Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
This requires the EZH1 SET domain, which augments AML1-ETO-dependent repression of tumor suppressor genes.
|
31699991 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Furthermore, we demonstrated that NASP depletion led to a global decrease of histone H3K9me1 modification associated with newly H3 processing, which occurred directly at the promoters of up-regulated anti-tumor genes BACH2 and RunX1T1.
|
30076957 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
CSF2RA, the gene encoding the α-subunit for GM-CSF, is significantly downregulated in t(8;21) (RUNX1-ETO or RE) leukemia patients, suggesting that it may serve as a tumor suppressor.
|
27389055 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We present evidence of an interplay between the tumor suppressor miR-29b-1 and the AML1-ETO (also designated RUNX1-RUNX1T1) oncogene that is encoded by the t(8;21).
|
28611288 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
RUNX1t1 is a C/EBPβ-associated tumor suppressor.
|
27522676 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data revealed a novel role for RUNX1T1 as a tumor-suppressor gene in CRC through modulation of multiple cellular pathways.
|
27798886 |
2016 |
Neoplasms
|
0.100 |
PosttranslationalModification
|
group |
BEFREE |
Our study identifies miR-193a and PTEN as targets for AML1/ETO and provides evidence that links the epigenetic silencing of tumor suppressor genes miR-193a and PTEN to differentiation block of myeloid precursors.
|
23223432 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
By focusing on the anti-apoptotic gene Bcl-2, the key regulator gene of granulocytic differentiation CCAAT/enhancer-binding protein α (CEBPA) and the tumor suppressor gene p14(ARF), we found that both AML1-ETO-expressing cell lines and t(8;21) leukemia samples displayed low levels of these three genes.
|
23673926 |
2013 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ΔAML1-ETO interacted with AML1-ETO and interfered with the trans-regulatory functions of remaining AML1-ETO oncoprotein, thus acting as a tumor suppressor that mediates the anti-leukemia effect of oridonin.
|
22461642 |
2012 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our gain- and loss-of-function experiments showed that miR-126/126* inhibited apoptosis and increased the viability of AML cells and enhanced the colony-forming ability of mouse normal bone marrow progenitor cells alone and particularly, in cooperation with AML1-ETO, likely through targeting Polo-like kinase 2 (PLK2), a tumor suppressor.
|
18832181 |
2008 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Each set of tumors shared a common clonal origin, as demonstrated by expression of identical, unique CDR IIIH sequences, shared somatic mutations in JH, and identical bcl-2 translocation breakpoints of microdissected ALL cells.
|
16966263 |
2006 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We found that AML1-ETO repressed the promoter of p14(ARF) tumor suppressor in transient transfection assays and reduced endogenous levels of p14(ARF) expression in multiple cell types.
|
12732181 |
2004 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Depletion of AML1/MTG8 correlates with an increased susceptibility of both Kasumi-1 and SKNO-1 cells to tumor growth factor beta(1) (TGF beta(1))/vitamin D(3)-induced differentiation, leading to increased expression of CD11b, macrophage colony-stimulating factor (M-CSF) receptor, and C/EBP alpha (CAAT/enhancer binding protein).
|
12480707 |
2003 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Because rearrangements of the 8q11-q13 region involving the PLAG1 gene have been described in lipoblastoma-another kind of benign adipose tumor--we used fluorescence in situ hybridization analysis to determine in the present case the chromosomal breakpoint on 8q was located between the ETO (8q22) and COX6C (8q22-q23) genes at a great distance from PLAG1.
|
11943344 |
2002 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
The t(8;21) fusion protein, AML1 ETO, specifically represses the transcription of the p14(ARF) tumor suppressor in acute myeloid leukemia.
|
12091906 |
2002 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Only retrospectively, using RT-PCR, did we detect the acute myeloid leukemia subset-specific fusion gene AML1/ETO in the frozen samples of the relapsed tumor, as well as in the otherwise unaffected bone marrow and peripheral blood (representing 'minimal initial disease' in the latter two samples).
|
11684288 |
2001 |
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Our results show that expression of a chimeric transcription factor encoded by the tumor related chromosomal translocation (8;21) involving the AML1 and ETO loci is sufficient to cause reorganization of PML domains.
|
10906759 |
2000 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data, which suggest that the MTG8 protein could be one of the tumour antigens recognized by CTLs, may be helpful in further investigations of TCR analysis in t(8;21) AML patients with HLA-A0201 who are in long-term remission.
|
11122105 |
2000 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
ETO-expressing cells grew to higher saturation densities and induced tumors following injection into irradiated and splenectomized nude mice.
|
9230207 |
1997 |