HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
about
The Functional Analysis of Histone Acetyltransferase MOF in TumorigenesisHDAC inhibitors and immunotherapy; a double edged sword?Mechanisms of Histone Deacetylase Inhibitor-Regulated Gene Expression in Cancer CellsBeyond the genome: epigenetic mechanisms in lung remodelingNew and emerging HDAC inhibitors for cancer treatmentMass spectrometric identification of ancient proteins as potential molecular biomarkers for a 2000-year-old osteogenic sarcomaRomidepsin in peripheral and cutaneous T-cell lymphoma: mechanistic implications from clinical and correlative dataPredicting Response to Histone Deacetylase Inhibitors Using High-Throughput Genomics.Induction of Apoptosis in Intestinal Toxicity to a Histone Deacetylase Inhibitor in a Phase I Study with Pelvic RadiotherapyB1, a novel HDAC inhibitor, induces apoptosis through the regulation of STAT3 and NF-κB.The therapeutic potential of class I selective histone deacetylase inhibitors in ovarian cancerPI3K/mTOR inhibition markedly potentiates HDAC inhibitor activity in NHL cells through BIM- and MCL-1-dependent mechanisms in vitro and in vivo.Metabolic Effects of Known and Novel HDAC and SIRT Inhibitors in Glioblastomas Independently or Combined with TemozolomideSystematic analysis of time-series gene expression data on tumor cell-selective apoptotic responses to HDAC inhibitors.Histone deacetylase inhibitors in clinical studies as templates for new anticancer agents.Increased levels of choline metabolites are an early marker of docetaxel treatment response in BRCA1-mutated mouse mammary tumors: an assessment by ex vivo proton magnetic resonance spectroscopyHistone deacetylase inhibitor SAHA epigenetically regulates miR-17-92 cluster and MCM7 to upregulate MICA expression in hepatoma.Targeting Histone Deacetylases in Diseases: Where Are We?Microarray gene expression profiling reveals potential mechanisms of tumor suppression by the class I HDAC-selective benzoylhydrazide inhibitors.The Therapeutic Potential of AN-7, a Novel Histone Deacetylase Inhibitor, for Treatment of Mycosis Fungoides/Sezary Syndrome Alone or with DoxorubicinA genome scale RNAi screen identifies GLI1 as a novel gene regulating vorinostat sensitivity.IκBα mediates prostate cancer cell death induced by combinatorial targeting of the androgen receptorSensitivity of osteosarcoma cells to HDAC inhibitor AR-42 mediated apoptosis.Identification of Synergistic, Clinically Achievable, Combination Therapies for OsteosarcomaCombining BET and HDAC inhibitors synergistically induces apoptosis of melanoma and suppresses AKT and YAP signaling.Extracellularly secreted APE1/Ref-1 triggers apoptosis in triple-negative breast cancer cells via RAGE binding, which is mediated through acetylation.Induction of MAPK- and ROS-dependent autophagy and apoptosis in gastric carcinoma by combination of romidepsin and bortezomibAnti-GD2 mAb and Vorinostat synergize in the treatment of neuroblastomaInhibition of the Autophagy Pathway Synergistically Potentiates the Cytotoxic Activity of Givinostat (ITF2357) on Human Glioblastoma Cancer Stem Cells.Synergistic Activity of N-hydroxy-7-(2-naphthylthio) Heptanomide and Sorafenib Against Cancer Stem Cells, Anaplastic Thyroid Cancer.Blocking downstream signaling pathways in the context of HDAC inhibition promotes apoptosis preferentially in cells harboring mutant Ras.APPL proteins modulate DNA repair and radiation survival of pancreatic carcinoma cells by regulating ATM.Moving Beyond the Androgen Receptor (AR): Targeting AR-Interacting Proteins to Treat Prostate Cancer.Epigenetics in esophageal cancers.Histone deacetylases and their inhibitors in cancer, neurological diseases and immune disorders.Selective class IIa HDAC inhibitors: myth or reality.Targeting chromatin to improve radiation response.Epigenetic modulation with histone deacetylase inhibitors in combination with immunotherapy.Targeting Chromatin-Mediated Transcriptional Control of Gene Expression in Non-Small Cell Lung Cancer Therapy: Preclinical Rationale and Clinical Results.Belinostat and vincristine demonstrate mutually synergistic cytotoxicity associated with mitotic arrest and inhibition of polyploidy in a preclinical model of aggressive diffuse large B cell lymphoma.
P2860
Q26771181-3F1A4445-4A23-41DE-9DDC-35A1DD2C0C5BQ26853102-98F0C63F-B8FD-4539-B64E-F490B0C687E1Q27015931-34B6D8A2-4B52-4D89-8F27-7D69034B7CE6Q27021767-D5321491-B7AE-4E2C-80F5-10A62EF1924BQ27022413-43543638-CC11-4523-9DF8-E4119DFA9A63Q28539210-9F8E26D9-ED3B-4FA9-80EF-3FE1C74A1502Q30936712-9EBB38A0-ACEB-4B3E-A6C6-87A073449A5CQ33425333-DE22C72A-1781-4F0F-A6E3-D43B08510A41Q33584050-EF0F85B8-213B-4C09-819D-23E31C5FBBBCQ33597695-89B5F825-0D4A-47F6-84AD-3075C99B489DQ33659166-4DC1771D-6F67-4E22-B5AE-2BB10700C74EQ34199935-F4CE2EA8-9C40-4E81-8F60-23D1AEF1E6E5Q34318242-79CBDA80-3C71-4710-9AA8-4F3CE9A45745Q34413200-2A3F8D57-9C56-4624-ADE5-D78708D52097Q35214924-A22C9987-64AF-4B7D-AFD0-8775F3BCA9E5Q35497704-E4BDC22F-9C90-4B9C-BF3A-B03C45610619Q35677697-3536718A-E8C6-48EF-AE75-120CB4498BC5Q35821728-9E46A608-478B-4001-B500-D7B69A30279EQ35884595-FF16D4AD-4AAA-4FDE-A02E-2C5E2916B9ACQ35890561-B480CCC2-8E97-4C5F-B889-2FFCC46B40DEQ35921565-DC6A64C4-E262-4BE5-9FC3-2E5CE198EB3AQ35933129-62D305A2-A8D8-42C8-ADC2-078716534903Q36256343-C8859580-020F-45BD-B2FC-16ABDC0AA4ADQ36316518-AC335CC9-18D4-458F-B01C-1DDFFBB5035BQ36356381-7782E86D-0E41-401B-8EE7-09C932DE24D5Q36414193-8DCCB551-7871-4886-AE30-A85EFD03ACB8Q36782473-0230FBA1-41F5-47F0-9740-D8709C3C6CD1Q37078946-2A76DA99-DB01-4CDF-B4B7-71087D9A563CQ37368670-1111A10B-14F2-40D9-BC29-E5C0BDB211EDQ37613829-2CFFB984-4F13-463C-B45B-EBF000AB7014Q37684405-1EC8AE70-3AAE-4F95-BF22-C3D7DB66531FQ37726159-A77AE2E0-A77C-4C5D-BD8B-F743FB31B062Q37737611-B9026D13-E9E9-4DCC-8786-62C7344AB263Q38210930-AAA90475-7774-43C6-AC73-524A9739AE68Q38240733-82606AC2-94DC-47CB-BECB-25F5B4809D25Q38246144-3B2C3B8C-083B-43AA-98F0-D039AE318617Q38290243-4BEDF892-EBCC-4D70-A5BA-307BDD22CD79Q38537768-ED2A9CB8-5BDD-4D95-94F8-A25E0F7CBCDFQ38582589-918F6D59-A74B-4AA8-AD9A-4254F1998D5BQ38735639-852FE952-FC4E-47E4-8E5A-85F2A6B569F8
P2860
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 28 February 2013
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
@en
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
@nl
type
label
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
@en
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
@nl
prefLabel
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
@en
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
@nl
P2093
P2860
P356
P1476
HDAC inhibitors induce tumor-cell-selective pro-apoptotic transcriptional responses.
@en
P2093
B P Martin
J E Bolden
K Jankowski
K L MacKenzie
R W Johnstone
P2860
P2888
P356
10.1038/CDDIS.2013.9
P577
2013-02-28T00:00:00Z
P5875
P6179
1050636858