 e that PTL may have therapeutic potential in childhood ALL and provide a basis for developing effecti

55 ngoing effort to define molecular relapse in childhood ALL.

56 Treatment results in childhood ALL continue to improve, and the expected curr

57 tion therapy have prognostic significance in childhood ALL, suggesting that patients with this findin

58 link Waf-1 RNA expression with p53 status in childhood ALL, our data show potential p53 inactivation

59 ics and response to high-dose MTX therapy in childhood ALL.

60 abnormalities, it lacks prognostic value in childhood ALL.

61 didates for clinical trials of venetoclax in childhood ALL.

62 We analyzed 137 B-lineage and 30 T-lineage childhood ALL cases using microarray analysis of DNA cop

63 Analyses of DPB1 supertypes showed a marked childhood ALL association with DP1, particularly for hig

64 The data indicate that although most childhood ALL cells express CD34 and CD38, leukemic cell

65 blastic leukemia (B-ALL) accounts for 10% of childhood ALL.

66 ted with differences in the tumor biology of childhood ALL.

67 tion in a significant proportion of cases of childhood ALL at the time of initial diagnosis.

68 Therefore, we studied 45 cases of childhood ALL with abnormalities of chromosome 11q23 for

69 an immunophenotypically distinct category of childhood ALL.

70 polymorphisms are important determinants of childhood ALL susceptibility and treatment outcome, and

71 lays an important role in the development of childhood ALL and provide new insights into the etiology

72 r the HLA-DR influence on the development of childhood ALL while confirming the recessive nature of t

73 n 11q are important events in development of childhood ALL.

74 ond neoplasms remains low after diagnosis of childhood ALL.

75 pport an immune mechanism in the etiology of childhood ALL involving the HLA-DPB1 gene in the context

76 arean section (C-section) in the etiology of childhood ALL.

77 nd provide new insights into the etiology of childhood ALL.

78 in treating asparaginase-resistant forms of childhood ALL.

79 rences in long-term cognitive functioning of childhood ALL patients based on corticosteroid randomiza

80 13q12-14 may contribute to leukemogenesis of childhood ALL and confer increased risk of treatment fai

81 c variations related to treatment outcome of childhood ALL, most of which were prognostic independent

82 otype does not affect etiology or outcome of childhood ALL.

83 ese results suggest that the pathogenesis of childhood ALL and allergy share a common biologic mechan

84 q loss may contribute to the pathogenesis of childhood ALL.

85 infrequently involved in the progression of childhood ALL.

86 ur less frequently during the progression of childhood ALL.

87 The incidence rate of childhood ALL was negatively associated with SEP among H

88 Although the risk of relapse of childhood ALL after 10 years in remission appears to be

89 Our results suggest an increased risk of childhood ALL after prelabour caesarean delivery.

90 ssociations between parental smoking risk of childhood ALL did not differ substantially by immunophen

91 nal risk factors, may play a role in risk of childhood ALL in American blacks.

92 The risk of childhood ALL was not linked to summary time-weighted av

93 rnal smoking was not associated with risk of childhood ALL, but the odds ratio for paternal smoking o

94 section was associated with a higher risk of childhood ALL, especially at the peak ages of incidence.

95 demonstrated little association with risk of childhood ALL.

96 hich they contributed to the overall risk of childhood ALL.

97 ation of the common cytogenetic subgroups of childhood ALL and overrepresentation of CRLF2-IL7R-JAK-S

98 tic leukemia (ALL) is a high-risk subtype of childhood ALL characterized by kinase-activating alterat

99 ysiology of specific cytogenetic subtypes of childhood ALL.

100 e in intelligence for 102 adult survivors of childhood ALL (age range, 26.6-54.7 years) during a medi

101 ional and social deficits among survivors of childhood ALL and BT.

102 rocognitive impairment in adult survivors of childhood ALL and warrants ongoing monitoring of brain h

103 We assessed 102 survivors of childhood ALL and Wilms' tumour, who had been free from

104 Structural MRI of long-term survivors of childhood ALL demonstrated smaller volumes of multiple b

105 Long-term survivors of childhood ALL exhibit excess mortality and morbidity.

106 Some survivors of childhood ALL experience fatigue many years after treatm

107 hoblastic leukemia (ALL), adult survivors of childhood ALL remain at risk for impaired fitness, body

108 was used to compare 1,765 adult survivors of childhood ALL to 2,565 adult siblings of childhood cance

109 Survivors of childhood ALL treated at St Jude Children's Research Hos

110 multisite study of young adult survivors of childhood ALL treated on CCG protocols after 1970 found

111 independent cohort of long-term survivors of childhood ALL treated with chemotherapy only.

112 r neurocognitive development in survivors of childhood ALL treated with chemotherapy-only protocols.

113 Results suggest long-term survivors of childhood ALL treated with CRT are at risk for progressi

114 may influence obesity in female survivors of childhood ALL, particularly those exposed to cranial rad

115 correction of GH deficiency in survivors of childhood ALL.

116 ively uncommon occurrence among survivors of childhood ALL.

117 hemotherapy-only regimens among survivors of childhood ALL.

118 ce susceptibility to obesity in survivors of childhood ALL.

119 cond population of 30 long-term survivors of childhood ALL; a fasting lipid and lipoprotein profile w

120 CRT used in the treatment of childhood ALL is associated with a greater rate of incre

121 ecularly targeted agent for the treatment of childhood ALL is warranted.

122 role of TEL/AML1 testing in the treatment of childhood ALL will require additional studies.

123 ong rationale for HD-MTX in the treatment of childhood ALL.

124 can be safely omitted from the treatment of childhood ALL.

125 e 9p21.3, a region that is deleted in 30% of childhood ALLs, suggesting the presence of causal polymo

126 Consistent with epidemiological findings on childhood ALL etiology, susceptibility to genetic lesion

127 f KIR genes and their cognate HLA ligands on childhood ALL risk.

128 ogenesis and progression of t(1;19)-positive childhood ALL.

129 y (LOH) of chromosome arm 11q in 113 primary childhood ALL samples using 14 microsatellite markers.

130 idence of activity in relapsed or refractory childhood ALL.

131 nduction regimens for relapsed or refractory childhood ALL.

132 an important role in the biology of relapsed childhood ALL, and is associated with disease progressio

133 ASNS may play in the onset of drug-resistant childhood ALL.

134 kemia (ALL) is a novel subgroup of high-risk childhood ALL.

135 Eight hundred forty-six childhood ALL patients who were newly diagnosed during 2

136 romosomal markers has provided evidence that childhood ALL cases may arise in utero.

137 lecular defects involving the Ikaros gene to childhood ALL.

138 c syndrome associated with predisposition to childhood ALL.

139 the sequence of genetic events that underlie childhood ALL and provide a framework for understanding

140 To identify genetic factors associated with childhood ALL risk in the Chinese population, we perform

141 s1121404 in WWOX) at 16q23.1 associated with childhood ALL susceptibility (odds ratio (OR) = 1.38, P

142 ative tumor suppressor genes associated with childhood ALL.

143 Emergency C-section was not associated with childhood ALL.

144 large independent data sets of patients with childhood ALL who were treated on different protocols.

145 more common among blacks but not whites with childhood ALL.