|
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Taken together, this study identifies SPIB as an important target of ETV6-RUNX1 in regulation of B-cell gene expression in t(12;21) leukemia.
|
30986496 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The most frequent chromosomal changes in subgroups divided according to WHO classification independent of treatment protocol and leukemia subtype were hyperdiploidy in 36 patients (with ≥50 chromosomes in 23 patients, with 47-49 chromosomes 13 patients) followed by translocation t(12;21) with ETV6/RUNX1 fusion detected by FISH in 18 (22%) patients.
|
27341996 |
2017 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Secondary chromosomal aberrations are necessary for development of overt leukemia in t(12;21)/ETV6-RUNX1-positive acute lymphoblastic leukemia (ALL).
|
27215399 |
2016 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
It is well-known that development of overt leukemia in t(12;21)-positive ALL requires secondary chromosomal aberrations although the full spectrum of these cytogenetic alterations is yet unsettled, and also, how they may be associated with disease outcome.
|
27664585 |
2016 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Interrogation of expression databases of 257 ALL samples demonstrated the specific down-regulation of the SPIB and IKZF3 genes (the latter encoding AIOLOS) in t(12;21) ALL, providing novel insight into the mechanism by which the translocation blocks B-cell development and promotes leukemia.
|
23704093 |
2013 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Although infant cases with t(12;21) did not display specific genetic abnormalities explaining the short latency to overt leukemia, the frequency of copy number abnormalities increased proportionally with age.
|
19665068 |
2009 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In the BCP group, cases with t(12;21) were characterized by a low MVD while patients with high-hyperdiploid leukaemia (HeH, 51-61 chromosomes) showed a high MVD compared to other BCP patients (P = 0.001 and 0.002 respectively).
|
19594745 |
2009 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Among them, the testis-specific SPANXB gene was the only one showing a high and uniform overexpression, irrespective of gender and presence of Xq duplication, suggesting that this gene plays an important pathogenetic role in t(12;21)-positive leukemia.
|
17690704 |
2007 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Further research is needed to explore whether the 2 to 7 years age incidence peak in childhood ALL harbor yet unidentified cytogenetic subsets with the same natural history as the high-hyperdiploid and t(12;21)-positive leukemias.
|
16912588 |
2006 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Genomic breakpoints in all the common chromosome translocations in leukemia, including t(4;11), t(9;11), t(8;21), inv(16), t(15;17), t(12;21), t(1;19) and t(9;22), have been cloned.
|
16893685 |
2006 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Translocations t(8;21) and t(12;21) have been shown to occur in the normal population (before birth) at a frequency that is 100-fold greater than the risk of developing the corresponding leukemia.
|
15054823 |
2004 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Analysis of additional cases of leukemia with translocations involving the MYC locus on 8q24 will be required to determine the frequency of association with the cryptic t(12;21)(p13;22), and the prognostic significance of the simultaneous occurrence of the translocations.
|
11106815 |
2000 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The FISH method clearly demonstrated that all patients with the TEL/AML1 fusion had subpopulations of leukemic cells with deletion of the normal TEL allele, which is significant for understanding the progression of leukemia with t(12;21).
|
9738986 |
1998 |
|
leukemia
|
0.100 |
AlteredExpression
|
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 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The t(8;21) creates a fusion protein between AML-1 and a gene of unknown function, mtg8 (ETO), whereas the t(12;21) fuses the TEL (translocation-ets-leukemia) transcription factor to the N-terminus of AML-1.
|
8834231 |
1995 |