Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE In comparison with Western cohorts, the incidence of t(9;22) (q34;q11)/BCR-ABL (14.60%) in B-ALL and HOX11 expression in T-ALL (25.24%) seemed to be much higher in our group, while the incidence of t(12;21) (p13;q22)/ETV6-RUNX1 (15.34%) seemed to be lower in Chinese pediatric patients. 22382891 2012
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE B-cell precursor childhood acute lymphoblastic leukemia with ETV6-RUNX1 (TEL-AML1) fusion has an overall good prognosis, but relapses occur, usually after cessation of treatment and occasionally many years later. 21482711 2011
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE In B-ALL KIBRA methylation was associated with ETV6/RUNX1 [t(12;21) (p13;q22)] chromosomal translocation (p = 0.0082) phenotype, suggesting that KIBRA may play an important role in t(12;21) leukemogenesis. 21173572 2011
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE EPOR mRNA is selectively and ectopically expressed in ETV6-RUNX1(+) ALL, but the presence of a functional EPOR on the cell surface and its role in leukemogenesis driven by ETV6-RUNX1 remains to be identified. 21900195 2011
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE ETV6/RUNX1 (E/R) (also known as TEL/AML1) is the most frequent gene fusion in childhood acute lymphoblastic leukemia (ALL) and also most likely the crucial factor for disease initiation; its role in leukemia propagation and maintenance, however, remains largely elusive. 22028862 2011
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE t(12;21)(p13;q22)[ETV6-RUNX1] is the most common chromosomal translocation in childhood acute lymphoblastic leukemia, and it can often be backtracked to Guthrie cards supporting prenatal initiation and high levels of circulating t(12;21)-positive cells at birth. 20713965 2011
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE However, the combined analysis also identified alterations affecting nuclear hormone response (24%) to be a characteristic feature of ETV6/RUNX1-positive ALL. 20513752 2010
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Together, these results suggest that the expression of hsa-mir-125b-2 in ETV6/RUNX1 ALL provides survival advantage to growth inhibitory signals in a p53-independent manner. 19890372 2010
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE In this cohort of Taiwanese children, the relative frequencies of the 4 translocations of B-lineage ALL were 8% with ALL-type t(9;22)/BCR-ABL1, 4% with (1;19)/TCF-PBX1, 2% with t(4;11)/MLL-AF4, and 17.6% with t(12;21)/ETV6-RUNX1. 20930648 2010
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Using ROC analysis, the most efficient model for predicting TEL/AML1-positive ALL combined CD9 (mean fluorescence intensity <or=20) and CD10 values (positive cells >40%). 19896186 2010
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE This study describes the cytogenetics of 33 children with ETV6-RUNX1 positive acute lymphoblastic leukemia (ALL) who had been in continuous complete remission for a minimum of 8.8 years [median event-free survival (EFS) 10.9 years]. 19998443 2010
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE "Driver" CNAs in another twin with ALL were all absent in the shared ETV6-RUNX1-positive preleukemic clone of her healthy co-twin. 20061556 2010
Childhood Acute Lymphoblastic Leukemia
0.400 AlteredExpression disease BEFREE Folylpolyglutamate synthetase (FPGS) activity was higher in B vs T lineage ALL (p<0.005), MTX influx and FPGS activity were higher in hyperdiploid vs non-hyperdiploid ALL (p<0.03), MTX influx and FPGS activity were lower in the t(12;21) (ETV6-RUNX1) subtype (p<0.05), and the ratio of FPGS to γ-glutamyl hydrolase (GGH) activity was lower in the t(1;19) (TCF3-PBX1) subtype (p<0.03) than other genetic subtypes. 21152005 2010
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE This study revealed that e.g., the t(12;21) [ETV6-RUNX1] subtype of ALL and the t(15;17) [PML-RARA] subtype of AML had transcriptional programs similar to those in normal Pro-B cells and promyelocytes, respectively. 20211010 2010
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE These frequencies were lower than those reported in the West, leading us to conduct a meta-analysis of ETV6-RUNX1 fusion and hyperdiploidy frequencies in childhood ALL based on published reports. 20658612 2010
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE We performed genome-wide methylation profiling using bacterial artificial chromosome arrays and promoter-specific analyses of high hyperdiploid and ETV6/RUNX1-positive ALLs. 19679565 2009
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE Compared to Europe, the ALL population in Nicaragua is older, has a higher proportion of poor prognostic clinical and hematological features and receives more intensive treatment, while patients with TEL/AML1 translocations and high-hyperdiploidy are clinically in the standard risk group. 19672974 2009
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE Chromosomal abnormalities, such as t(9;22)(q34;q11) (ABL/BCR), t(12;21)(p13;q22) (TEL/AML1), and t(11q23) (MLL) are independent prognostic indicators in childhood acute lymphoblastic leukemia resulting in risk adapted therapy. 19875970 2009
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE In the current study (26 cases), the frequencies of the most frequent genetic rearrangements TEL-AML1, MLL/AF4, BCR-ABL (major and minor) in ALL in children from Mexico City were determined. 19579075 2009
Childhood Acute Lymphoblastic Leukemia
0.400 GeneticVariation disease BEFREE The TEL-AML1 gene fusion, the hallmark translocation in Childhood Acute Lymphoblastic Leukemia and the first hit, occurs years before the clinical disease, most often in utero. 19570513 2009
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Cluster analysis of genomic ETV6-RUNX1 (TEL-AML1) fusion sites in childhood acute lymphoblastic leukemia. 19081626 2009
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE AML1 amplification is a common finding in childhood ALL, and itis observed as an increase in gene copy number by the FISH analysis. 19927343 2009
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Our data together with published results on TEL/AML1 positive ALL suggest that frequencies of additional TEL and AML1 mutations are, with the exception of loss of untranslocated TEL, higher in first relapses than in initial disease. 19594616 2009
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Chromosome translocation to generate the TEL-AML1 (also known as ETV6-RUNX1) chimeric fusion gene is a frequent and early or initiating event in childhood acute lymphoblastic leukemia (ALL). 19287094 2009
Childhood Acute Lymphoblastic Leukemia
0.400 Biomarker disease BEFREE Therefore, the use of HdI in the differentiation of leukemic DC from patients with TEL/AML1-positive ALL is recommended. 19129484 2009