|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.130 |
Biomarker
|
disease |
BEFREE |
Understanding inflammation in the context of BET protein regulation may provide a basis for designing promising therapeutics for T2D and breast cancer.
|
27491296 |
2017 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.130 |
GeneticVariation
|
disease |
GWASDB |
A genome-wide association study in American Indians implicates DNER as a susceptibility locus for type 2 diabetes.
|
24101674 |
2014 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.130 |
Biomarker
|
disease |
BEFREE |
SUMMARY: BETonMACE will determine whether the addition of the selective BET protein inhibitor apabetalone to contemporary standard of care for ACS reduces cardiovascular morbidity and mortality in patients with type 2 diabetes.Results are expected in 2019.
|
31520897 |
2019 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.130 |
Biomarker
|
disease |
BEFREE |
These studies implicate DNER as a susceptibility gene for T2DM in American Indians.
|
24101674 |
2014 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.130 |
GeneticVariation
|
disease |
GWASCAT |
A genome-wide association study in American Indians implicates DNER as a susceptibility locus for type 2 diabetes.
|
24101674 |
2014 |
|
Autistic Disorder
|
0.100 |
GeneticVariation
|
disease |
GWASDB |
Individual common variants exert weak effects on the risk for autism spectrum disorders.
|
22843504 |
2012 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Here, we demonstrate that AMPK maintains the epigenome of MLL-rearranged AML by linking acetyl-coenzyme A (CoA) homeostasis to Bromodomain and Extra-Terminal domain (BET) protein recruitment to chromatin.
|
31697807 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
These findings provide novel insight on how BET inhibitor can induce apoptosis in AML, and further support the development of BET inhibitors as a promising therapeutic strategy against AML.
|
29996811 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Bromodomain and extra-terminal (BET) protein inhibitors have been reported as treatment options for acute myeloid leukemia (AML) in preclinical models and are currently being evaluated in clinical trials.
|
29491412 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
This finding may guide pharmacological treatment to enhance the clinical utility of such targeted therapies in AML and potentially other BET proteins-driven diseases.
|
31266503 |
2019 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Interestingly, Mll3-suppressed leukemias, like human -7/del(7q) AMLs, are refractory to conventional chemotherapy but sensitive to the BET inhibitor JQ1.
|
24794707 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Here, we demonstrate the sensitizing effects of the histone hyperacetylation-inducing pan-histone deacetylase (HDAC) inhibitor panobinostat on human acute myelogenous leukemia (AML) blast progenitor cells (BPC) to the BET protein antagonist JQ1.
|
24435446 |
2014 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
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
|
0.100 |
Biomarker
|
disease |
BEFREE |
The bromodomain and extraterminal (BET) protein BRD4 is a therapeutic target in acute myeloid leukemia (AML).
|
26626481 |
2015 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Treatment with a BET inhibitor resulted in significant antitumor activity in xenograft models of Burkitt's lymphoma and acute myeloid leukemia.
|
21949397 |
2011 |
|
Leukemia, Myelocytic, Acute
|
0.100 |
Biomarker
|
disease |
BEFREE |
Moreover, treatment with BET protein inhibitor or degrader (BET-proteolysis targeting chimera) repressed RUNX1 and its targets, inducing apoptosis and improving survival of mice engrafted with AML expressing mtRUNX1.
|
31023702 |
2019 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Herein our results expanded the understanding of the mechanism for BET inhibitors OTX015 in MM.
|
30048594 |
2018 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We explored the transcriptional and functional interrelationship between E2F transcription factors and BET transcriptional co-activators in multiple myeloma.
|
30590042 |
2018 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Efficacy of JQ1 in three murine models of multiple myeloma establishes the therapeutic rationale for BET bromodomain inhibition in this disease and other malignancies characterized by pathologic activation of c-Myc.
|
21889194 |
2011 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The BET bromodomain inhibitor CPI203 improves lenalidomide and dexamethasone activity in <i>in vitro</i> and <i>in vivo</i> models of multiple myeloma by blockade of Ikaros and MYC signaling.
|
28751557 |
2017 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Pharmacologic inhibition of BET protein binding has been shown to inhibit tumor growth in MYC-dependent cancers, such as multiple myeloma.
|
26253517 |
2015 |
|
Multiple Myeloma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The homeobox transcription factor MEIS2 is a regulator of cancer cell survival and IMiDs activity in Multiple Myeloma: modulation by Bromodomain and Extra-Terminal (BET) protein inhibitors.
|
30975979 |
2019 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our studies further underscored that the BET inhibitor OTX015 sensitized MM cells by interrupting several pathways and genes critical for MM cell proliferation and drug response, which provided the rationale for multiple myeloma therapy with OTX015 combined with conventional chemotherapeutic drugs.
|
30339013 |
2018 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We found that treatment of human multiple myeloma (MM) cells with the small-molecular inhibitor of BET bromodomains, (+)-JQ1, selectively downregulated <i>MYC</i> transcription, which is similar to what was reported in the original study (Figure 3B; Delmore et al., 2011).
|
28100400 |
2017 |
|
Multiple Myeloma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Collectively, these data qualify BMI-1 as a candidate for targeted therapy in MM alone or in combinations with epigenetic inhibitors directed to PRC2/EZH2 or BET bromodomains.
|
29262596 |
2017 |