The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells - Wikidata - wikimedia - TriplyDB

The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells

The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells

http://www.wikidata.org/entity/Q36658033

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Novel histone deacetylase inhibitors in clinical trials as anti-cancer agents Epimutational profile of hematologic malignancies as attractive target for new epigenetic therapies Histone acetylation: novel target for the treatment of acute lymphoblastic leukemia Linking epithelial-to-mesenchymal-transition and epigenetic modifications Targeting histone deacetylases for cancer therapy: from molecular mechanisms to clinical implications Trials with 'epigenetic' drugs: an update Histone Deacetylase (HDAC) Inhibitor Kinetic Rate Constants Correlate with Cellular Histone Acetylation but Not Transcription and Cell Viability Dietary phytochemicals, HDAC inhibition, and DNA damage/repair defects in cancer cells Multiple mechanisms determine the sensitivity of human-induced pluripotent stem cells to the inducible caspase-9 safety switch Phase II study of vorinostat for treatment of relapsed or refractory indolent non-Hodgkin's lymphoma and mantle cell lymphoma Treatment 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 leukemia The 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 lymphocytes Synergistic 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 lymphoma Painful pathways induced by TLR stimulation of dorsal root ganglion neurons Biomarkers 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 development A 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 malignancies SIRT1 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.

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The novel histone deacetylase inhibitor, LBH589, induces expression of DNA damage response genes and apoptosis in Ph- acute lymphoblastic leukemia cells

http://www.wikidata.org/entity/Q36658033

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2008 nî lūn-bûn

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Agnes Juhasz

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Anna Scuto

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Claudia Kowolik

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Leo Kretzner

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Mark Kirschbaum

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Peter Atadja

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Ravi Bhatia

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Richard Jove

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Stephen Forman

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Vinod Pullarkat

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P2860

siRNA target site secondary structure predictions using local stable substructures

GADD45gamma, down-regulated in 65% hepatocellular carcinoma (HCC) from 23 chinese patients, inhibits cell growth and induces cell cycle G2/M arrest for hepatoma Hep-G2 cell lines

Loss of expression of GADD45 gamma, a growth inhibitory gene, in human pituitary adenomas: implications for tumorigenesis

p53-independent induction of Gadd45 by histone deacetylase inhibitor: coordinate regulation by transcription factors Oct-1 and NF-Y

GADD45b and GADD45g are cdc2/cyclinB1 kinase inhibitors with a role in S and G2/M cell cycle checkpoints induced by genotoxic stress

Clinical development of histone deacetylase inhibitors as anticancer agents

Gadd45gamma is androgen-responsive and growth-inhibitory in prostate cancer cells

Myc suppresses induction of the growth arrest genes gadd34, gadd45, and gadd153 by DNA-damaging agents

Histone deacetylase inhibitors and the promise of epigenetic (and more) treatments for cancer

DNA methylation patterns at relapse in adult acute lymphocytic leukemia.

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