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1 thogenesis, natural history, and etiology of childhood leukemia.
2 ic-related contaminants, affects the risk of childhood leukemia.
3 cations in utero leading to infant and early childhood leukemia.
4 to an increased risk of cancer, particularly childhood leukemia.
5 (ALL) represents the most refractory type of childhood leukemia.
6 roved protein drug used for the treatment of childhood leukemia.
7 s associated with the most common subtype of childhood leukemia.
8 ears to be associated with a reduced risk of childhood leukemia.
9 ration of breastfeeding and the incidence of childhood leukemia.
10 dicted RF-EMF exposure from broadcasting and childhood leukemia.
11 ociated with a slightly higher risk of acute childhood leukemia.
12 evaluate the association between allergy and childhood leukemia.
13 ctase 1 (NQO1), had no significant effect on childhood leukemia.
14 y of residential magnetic field exposure and childhood leukemia.
15  examined the association between NQO1*2 and childhood leukemia.
16 ociation between magnetic field exposure and childhood leukemia.
17 sive smoking may be important in the risk of childhood leukemia.
18 ron supplement use may be protective against childhood leukemia.
19 ighlight parallels between DS AMKL and other childhood leukemias.
20 ated in human leukemias, but rarely in early childhood leukemias.
21 en identified in Noonan syndrome and various childhood leukemias.
22 Noonan syndrome and a significant portion of childhood leukemias.
23 ich had long been recognized as disrupted in childhood leukemia, also plays a role in the CNS.
24             Relative to those survivors with childhood leukemia, an increased risk was observed for a
25 amples from a study of electrical wiring and childhood leukemia and a study of diet and glioma.
26 ty of combination chemotherapy to cure acute childhood leukemia and advanced Hodgkin's disease in the
27                                 Survivors of childhood leukemia and brain tumors, particularly those
28 kes that occur in > or = 5-year survivors of childhood leukemia and brain tumors.
29 widely used drugs for the treatment of acute childhood leukemia and chronic myelocytic leukemia.
30 rts describing the effect of NQO1 in de novo childhood leukemia and conducted a meta-analysis of 7 ca
31 the role of P-gp-mediated drug resistance in childhood leukemia and confirms that P-gp expression and
32  new development in the induction therapy of childhood leukemia and lymphoma in the United States is
33 a significant late toxicity of treatment for childhood leukemia and lymphoma.
34 nce known as "wire coding"), but not between childhood leukemia and measurements of 60-Hz residential
35         Carriers might be at greater risk of childhood leukemia and non-Hodgkin lymphoma and those di
36 e suggested that meta-analyses of studies on childhood leukemia and proximity to gasoline stations sh
37  identified evidence of associations between childhood leukemia and several different potential metri
38 de novel insight into the natural history of childhood leukemia and suggest that consequent to a pren
39  Previous studies found associations between childhood leukemia and surrogate indicators of exposure
40                                   Studies of childhood leukemia and the potential etiologic role of g
41 f-function Shp2 mutations have been found in childhood leukemias and Noonan syndrome.
42 cell signaling pathways, are associated with childhood leukemias and solid tumors.
43 r all cancers, 0.55 (95% CI: 0.26, 1.19) for childhood leukemia, and 1.68 (95% CI: 0.98, 2.91) for ch
44 stic leukemia (T-ALL), an aggressive form of childhood leukemia, and study the emergence of phenotypi
45 ment of further evidence for fetal origin of childhood leukemias, and additional evidence to support
46 associated with a markedly increased risk of childhood leukemias, and identification of chromosome 21
47 NX1) is the most common translocation in the childhood leukemias, and is a prenatal mutation in most
48 hatase) are associated with Noonan syndrome, childhood leukemias, and sporadic solid tumors.
49                              The majority of childhood leukemias are precursor B-cell acute lymphobla
50     Thiopurines are a standard treatment for childhood leukemia, but like all chemotherapeutics, thei
51      The present analysis included 327 acute childhood leukemia cases (281 acute lymphoblastic leukem
52                 The study compared the 2,760 childhood leukemia cases diagnosed in France between 200
53 ent meta-analyses results, 14% to 19% of all childhood leukemia cases may be prevented by breastfeedi
54 e was associated with a reduction in risk of childhood leukemia diagnosed between the ages of 2 and 1
55 nuous doxorubicin infusion over 48 hours for childhood leukemia did not offer a cardioprotective adva
56            The molecular characterization of childhood leukemias directly affects our treatment strat
57 in methionine synthase could mediate risk of childhood leukemia, either via effects on DNA methylatio
58 ole of NQO1 polymorphisms in the etiology of childhood leukemia, especially among MLL-positive leukem
59 in C and/or potassium may reduce the risk of childhood leukemia, especially if they are consumed on a
60                                              Childhood leukemia frequently starts before birth, durin
61  a matched case-control study of the risk of childhood leukemia from exposure to residential electric
62  Recent identification of SHP-2 mutations in childhood leukemia further emphasizes the importance of
63  of birth, in contrast to previously studied childhood leukemia fusions, t(12;21), t(8;21), and t(4;1
64 f human milk to mixed-fed infants with acute childhood leukemia, generally, and acute lymphoblastic l
65 ausal link between outdoor air pollution and childhood leukemia has been proposed, but some older stu
66 ation between child's early diet and risk of childhood leukemia has remained largely unexplored.
67        Significant elevations in the risk of childhood leukemia have been associated with environment
68 s in therapy, primarily intensification, for childhood leukemias have significantly improved cure rat
69 ys the progress of epidemiologic research on childhood leukemia in 1996.
70  (first 2 years) are associated with risk of childhood leukemia in a 1995-2002 case-control study of
71 t has been associated with increased risk of childhood leukemia in Los Angeles and elsewhere in North
72 t studies that have investigated the risk of childhood leukemia in relation to exposure either to mot
73 inone carcinogens, have been associated with childhood leukemia in some studies, although the observe
74               The odds ratios for developing childhood leukemia in the highest exposure category were
75 phoblastic leukemia, the predominant type of childhood leukemia in the United States and many Europea
76        An expert panel reviewed a cluster of childhood leukemias in Fallon, Nevada, and suggested the
77 tfeeding for 6 months or more may help lower childhood leukemia incidence, in addition to its other h
78     Remaining challenges in the treatment of childhood leukemia include 1) the development of specifi
79 tained from 12 case-control studies from the Childhood Leukemia International Consortium (CLIC, 1974-
80 11 case-control studies participating in the Childhood Leukemia International Consortium (enrollment
81 d data from 13 case-control studies from the Childhood Leukemia International Consortium done in nine
82 hed cause of adult leukemia, but its role in childhood leukemia is less clear.
83 motherapy, but its role in the management of childhood leukemia is unclear.
84                                              Childhood leukemia may be associated with traffic-relate
85                               In contrast to childhood leukemia, no pooled analyses of childhood brai
86      Severe sepsis during treatment of acute childhood leukemia occurred in 46 participants (7.1%).
87 22) is the most common gene rearrangement in childhood leukemia, occurring in approximately 25% of pe
88 ger was associated with a 19% lower risk for childhood leukemia (odds ratio, 0.81; 95% CI, 0.73-0.89)
89 ed was associated with an 11% lower risk for childhood leukemia (odds ratio, 0.89; 95% CI, 0.84-0.94)
90 V6-RUNX1), the most common fusion protein in childhood leukemia, on miRNA expression and the leukemic
91                               No increase in childhood leukemia or other cancers has been documented.
92 d to be associated with an increased risk of childhood leukemia, particularly among young children.
93 proximately linearly associated with risk of childhood leukemia, particularly for acute myeloid leuke
94 40%) and 52 of 190 (27.4%) bone marrows from childhood leukemia patients demonstrated hypermethylatio
95 ng associations between parental smoking and childhood leukemia, possibly because previous studies us
96 ons and applied to a candidate gene study of childhood leukemia (Quebec Childhood Leukemia Study, 198
97 ortality; whether a similar effect exists in childhood leukemia remains controversial.
98  leukemia, but whether it is associated with childhood leukemia remains unclear.
99 the association between parental smoking and childhood leukemia remains unclear.
100 ic leukemia (ALL) is the most common form of childhood leukemia, representing 75% to 80% of cases of
101 eQTLs and shows their potential influence on childhood leukemia research.
102 o support an association between benzene and childhood leukemia risk, with no indication of any thres
103 llicit) during pregnancy might be related to childhood leukemia risk.
104 may be associated with slightly higher acute childhood leukemia risk.
105  ratio (SIR) = 1.90, 95% CI: 1.01, 3.24) and childhood leukemia (SIR = 14.5, 95% CI: 1.75, 52.2), the
106  469 households from the Northern California Childhood Leukemia Study (1999-2007).
107 89) and controls (n = 205) in the California Childhood Leukemia Study (CCLS) from 1995-2008 was compa
108  (n=567) enrolled in the Northern California Childhood Leukemia Study (NCCLS) compared with populatio
109 ollected from participants of the California Childhood Leukemia Study at various intervals from 1999
110 useholds enrolled in the Northern California Childhood Leukemia Study during 2001-2006, trained inter
111 om 293 households in the Northern California Childhood Leukemia Study during two sampling rounds (fro
112 e collected from 289 homes in the California Childhood Leukemia Study during two sampling rounds from
113 ate gene study of childhood leukemia (Quebec Childhood Leukemia Study, 1980-2000).
114 mia were examined in the Northern California Childhood Leukemia Study, a case-control study, between
115 etreatment tumor samples from the California Childhood Leukemia Study.
116  race/ethnicity from the Northern California Childhood Leukemia Study.
117 ata (1995-2002) from the Northern California Childhood Leukemia Study.
118                                        Other childhood leukemias, such as non-infant pre-B-cell acute
119 lasts of adult patients and early relapse in childhood leukemia, suggest that GRP78 is a novel therap
120 nation in the first year of life and risk of childhood leukemia (summary odds ratio (OR) 0.58 [95% co
121 ensive follow-up programs play a key role in childhood leukemia survivor care.
122                   Epidemiological studies of childhood leukemia survivors reveal an alarmingly high i
123                  The Therapeutic Advances in Childhood Leukemia (TACL) Consortium was assembled to as
124 erinatal factors have been linked to risk of childhood leukemia, testicular cancer, and breast cancer
125 phoblastic leukemia (T-ALL) is an aggressive childhood leukemia that is caused by the accumulation of
126 tween paternal military service and risk for childhood leukemia, the authors analyzed data from three
127 e success of L-asparaginase as a therapy for childhood leukemia, the data suggest that intracellular
128 nfections are a frequent complication during childhood leukemia treatment.
129 s study did not understand randomization for childhood leukemia trials.
130 onocytic leukemia (JMML) is a poor-prognosis childhood leukemia usually caused by RAS-pathway mutatio
131  1987 to 2014, the summary relative risk for childhood leukemia was 1.96 (95% confidence interval (CI
132 ng the association between breastfeeding and childhood leukemia was conducted on PubMed, the Cochrane
133 ng MeiHMM to 509 children with DS-associated childhood leukemia, we demonstrate that NDJ error is ass
134             Parental smoking and the risk of childhood leukemia were examined in the Northern Califor
135 ociated with a slightly higher risk of acute childhood leukemia, whereas evidence comparing never fee
136 s been associated with the increased risk of childhood leukemia, which arises from mutations induced
137 tion strategies were evaluated in a study of childhood leukemia, which commenced in California in 199
138               The population of survivors of childhood leukemia who reach adulthood is growing due to
139 cohort study included 644 adult survivors of childhood leukemia who were diagnosed between January 1,
140  additional new evidence for associations of childhood leukemia with both residential proximity to ga
141 stigated recently include the association of childhood leukemia with infection and with birth weight.
142 meta-analysis, we identified associations of childhood leukemia with occupational and household produ
143 KMT2A-rearranged infant ALL is an aggressive childhood leukemia with poor prognosis.

 
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