Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
It demonstrated that DNER could enhance the proliferation and metastasis of breast cancer cells in vitro and significantly increases tumor growth in vivo.
|
31408676 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In PDA cells, growth factors promote AKT-ACLY signaling and histone acetylation, and both cell proliferation and tumor growth can be suppressed by concurrent BET inhibition and statin treatment.
|
30626590 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The optimized dimethylisoxazole aryl-benzimidazole inhibitor exhibited high potency towards BRD4 and related BET proteins in biochemical and cell-based assays and inhibited tumor growth in two proof-of-concept preclinical animal models.
|
30606676 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Alterations in transcriptional programs promote tumor development and progression and are targetable by bromodomain and extraterminal (BET) protein inhibitors.
|
30610113 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In a MV4-11 mouse xenograft model, 47 caused 67% of tumor growth inhibition and was less toxic than a pan BET inhibitor 1 at high doses.
|
31461688 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Experimental data have demonstrated the involvement of some BET proteins in many pathological conditions, including tumor development, infections, autoimmunity, and inflammation.
|
31780938 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
To this end, the mechanisms by which BET proteins regulate chromatin remodeling and promote tumor-associated inflammation have been heavily studied over the past decade.
|
30832981 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Disrupting MLV integrase:BET protein interaction biases integration into quiescent chromatin and delays but does not eliminate tumor activation in a MYC/Runx2 mouse model.
|
31815961 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In this study, we explore new strategy to overcome BET inhibitor resistance in MPNST.<b>Experimental Design:</b> Through modeling tumor evolution by studying genetic changes underlying the development of MPNST, a lethal sarcoma with no effective medical treatment, we identified a targetable addiction to BET bromodomain family member BRD4 in MPNST.
|
30796033 |
2019 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Work is ongoing to determine the role of visceral adiposity in c-Myc activity in several tissues and determine the inhibitory effect of I-BET on VAT-promoted tumors <i>in vivo</i><i>Cancer Prev Res; 11(3); 129-42.
|
29246955 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Combining BET and MEK inhibitors synergistically curbed the growth of <i>NRAS</i>-mutant melanoma and prolonged the survival of mice bearing tumors refractory to MAPK inhibitors and immunotherapy.
|
29650805 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
BET inhibitors display anti-tumor activity in pancreatic cancer, however the cells often develop resistance after a long-term treatment and the underlying molecular basis is not fully understood.
|
30201002 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We discovered a positive feedback loop, in which the activation of p38 and AKT downstream from the altered FGFR3 upregulates <i>MYC</i> mRNA levels and stabilizes MYC protein, respectively, leading to the accumulation of MYC, which directly upregulates <i>FGFR3</i> expression by binding to active enhancers upstream from <i>FGFR3</i> Disruption of this FGFR3/MYC loop in bladder cancer cell lines by treatment with FGFR3, p38, AKT, or BET bromodomain inhibitors (JQ1) preventing <i>MYC</i> transcription decreased cell viability <i>in vitro</i> and tumor growth <i>in vivo</i> A relevance of this loop to human bladder tumors was supported by the positive correlation between <i>FGFR3</i> and <i>MYC</i> levels in tumors bearing <i>FGFR3</i> mutations, and the decrease in FGFR3 and MYC levels following anti-FGFR treatment in a PDX model bearing an <i>FGFR3</i> mutation.
|
29463565 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Consistently, genetic disruption of <i>HOXB13</i> or pharmacological suppression of its mRNA and protein expression by the novel dual-activity BET bromodomain-kinase inhibitors directly correlates with rapid induction of apoptosis, potent inhibition of tumor cell proliferation and cell migration, and suppression of CRPC growth.
|
30242092 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We also demonstrate that KDM6A-deficient pancreatic cancer is selectively sensitive to BET inhibitors, which reversed squamous differentiation and restrained tumor growth in vivo, highlighting a therapeutic niche for patient tailored therapies.
|
29533787 |
2018 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Compound BDF-1253 efficiently suppressed the expression of BET downstream genes, impaired RCC cells viability via inducing cell cycle arrest and apoptosis, and decreased tumor growth in RCC xenografts.
|
30385738 |
2018 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Markers such as SERPINI1, ZCCHC24, and ZMYND8 were modulated by ABBV-075 and other BET inhibitors across cancer cell lines and xenograft tumors but not in blood and skin.
|
27903752 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
In multiple murine xenograft models of human breast cancer, BETd-246 and a further optimized analogue BETd-260 effectively depleted BET proteins in tumors and exhibited strong antitumor activities at well-tolerated dosing schedules.
|
28209615 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The Neuroblastoma New Drug Development Strategy (NDDS) has: 1) established a group with expertise in drug development; 2) prioritised targets and drugs according to tumour biology (target expression, dependency, pre-clinical data; potential combinations; biomarkers), identifying as priority targets ALK, MEK, CDK4/6, MDM2, MYCN (druggable by BET bromodomain, aurora kinase, mTORC1/2) BIRC5 and checkpoint kinase 1; 3) promoted clinical trials with target-prioritised drugs.
|
28604107 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The BET inhibitor JQ1 selectively impairs tumour response to hypoxia and downregulates CA9 and angiogenesis in triple negative breast cancer.
|
27292261 |
2017 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Pharmacologic inhibition of BET bromodomains enhanced survival in a PDAC GEM model and inhibited growth of human-derived xenograft tumors.
|
27169995 |
2016 |
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Tumor development was suppressed dose dependently in a xeno-transplant model in immune deficient mice, overall indicating that ES may be susceptible to treatment with epigenetic inhibitors blocking BET bromodomain activity and the associated pathognomonic EWS-ETS transcriptional program.
|
26623725 |
2016 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Combined treatment with the multitargeted DDR2 inhibitor dasatinib and BET inhibitor JQ1 inhibited tumor growth in vitro and in vivo.
|
26206333 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Our data unravel a previously unappreciated mechanism through which BET proteins control tumor growth of glioblastoma cells and suggest that modulation of lncRNA networks may, in part, mediate the antiproliferative effects of many epigenetic inhibitors currently in clinical trials for cancer and other diseases.
|
26111795 |
2015 |
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Selective inhibition of BET bromodomain epigenetic signalling interferes with the bone-associated tumour vicious cycle.
|
24646477 |
2014 |