|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The data reveal a strong association of t(12;21) with B-cell precursor ALL, especially with myeloid marker expression.
|
11129441 |
2000 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Although the true pathogenetic significance of the mutations must await future functional evaluations, this study provides a first estimate of the mutational burden at the genetic level of t(12;21)-positive childhood ALL.
|
22094584 |
2012 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Half of the karyotypically "normal" ALL cases examined have been found to have abnormal clones with t(12;21) rearrangement and/or hyperdiploidy by this specially designed FISH assay.
|
12847317 |
2003 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In this study, bone marrow samples from 30 children with ALL from southern Brazil were evaluated by fluorescence in situ hybridization (FISH) for the t(12;21), using locus specific probes to detect the TEL/AML1 rearrangement.
|
15289014 |
2004 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The TEL-AML1 fusion gene, created by the t(12;21), is the most common genetic alteration in childhood acute lymphoblastic leukemia and is associated with a favorable outcome.
|
10049061 |
1999 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Thus we conclude that the TEL allele not involved in t(12;21) is inconstantly lost in patients with this subtype of ALL and occurs on the 12p- chromosome.
|
8558923 |
1996 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Sequencing analysis of >1,000 pediatric cancer genomes identified the NSD2 p.E1099K alteration in 14% of t(12;21) ETV6-RUNX1-containing ALLs.
|
24076604 |
2013 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In order to characterize the incidence of the t(12;21) at both the chromosomal level as well as the RNA transcript level, we have used a combination of classical cytogenetics, reverse transcriptase-polymerase chain reaction (RT-PCR), and fluorescence in situ hybridization (FISH) to examine the bone marrow of 34 children diagnosed with B-cell precursor ALL.
|
8913730 |
1996 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
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
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Microarray-based identification of several translocations has been performed in acute lymphoblastic leukemia (ALL), leading to the discovery of t(1;19), t(12;21), and 11q23 translocations, and in acute myeloid leukemia (AML), finding t(8;21), inv(16), and t(15;17).
|
14704033 |
2003 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
These results provide mechanistic insight into the role of the t(12;21) translocation in the initiation of common B cell precursor ALL.
|
15155899 |
2004 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The mRNA levels of AS between t(12;21)(-) ALL and healthy controls did not differ.
|
12433682 |
2003 |
|
Childhood Acute Lymphoblastic Leukemia
|
0.100 |
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
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Patients with standard-risk ALL, who received the longest maintenance therapy, had the highest adjusted hazard of second cancer (hazard ratio [HR], intermediate vs. standard risk: 0.16, 95% CI: 0.06-0.43, P < 0.001; HR, high vs. standard risk: 0.09, 95% CI: 0.02-0.49, P = 0.006); no significant effects of protocol, age, or white blood cell count at diagnosis, ALL HeH, or t(12;21)[ETV6/RUNX1] were observed.
|
28500740 |
2017 |
|
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 |
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 |
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 |
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 |
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 |
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 |