|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Selective HDAC6 inhibitors (Tubathian A, Tubastatin A, Tubacin and Ricolinostat) and a non-selective HDAC inhibitor (Vorinostat) were evaluated on cancer cell lines derived from multiple tumour types in both an in vitro and in vivo setting as potential cancer therapeutics.
|
30694564 |
2019 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
<i>In vivo</i>, the MEK-HDAC inhibitor combination outperformed either agent alone, leading to a long-term decrease of tumor growth in both subcutaneous and liver metastasis models and the suppression of adaptive PI3K/AKT and YAP signaling.
|
31227503 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We then performed CRISPR screening to identify which HDAC among the class I HDACs is responsible for tumor growth inhibition in eRMS.
|
31113472 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Cytotoxicity due to the epigenetic regulation of tumor-associated genes by HDAC inhibitors has also been reported.
|
30987296 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Further evaluations indicated that C02S could inhibit DNMT and HDAC at cellular levels, thereby inversing mutated methylation and acetylation and increasing expression of tumor suppressor proteins.
|
30901675 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Additionally, the in vivo study found melatonin exerted anti-proliferative and pro-apoptotic effects on xenograft tumors which were also strengthened by HDAC9 knockdown.
|
31090223 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Combined targeting of HBP1 by PI<sub>3</sub>K antagonists and MYCN signaling by BET- or HDAC-inhibitors blocks MYCN activity and significantly reduces tumor growth, suggesting a novel targeted therapy option for high-risk neuroblastoma.
|
30538293 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
This behavior was coupled to vimentin and connexin 43 gene expression downregulation, suggesting that HDAC activity blockade downgrades GBM aggressiveness mostly due to tumor cell competence and plasticity modulation <i>in vitro</i>.
|
31531023 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Thus, HDAC1 inhibitors have emerged as the potential therapeutic leads against multiple human cancers, as they can block the activity of particular HDACs, renovate the expression of several tumour suppressor genes and bring about cell differentiation, cell cycle arrest and apoptosis.
|
29732991 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
DNMT and HDAC and expression pattern of certain tumor-suppressor genes.
|
31112703 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
There was a significant correlation between tumor differentiation and HDAC9.
|
31078148 |
2019 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
HDACs are considered potential targets for tumor drug discovery and hydroxamates are known inhibitors of HDACs.
|
31326241 |
2019 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Moreover, combined treatment of HDAC inhibitors and EZH2 inhibitors at sublethal doses synergistically induced histone H3K27 acetylation and target gene expression, leading to rapid induction of apoptosis and growth suppression of SCCOHT cells and xenografted tumors.
|
30232145 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Knock down of eIF2α, ATM, AMPKα, ULK1, Beclin1 or ATG5 reduced tumor cell killing by the niraparib plus HDAC inhibitor combination.
|
29923797 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Histone deacetylase 6 (HDAC6) is a unique member of the HDAC family that not only participates in histone acetylation and deacetylation but also targets several nonhistone substrates, such as α-tubulin, cortactin, and heat shock protein 90 (HSP90), to regulate cell proliferation, metastasis, invasion, and mitosis in tumors.
|
30176876 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
In studies of PDAC cells and 2 mouse models of PDAC, we found a dual inhibitor of GSK3B and HDACs (Metavert) to induce cancer cell apoptosis, reduce migration and expression of stem cell markers, and slow growth of tumors and metastases.
|
30144430 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
HDAC4 knockdown with or without an HDAC inhibitor significantly delayed tumor growth in a radiation-treated xenograft model.
|
28646552 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Expression of the tumour suppressor genes (TSGs) [MGMT, RARβ, p21, E-cadherin, DAPK1] as well the methylation status of their promoters were examined alongwith the activity levels of DNMT and HDAC enzymes after treatment with genistein.
|
28925878 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Herein, we developed a hybrid HDAC inhibitor that sensitized solid tumours to HDAC-targeted treatment.
|
30429882 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Some histone deacetylases (HDACs) promote tumor cell growth and pan- or selective HDAC inhibitors are active in some cancers; however, the pivotal HDAC enzyme and its functions in human diffuse large B-cell lymphoma (DLBCL) remain largely unknown.
|
29876933 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Transcriptome analysis of GEP-NET-derived cells, perturbed with a library of 107 compounds, identified the HDAC class I inhibitor entinostat as a potent inhibitor of master regulator activity for 42% of metastatic GEP-NET patients, abrogating tumor growth in vivo.
|
29915428 |
2018 |
|
Neoplasms
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Recently, we have discovered that drug combinations which cause a rapid and intense autophagosome formation also can modulate the expression of HDAC proteins that control tumor cell immunogenicity via their regulation of PD-L1 and MHCA.
|
29405973 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Overall, our findings establish RASSF4 as a tumor-suppressive hub in MM and provide a mechanistic rationale for combining trametinib with HDAC inhibitors or bortezomib to treat patients with tumors exhibiting low RASSF4 expression.<b>Significance:</b> These findings provide a mechanistic rationale for combining trametinib with HDAC inhibitors or bortezomib in patients with multiple myeloma whose tumors exhibit low RASSF4 expression.<i></i>.
|
29259009 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
We have used human and murine cell culture models, atomic force microscopy (AFM), microarray analyses, CAF/tumour cell spheroid co-cultures and transgenic fibroblast reporter mice to study how targeting HDACs using small molecule inhibitors or siRNAs re-directs CAF differentiation and function in vitro and in vivo.
|
29695769 |
2018 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
<i>In vivo</i>, neratinib and HDAC inhibitors interacted to suppress the growth of 4T1 mammary tumors, an effect that was enhanced by an anti-PD-1 antibody.
|
29163826 |
2017 |