Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, LINC00319 expression was demonstrated proportional to MYC level in AML samples and transcriptionally regulated by MYC.
|
30587342 |
2019 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Glycogen synthase kinase-3 (GSK-3) and protein phosphatase 2A (PP2A) are two crucial signaling molecules involved in the AML pathogenesis and MYC stability.
|
31623866 |
2019 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Global transcriptomic analysis revealed that POLR2A knockout strongly impaired growth of AML cells by selectively depleting a substantial set of AML-related oncogenic and anti-apoptosis genes such as MYC, RUNX2, MEIS1, CDC25A and BCL-2.
|
31574286 |
2019 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
This mechanism is also operative in human AML patients where low RBM25 levels are associated with high MYC activity and poor outcome.
|
30635567 |
2019 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
We conclude that MYC immunopositivity is an important prognostic factor in patients with untreated AML, particularly those at higher risk for relapse.
|
29741984 |
2019 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Acute Myeloid Leukemia (AML): Upregulation of BAALC/MN1/MLLT11/EVI1 Gene Cluster Relate With Poor Overall Survival and a Possible Linkage With Coexpression of MYC/BCL2 Proteins.
|
28362701 |
2018 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia.
|
29958106 |
2018 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Correction to: MYC-dependent downregulation of telomerase by FLT3 inhibitors is required for their therapeutic efficacy on acute myeloid leukemia.
|
29744585 |
2018 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Collectively, PKC412 downregulates hTERT expression and telomerase activity in a MYC-dependent manner and this effect is required for its optimal anti-AML efficacy, while hTERT over-expression confers AML cells resistance to a targeted therapeutic agent PKC412.
|
29080039 |
2018 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Highest expression of MYC was noted in AML patients with favourable cytogenetic risk group.
|
26856970 |
2017 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The expression levels of some markers for AML subtypes and c-MYC regulated genes were considered potential predictors of response to ADI-PEG20.
|
28900115 |
2017 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Altogether, we discovered a novel molecular mechanism mediating the GM-CSF-induced reduction in leukemic potential of RE cells, and our findings support MYC inhibition as an effective strategy for reducing the leukemogenicity of t(8;21) AML.
|
27389055 |
2017 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
The recent discovery that epigenetic readers of the bromodomain (BRD) and extraterminal (BET) protein family, are crucial for AML maintenance by transcription of oncogenic c-MYC lead to rapid development of BET inhibitors entering clinical trials.
|
28541716 |
2017 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Here we show that acute myeloid leukemia (AML) cells require the BRD9 subunit of the SWI-SNF chromatin-remodeling complex to sustain MYC transcription, rapid cell proliferation and a block in differentiation.
|
27376689 |
2016 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Studies showed that miR-17-92 cluster regulation was, surprisingly, independent of transcription factors c-MYC and E2F in these cells; instead all-trans-retinoic acid (ATRA), a drug used for terminally differentiating AML subtypes, markedly suppressed miR-17-92 expression and increased PHLPP2 protein levels and phosphatase activity.
|
26868909 |
2016 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Collectively, our data reveal a previously unappreciated signaling pathway involving the MLL-fusion/MYC⊣miR-26a⊣TET1 signaling circuit, in which miR-26a functions as an essential tumor-suppressor mediator and its transcriptional repression is required for the overexpression and oncogenic function of TET1 in MLL-rearranged AML.
|
26791235 |
2016 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
CTD_human |
JQ1, a bromodomain and extra-terminal bromodomain inhibitor, demonstrated both in vitro and in vivo efficacy against several MYC-overexpressing AMLs.
|
25956709 |
2015 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Herein we present a case of AML with MYC amplification in marker chromosomes and a microdeletion of chromosome 7 below cytogenetic resolution.
|
25800664 |
2015 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
Overexpression of GYS1, MIF, and MYC is associated with adverse outcome and poor response to azacitidine in myelodysplastic syndromes and acute myeloid leukemia.
|
25487600 |
2015 |
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Acute myeloid leukemia with MYC rearrangement and JAK2 V617F mutation.
|
26382622 |
2015 |
Leukemia, Myelocytic, Acute
|
0.400 |
AlteredExpression
|
disease |
BEFREE |
Increased expression of c-MYC is observed in both Acute Myeloid Leukemia (AML) and T-cell Acute Lymphoblastic Leukemia (T-ALL).
|
26517351 |
2015 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
JQ1, a bromodomain and extra-terminal bromodomain inhibitor, demonstrated both in vitro and in vivo efficacy against several MYC-overexpressing AMLs.
|
25956709 |
2015 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
To review 5 important recent advances in hematopathology: (1) detection and prognostic implication of MYC in diffuse large B-cell lymphomas, (2) determining origin and prognosis through immunoglobulin gene usage in mature B-cell neoplasms, (3)detecting minimal residual disease in multiple myeloma, (4) using genome-wide analysis in myelodysplastic syndromes, and (5) employing whole-genome sequencing in acute myeloid leukemias.
|
24576034 |
2014 |
Leukemia, Myelocytic, Acute
|
0.400 |
Biomarker
|
disease |
BEFREE |
SIRT1 activation by a c-MYC oncogenic network promotes the maintenance and drug resistance of human FLT3-ITD acute myeloid leukemia stem cells.
|
25280219 |
2014 |
Leukemia, Myelocytic, Acute
|
0.400 |
GeneticVariation
|
disease |
BEFREE |
Highly activated SYK is predominantly found in FLT3-ITD positive AML and cooperates with FLT3-ITD to activate MYC transcriptional programs.
|
24525236 |
2014 |