CD6, CD6 molecule, 923

N. diseases: 216; N. variants: 8
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE Childhood acute lymphoblastic leukemia (ALL) with t(12;21), which results in expression of the ETV6/RUNX1 fusion gene, is the most common chromosomal lesion in precursor-B (pre-B) ALL. 26580398 2015
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE Forty-one of the patients had chromosome 21 abnormalities, including t(8;21) in 6 of the patients with AML, t(12;21) in 8 patients with ALL, acquired trisomy 21 in 17 patients, tetrasomy 21 in 7 patients, and constitutional trisomy 21 (Down syndrome) in 3 patients. 11023523 2000
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE The data demonstrate that nested-RT-PCR is a suitable tool for diagnosing t(12;21)-positive ALL, that these patients constitute a clinically distinct subgroup of ALL patients, and that the method could also be used to monitor MRD in these patients. 10774753 2000
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE This includes cell lines derived from patients with relapsed disease featuring cytogenetic anomalies such as t(12;21), Philadelphia chromosome t(9;22), t(1;19) as well as a cell line carrying t(17;19) from a patient with de novo ALL. 21960246 2012
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE It also stratified patients with high hyperdiploidy and t(12;21) ALL into 2 subgroups with different probability of relapse. 19965625 2010
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE The t(12;21) translocation is the most common reciprocal chromosomal rearrangement in pediatric acute lymphoblastic leukemia (ALL). 12621238 2003
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE The overall incidence of the t(12;21) in pediatric ALL is 18.9%. 9226156 1997
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE A total of 69 patients of B lineage ALL, 35 children (32 males, 3 females) and 34 young adults (27 males, 7 females) were studied by multiplex RT-PCR to determine the relative frequency of t(9;22), t(12;21), t(1;19), and t(4;11,). 15114604 2004
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE The fusion protein TEL-AML1 in t(12;21)+ acute lymphoblastic leukemia (ALL) recruits co-repressors and histone deacetylases (HDAC), which transrepress AML1 target genes. 16330447 2005
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE Notably, the t(12;21) translocation leading to an ETV6-AML1 fusion gene is the most common genetic alteration found in childhood acute lymphoblastic leukemia. 30341373 2018
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE TEL-AML1 fusion oncogene (t 12; 21) is the most common chromosomal abnormality in childhood acute lymphoblastic leukemia (ALL). 24870754 2014
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE Majority of the patients had<br /> pre-B-cell ALL (88.7%), WBC count <50, 000/μL at diagnosis (76.1%, median = 13.5/μL with a range of 0.51-553.0/<br /> μL) with involvement of central nervous system (CNS) disease in 8.5%patients.Different common chromosomal<br /> anomalies or abnormalities, including t(12, 21) translocation, MLL genre arrangements, trisomy (4, 10, 17)and others,<br /> were detected. 31759364 2019
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE Genes that were differentially expressed between BCP ALL subtypes were enriched to distinct signaling pathways with dic(9;20) enriched to TP53 signaling, t(9;22) to interferon signaling, as well as high hyperdiploidy and t(12;21) to apoptosis signaling. 22173241 2012
Childhood Acute Lymphoblastic Leukemia
0.100 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
0.100 GeneticVariation disease BEFREE Recent technical improvements in the detection of such aberrations have demonstrated that the previously unrecognized chromosomal translocation t(12;21) is the most prevalent structural aberration in childhood acute lymphoblastic leukemia. 10084082 1999
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE In order to investigate whether the t(12;21) could give a molecular clue as to the precise basis of the etiologic association between DS and acute lymphoblastic leukemia, we tested a series of 11 consecutive cases of ALL in DS children for the presence of the TEL/AML1 transcript, by RT-PCR analysis. 9177434 1997
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE These data show the coexistence of multiple genetic defects in childhood B-lineage ALL Cell lines with t(12;21) will facilitate the study of TEL-AML1 and AML1-TEL fusion proteins as well as TEL and CDKN2 gene inactivation in leukemia transformation and progression. 8704231 1996
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE The t(12;21) translocation is the most common genetic rearrangement in childhood acute lymphoblastic leukemia (ALL) and gives rise to the TEL-AML1 fusion gene. 25893288 2015
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE The results show that rearrangements of 6p are also non-random events t(12;21)-positive ALL. 17418891 2008
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE Only children with B-lineage ALL who lack these abnormalities detected by conventional cytogenetics will probably benefit from additional testing by molecular methods to detect the t(12;21). 10482981 1999
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE We studied the relation between t(12;21), determined by fluorescence in situ hybridization or polymerase chain reaction, and in vitro drug resistance, measured by the MTT assay, in childhood B-lineage ALL at diagnosis. 10910927 2000
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE The modal chromosome numbers, incidence, types, and numbers of additional abnormalities, genomic imbalances, and chromosomal breakpoints in the 245 karyotypically informative cases, as well as in 152 previously reported cytogenetically characterized t(12;21)-positive ALLs in the same age group, were ascertained. 17285576 2007
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE Eleven patients with pro-B cell or B cell type ALL (9 children with ALL, 2 adults with ALL) had numerical changes of chromosome 21 (gain 1 or 2 chromosome 21), among them, 10 patients had no structural alteration of chromosome 21, and one was combined by t (12; 21). 14527352 2003
Childhood Acute Lymphoblastic Leukemia
0.100 Biomarker disease BEFREE Fluorescence in situ hybridization (FISH) analysis was applied to detect t(12;21) using two yeast artificial chromosome probes and cosmid probes covering the TEL(ETV6) and the AML1 gene to clarify the incidence of abnormality of t(12;21) in Japanese childhood acute lymphoblastic leukemia (ALL). 9738986 1998
Childhood Acute Lymphoblastic Leukemia
0.100 GeneticVariation disease BEFREE We report that fusion of TEL to AML1 is specifically observed in at least 16% of the childhood B-lineage acute lymphoblastic leukemia (ALL) investigated, none of which had been previously identified as harboring t(12;21). 7492786 1995