|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Importantly, results from preclinical studies using an in vivo mouse model also demonstrated that combining RT with ASC-J9<sup>®</sup> to target AR led to better therapeutic efficacy to suppress PCa progression.
|
30692044 |
2019 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
These dual functions of ASC-J9<sup>®</sup> to suppress PCa proliferation and invasion (via altering STAT3 sumoylation) may help us to develop a better anti-AR compound that may overcome the current antiandrogens' unwanted side-effect of increasing the metastasis to better suppress the castration-resistant PCa progression.
|
29425687 |
2018 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
New therapeutic approaches via directly targeting the AR with ASC-J9<sup>®</sup>, Cisplatin, EPI-001, Niclosamide, and VPC compounds as well as silencing AR with siRNAs or non-coding RNAs have been developed to further suppress PCa at the castration resistant stages.
|
28323036 |
2017 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Androgen deprivation therapy-enzalutamide treatment may not be the best choice for prostate cancer patients who have higher expression of the Malat1/androgen receptor splicing variant 7 axis, and new therapies using Malat1-short interfering RNA or ASC-J9<sup>®</sup> may be developed in the future to better suppress enzalutamide-resistant prostate cancer.
|
28528814 |
2017 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Together, these results suggest that targeting PCa S/P cells with ASC-J9(®) or inhibitors to interrupt the EZH2/STAT3 and/or Akt/EZH2/STAT3 signals may become a new therapy to overcome the unwanted side effects of Casodex or Enzalutamide to further suppress the PCa metastasis.
|
27045473 |
2016 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Current evidence suggests that stromal AR may play positive roles to promote BPH and PCa progression, and targeting stromal AR selectively with AR degradation enhancer, ASC-J9, may allow development of better therapies with fewer adverse effects to battle BPH and PCa.
|
25432062 |
2015 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Targeting the AR-PrLZ complex via ASC-J9® or PrLZ-siRNA resulted in suppression of PCa growth in various human PCa cells and in vivo mouse PCa models.
|
23104178 |
2013 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Using various human PCa cell lines and three different mouse models, we concluded that targeting PCa non-stem/progenitor cells with AR degradation enhancer ASC-J9 and targeting PCa stem/progenitor cells with 5-azathioprine and γ-tocotrienol resulted in a significant suppression of the tumors at the castration resistant stage.
|
22831834 |
2013 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results demonstrate that ASC-J9 could serve as an AR degradation enhancer that effectively suppresses PCa development/progression in the androgen-sensitive and castration-resistant stages.
|
23219429 |
2013 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
In this study, we investigated the association of BMI1 expression, promoter methylation of CDKN2a (p16(INK4a) and p14(ARF)) and TMS1 with pathological variables (Gleason score, TNM stage, perineural invasion) in prostate cancer (PCa).
|
21912429 |
2011 |
|
Malignant neoplasm of prostate
|
0.100 |
Biomarker
|
disease |
BEFREE |
Our study demonstrates that methylation-mediated silencing of TMS1/ASC is a frequent event in prostate cancer, thus identifying a new potential diagnostic and prognostic marker for the treatment of the disease.
|
16848908 |
2006 |
|
Malignant neoplasm of prostate
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
Methylation of the ASC gene promoter is both a frequent and early event in prostate cancer carcinogenesis.
|
16425203 |
2006 |