|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
WW domain binding protein 1-like (WBP1L), also known as outcome predictor of acute leukaemia 1 (OPAL1), is a transmembrane adaptor protein, expression of which correlates with ETV6-RUNX1 (t(12;21)(p13;q22)) translocation and favourable prognosis in childhood leukaemia.
|
31845480 |
2020 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
The modification of this translocation may lead to reducing effects of the fusion gene's damaging and the dosage compensation related to ETV6 and RUNX1 genes and subsequently reduce the effects of leukemia.
|
31602594 |
2020 |
|
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Protein lysine 43 methylation by EZH1 promotes AML1-ETO transcriptional repression in leukemia.
|
31699991 |
2019 |
|
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In survival analyses based on LinkedOmics, higher expression of RUNX1 and RUNX2 indicated a better overall survival (OS), but with no significance, whereas increased RUNX3 revealed a poor OS in leukemia.
|
30719500 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Co-expression of two mutant genes increased myeloid stem cells in animal model, suggesting that cooperation of RUNX1 and ASXL1 mutations played a critical role in leukemia transformation.
|
31640815 |
2019 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
A 4-log-stage linearity of R2 ≥ 99.81% and a sensitivity of one leukemia associated ETV6-RUNX1 mutant DNA copy in a background of 100 000 wild-type DNA copies are achieved.
|
31139783 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Most importantly, MLT reduced the infiltration of leukaemia blasts, decreased the frequency of leukaemia stem cells (LSCs) and prolonged the overall survival in AML1-ETO-induced murine leukaemia.
|
31119862 |
2019 |
|
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 |
AML1-ETO (AE) is a fusion transcription factor, generated by the t(8;21) translocation, that functions as a leukemia promoting oncogene.
|
31664040 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Inhibition of autophagy by hydroxychloroquine, a well-tolerated autophagy inhibitor, reduced cell viability in both ETV6-RUNX1-positive cell lines and primary acute lymphoblastic leukemia samples, and selectively sensitized primary ETV6-RUNX1-positive leukemia samples to L asparaginase.
|
30381299 |
2019 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Second, in a small fraction of these cases, the postnatal acquisition of secondary genetic changes (primarily V(D)J recombination-activating protein (RAG) and activation-induced cytidine deaminase (AID)-driven copy number alterations in the case of ETS translocation variant 6 (ETV6)-runt-related transcription factor 1 (RUNX1)<sup>+</sup> ALL) drives conversion to overt leukaemia.
|
29784935 |
2018 |
|
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
R-E dominance negatively inhibits global gene expression regulated by RUNX1, a master transcription factor for hematopoiesis, causing increased self-renewal and blocked cell differentiation of hematopoietic progenitor cells, and eventually leukemia initiation.
|
29721072 |
2018 |
|
leukemia
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Our data suggest that miR-130a is directly activated by AML1/ETO, and may act as a factor which is associated with leukemia burden, event-free survival, and chemotherapy sensitivity in t(8;21) AML.
|
29493383 |
2018 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Normal CBF function is essential for activity of AML1-ETO, product of the t(8;21), and for survival of several leukemias lacking RUNX1 mutations.
|
29249175 |
2018 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
In contrast, chromosomal translocations involving RUNX1 are detectable in utero, suggesting an initiating role in leukemias.
|
29052866 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
In addition, recent studies reported by us and other groups suggested that WT RUNX1 is needed for survival and proliferation of certain types of leukemia.
|
29883054 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our data demonstrate that RUNX1/ETO maintains leukemia by promoting cell cycle progression and identifies G1 CCND-CDK complexes as promising therapeutic targets for treatment of RUNX1/ETO-driven AML.
|
30300583 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Deletions affecting the transcriptional coregulator BTG1 are frequently observed in ETV6-RUNX1-positive leukemia.
|
29408281 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our previous study demonstrated that HDAC inhibitor phenylbutyrate (PB) could induce AML1-ETO positive leukemia cell line Kasumi-1 cells to undergo differentiation and apoptosis accompanied by significant changes in gene expression profile.
|
29518627 |
2018 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Lympho-myeloid restricted early thymic progenitors (ETPs) are postulated to be the cell of origin for ETP leukemias, a therapy-resistant leukemia associated with frequent co-occurrence of EZH2 and RUNX1 inactivating mutations, and constitutively activating signaling pathway mutations.
|
29438697 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest that chromosomal rearrangements may activate RUNX1 by perturbing its transcriptional control to contribute to AML pathogenesis, in keeping with an emerging oncogenic role of RUNX1 in leukemia.
|
30157851 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Disruption of VPS13B may thus cause the unusual features of RUNX1-RUNX1T1 leukemia.
|
29264741 |
2018 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings suggest ETV6-RUNX1 is associated with space-time clustering of CL and are consistent with an infection interacting with that oncogene in early life leading to clinical leukemia.
|
28129329 |
2017 |
|
leukemia
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Our findings represent the first characterization of this CASC15 in RUNX1-translocated leukemia, and point towards a mechanistic basis for its action.
|
28724437 |
2017 |
|
leukemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus, deregulation of both AML1 and Notch target genes is required for the development of AE9a-driven leukemia.
|
28360416 |
2017 |