The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells
about
Novel histone deacetylase inhibitors in clinical trials as anti-cancer agentsEpimutational profile of hematologic malignancies as attractive target for new epigenetic therapiesHistone acetylation: novel target for the treatment of acute lymphoblastic leukemiaLinking epithelial-to-mesenchymal-transition and epigenetic modificationsTargeting histone deacetylases for cancer therapy: from molecular mechanisms to clinical implicationsTrials with 'epigenetic' drugs: an updateHistone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell ViabilityDietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cellsMultiple mechanisms determine the sensitivity of human-induced pluripotent stem cells to the inducible caspase-9 safety switchPhase II study of vorinostat for treatment of relapsed or refractory indolent non-Hodgkin's lymphoma and mantle cell lymphomaTreatment of resistant metastatic melanoma using sequential epigenetic therapy (decitabine and panobinostat) combined with chemotherapy (temozolomide).Phase 1 dose-escalation study of oral abexinostat for the treatment of patients with relapsed/refractory higher-risk myelodysplastic syndromes, acute myeloid leukemia, or acute lymphoblastic leukemia.Interconnecting molecular pathways in the pathogenesis and drug sensitivity of T-cell acute lymphoblastic leukemiaThe HDAC inhibitor LBH589 (panobinostat) is an inhibitory modulator of aromatase gene expression.PI3K/mTOR inhibition markedly potentiates HDAC inhibitor activity in NHL cells through BIM- and MCL-1-dependent mechanisms in vitro and in vivo.Mutated in colorectal cancer (MCC) is a novel oncogene in B lymphocytesSynergistic antitumor interactions between MK-1775 and panobinostat in preclinical models of pancreatic cancer.STAT3 inhibition is a therapeutic strategy for ABC-like diffuse large B-cell lymphomaPainful pathways induced by TLR stimulation of dorsal root ganglion neuronsBiomarkers of histone deacetylase inhibitor activity in a phase 1 combined-modality study with radiotherapy.Molecular Mechanism of the Cell Death Induced by the Histone Deacetylase Pan Inhibitor LBH589 (Panobinostat) in Wilms Tumor Cells.Targeting paediatric acute lymphoblastic leukaemia: novel therapies currently in developmentA phase 2 study of vorinostat for treatment of relapsed or refractory Hodgkin lymphoma: Southwest Oncology Group Study S0517.Stemness of B-cell progenitors in multiple myeloma bone marrow.Inhibition of the proliferation of acquired aromatase inhibitor-resistant breast cancer cells by histone deacetylase inhibitor LBH589 (panobinostat).Synergistic anti-leukemic interactions between panobinostat and MK-1775 in acute myeloid leukemia ex vivo.p53-Independent, normal stem cell sparing epigenetic differentiation therapy for myeloid and other malignanciesSIRT1 activation enhances HDAC inhibition-mediated upregulation of GADD45G by repressing the binding of NF-κB/STAT3 complex to its promoter in malignant lymphoid cells.HDAC inhibitor, scriptaid, induces glioma cell apoptosis through JNK activation and inhibits telomerase activity.HDAC inhibition by LBH589 affects the phenotype and function of human myeloid dendritic cells.The role of HDACs inhibitors in childhood and adolescence acute leukemias.Targeting epigenetics through histone deacetylase inhibitors in acute lymphoblastic leukemia.Emerging promise of epigenetics and DNA methylation for the diagnosis and management of women's cancers.Panobinostat for the treatment of multiple myeloma.Relapsed or refractory pediatric acute lymphoblastic leukemia: current and emerging treatments.Targeting c-FLICE-like inhibitory protein (CFLAR) in cancer.Genetic syndromes caused by mutations in epigenetic genes.Epigenetic regulation of cell signaling pathways in acute lymphoblastic leukemia.Preclinical activity of LBH589 alone or in combination with chemotherapy in a xenogeneic mouse model of human acute lymphoblastic leukemia.Cytomegalovirus induces apoptosis in acute leukemia cells as a virus-versus-leukemia function.
P2860
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P2860
The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells
description
2008 nî lūn-bûn
@nan
2008年の論文
@ja
2008年論文
@yue
2008年論文
@zh-hant
2008年論文
@zh-hk
2008年論文
@zh-mo
2008年論文
@zh-tw
2008年论文
@wuu
2008年论文
@zh
2008年论文
@zh-cn
name
The novel histone deacetylase ...... e lymphoblastic leukemia cells
@ast
The novel histone deacetylase ...... e lymphoblastic leukemia cells
@en
type
label
The novel histone deacetylase ...... e lymphoblastic leukemia cells
@ast
The novel histone deacetylase ...... e lymphoblastic leukemia cells
@en
prefLabel
The novel histone deacetylase ...... e lymphoblastic leukemia cells
@ast
The novel histone deacetylase ...... e lymphoblastic leukemia cells
@en
P2093
P2860
P1433
P1476
The novel histone deacetylase ...... e lymphoblastic leukemia cells
@en
P2093
Agnes Juhasz
Anna Scuto
Claudia Kowolik
Leo Kretzner
Mark Kirschbaum
Peter Atadja
Ravi Bhatia
Richard Jove
Stephen Forman
Vinod Pullarkat
P2860
P304
P356
10.1182/BLOOD-2007-10-117762
P407
P577
2008-03-18T00:00:00Z