|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our findings demonstrate that MYC suppression is an important pharmacodynamic marker of BET bromodomain inhibitor response and suggest that targeting MYC may be a promising therapeutic strategy to overcome de novo BET bromodomain inhibitor resistance in prostate cancer.
|
30846826 |
2019 |
|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Compounds inducing the pharmacologic degradation of BET proteins effectively target the major oncogenic drivers of prostate cancer, and ultimately present a potential advance in the treatment of mCRPC.
|
30918020 |
2019 |
|
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Here, we show that targeting BET bromodomains using the small molecule inhibitor JQ1 decreased PD-L1 expression and mitigated tumor progression in prostate cancer models.
|
31653272 |
2019 |
|
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
The novel BET-CBP/p300 dual inhibitor NEO2734 is active in SPOP mutant and wild-type prostate cancer.
|
31559706 |
2019 |
|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Structural Insights into BET Client Recognition of Endometrial and Prostate Cancer-Associated SPOP Mutants.
|
31026449 |
2019 |
|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
BET bromodomain inhibition blocks the function of a critical AR-independent master regulator network in lethal prostate cancer.
|
30996246 |
2019 |
|
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Thus, QD-IIQAS is an easy and accurate method for assessing DNER and the DNER expression was an independent prognostic factor in prostate cancer.
|
29843212 |
2018 |
|
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We evaluated how bromodomain and extra-terminal (BET) protein inhibitors (BETi) abrogate aberrant AR signaling in CRPC.<b>Experimental Design:</b> We determined associations between BET expression, AR-driven transcription, and patient outcome; and the effect and mechanism by which chemical BETi (JQ1 and GSK1210151A; I-BET151) and BET family protein knockdown regulates AR-V7 expression and AR signaling in prostate cancer models.<b>Results:</b> Nuclear BRD4 protein expression increases significantly (<i>P</i> ≤ 0.01) with castration resistance in same patient treatment-naïve (median <i>H</i>-score; interquartile range: 100; 100-170) and CRPC (150; 110-200) biopsies, with higher expression at diagnosis associating with worse outcome (HR, 3.25; 95% CI, 1.50-7.01; <i>P</i> ≤ 0.001).
|
29555663 |
2018 |
|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, our results elucidate the tumor-suppressor role of SPOP in prostate cancer in which it acts as a negative regulator of BET protein stability and also provide a molecular mechanism for resistance to BET inhibitors in individuals with prostate cancer bearing SPOP mutations.
|
28805820 |
2017 |
|
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
We identified JQ1, a BET bromodomain inhibitor previously implicated in regulating MYC expression and demonstrated role in prostate cancer, abrogates PAICS expression in several prostate cancer cells.
|
27550065 |
2017 |
|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Intrinsic BET inhibitor resistance in SPOP-mutated prostate cancer is mediated by BET protein stabilization and AKT-mTORC1 activation.
|
28805822 |
2017 |
|
Prostate carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
Specifically, we provide a molecular rationale for the use of BET inhibitors to treat patients with endometrial but not prostate cancer who harbor SPOP mutations.
|
28805821 |
2017 |
|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Areas covered: We speculate that a combination approach using inhibitors of BET proteins (BETi) with other targeted therapies may be required to improve the therapeutic index of BET inhibition in the management of prostate cancer.
|
29032717 |
2017 |
|
Prostate carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Regulation of the glucocorticoid receptor via a BET-dependent enhancer drives antiandrogen resistance in prostate cancer.
|
28891793 |
2017 |
|
Prostate carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Recent data indicates that BET bromodomain proteins regulate ERG gene fusion and MYC gene expression in prostate cancer, suggesting possible synergistic targeted therapeutics in ERG-positive/MYC high tumors.Prostate 76:845-853, 2016.
|
27159573 |
2016 |