|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
A unique feature was the detection of a specific chromosomal deletion at 1p32 involving the tal-1 gene, an abnormality previously described only in aggressive T-cell neoplasms.
|
7604814 |
1995 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Among the quiescent genes activated by rearrangement, expression of cyclin D1 (due to rearrangement of the CCND1 [BCL-1] gene) is a near-specific marker of t(11;14) in mantle cell lymphoma; BCL-2 expression distinguishes follicular lymphoma cells from their nonneoplastic counterparts in reactive germinal centers and appears to be an independent prognostic marker in diffuse large cell lymphoma; and TAL-1 (SCL) expression identifies T-cell acute lymphoblastic neoplasms in which this gene is activated.
|
11781220 |
2002 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Collectively, our findings provide initial evidence for a novel role of FOXP3 as a tumor suppressor in T-ALL through modulation of TAL1 transcriptional activity.
|
26686090 |
2016 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Evaluation of the expression of three T-cell malignancy associated genes showed that Rhombotin-2 (RBTN-2 also known as Lmo-2), TAL-1 (also known as SCL), and HOX-11 were expressed in 100%, 40%, and 0% of the murine tumors, respectively.
|
9116269 |
1997 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Five fusions found exclusively in tumour samples could be considered pathogenic (NFYG-TAL1, RIC3-TCRBC2, SLC35A3-HIAT1, PICALM MLLT10 and MLLT10-PICALM).
|
30914738 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, in vitro analysis of primary patient samples indicated that some immature, TLX3- or HOXA-positive primary T-ALLs are highly sensitive to BCL-2 inhibition, whereas TAL1 driven tumors mostly showed poor ABT-199 responses.
|
25301704 |
2014 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In this review, we focus on the oncogenic transcription factor TAL1 and the tumor-suppressor E-proteins and discuss the malignant cell state, the transcriptional circuit, and the consequence of molecular abnormalities in T-ALL.
|
28652130 |
2017 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, we show that, in human TAL1-expressing T-ALL cell lines, TAL1 directly activates NKX3.1, a tumor suppressor gene required for prostate stem cell maintenance.
|
20855495 |
2010 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Overexpression of miR-223 also leads to marked down-regulation of FBXW7 protein expression, whereas knockdown of TAL1 leads to up-regulation of FBXW7 protein levels, with a marked reduction of its substrates MYC, MYB, NOTCH1, and CYCLIN E. We conclude that TAL1-mediated up-regulation of miR-223 promotes the malignant phenotype in T-ALL through repression of the FBXW7 tumor suppressor.
|
23857984 |
2013 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The data also provide formal proof that TAL1 is an oncogene, apparently acting as a tumour promoter in this system.
|
8605871 |
1996 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
These results are further supported by low level expression of SCL in these tumors (as assessed by a polymerase chain-reaction-based method).
|
1625484 |
1992 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
We sequenced the heterodimerization domain and the PEST domain of Notch1 in our mouse model of TAL1-induced leukemia and found that 74% of the tumors harbor activating mutations in Notch1.
|
16166587 |
2006 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Whereas the tumors which arise in SCL/LMO1 double transgenic mice are typically diploid or pseudodiploid, the cell lines were all grossly aneuploid, suggesting the possibility that additional genetic events were selected for in vitro.
|
11243382 |
2001 |