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Gene Expression during Panobinostat Dosing

ABSTRACT: A clinical study evaluating the dosing of an oral HDACi panobinostat in patient infected with HIV-1. Dosing was 20 mg orally, 3 times weekly, every other week for a total of 8 weeks. Gene expression was evaluated in whole PBMCs at baseline (Visit 2), after 3 doses (Visit 4), 4 weeks after dosing (Visit 12) and 6 months after dosing (Visit 13) using the Affymetrix HTA 2.0 gene expression chip

ORGANISM(S): Homo sapiens

PROVIDER: GSE109792 | GEO | 2018/01/30

REPOSITORIES: GEO

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Gene Expression during Panobinostat Dosing

Project description:Gene Expression during Panobinostat Dosing

| PRJNA432059 | ENA

RNAseq to investigate transcriptional changes in human MM cell lines due to panobinostat, 5-Azacytidine, panobinostat+5-Azacytidine or n-methyl-2-pyrroldine (NMP) treatments.

Project description:Purpose: We applied RNA sequencing technology for high-throughput analysis of transcriptional changes within human MM cell lines JJN3 and U266 due to individual and combination drug treatment. Methods: JJN3 and U266 cells were treated with pan-HDACi panbobinostat, DNMTi 5-Azacytidine, panobinostat+5-Azacytidine or NMP for 4h or 24h in triplicate and transcriptional changes assessed by RNAseq using Illumina HiSeq platform. Specifically, JJN3 cells were treated with 10nM panobinostat, 2.5µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. U266 cells were treated with 10nM panobinostat, 10µM 5-Azacytidine, panobinostat+5-Azacytidine (at given doses), or 10mM NMP. Results: We report unique and overlapping transcriptional signatures that lead to the induction of apoptosis in human MM cell lines in a cell-specific manner due to individual or combination treatments. Conclusions: A detailed analysis of differential transcriptional events in human MM cell lines due to HDACi, DNMTi, HDACi+DNMTi and NMP appear to define the molecular events leading to apoptosis and drug mechanism of action. We tested triplicate experiments at 4h and 24hr time points in JJN3 and U266 cell lines against vehicle control treated cells.

2014-04-09 | E-GEOD-56623 | biostudies-arrayexpress

Myc-driven medulloblastoma cells treated with Panobinostat (LBH589)

Project description:Mouse MycT58A/DNp53 (MP) medulloblastoma cells were treated with DMSO or HDAC inhibitor (HDACi) panobinostat for 6 or 12 hours in vitro. Gene expression profiling was performed to compare cells treated with panobinostat and DMSO.

2015-06-02 | GSE69410 | GEO

Analysis of gene expression in human malignant rhabdoid cells following prolonged treatment with the histone deacetylase inhibitor, Panobinostat

Project description:We hypothesized that prolonged treatment of malignant rhabdoid tumor cells with low-dose HDACi will drive cellular differentiation. We assessed changes in gene expression following 21 days treatment with the HDACi, Panobinostat, versus a DMSO vehcile control in three human MRT cell lines. Total RNA obtained from three human malignant rhabdoid tumor cell lines (G401, SJSC, STM91-01) cultured for 21 days in the presence of low-dose Panobinostat was compared to 21-day treated DMSO control cells. All treatments and cell lines were performed in triplicate.

2016-03-01 | E-GEOD-76664 | biostudies-arrayexpress

RNAseq to investigate transcriptional changes in human MM cell lines due to panobinostat, 5-Azacytidine, panobinostat+5-Azacytidine or n-methyl-2-pyrroldine (NMP) treatments.

2014-04-09 | GSE56623 | GEO

Atypical Teratoid Rhabdoid Tumours Are Susceptible to Panobinostat-Mediated Differentiation Therapy

Project description:Atypical teratoid rhabdoid tumour (ATRT) is a rare but highly aggressive undifferentiated solid tumour arising in the central nervous system and predominantly affecting infants and young children. ATRT is exclusively characterised by the inactivation of SMARCB1, a member of the SWI/SNF chromatin remodelling complex that is essential for the regulation of large sets of genes required for normal development and differentiation. Histone deacetylase inhibitors (HDACi) are a promising anticancer therapy and are able to mimic the normal acetylation functions of SMARCB1 in SMARCB1-deficient cells and drive multilineage differentiation in extracranial rhabdoid tumours. However, the potential efficacy of HDACi in ATRT is unknown. Here, we show that human ATRT cells are highly responsive to the HDACi panobinostat and that sustained treatment leads to growth arrest, increased cell senescence, decreased clonogenicity and induction of a neurogenesis gene expression profile. Furthermore, in an orthotopic ATRT xenograft model, continuous panobinostat treatment inhibits tumour growth, increases survival and drives neuronal differentiation as shown by the expression of the neuronal marker, TUJ1. Collectively, this preclinical study supports the therapeutic potential of panobinostat-mediated differentiation therapy for ATRT.

2024-09-08 | GSE276501 | GEO

Analysis of gene expression in human malignant rhabdoid cells following prolonged treatment with the histone deacetylase inhibitor, Panobinostat

2016-03-01 | GSE76664 | GEO

Comparison of gene expression between control and Panobinostat treated Notch1-driven T-ALL

Project description:T-cell acute lymphoblastic leukaemia (T-ALL) is a disease characterized by the uncontrolled clonal proliferation of immature lymphoid cells. Despite improvement in remission rates using conventional chemotherapeutics, the prognosis for T-ALL remains poor due to disease relapse associated with intrinsic, or acquired tumor cell resistance to the initial therapies. Although T-ALL is a genetically heterogenous disease, mutations resulting in activation of the Notch-1 signaling pathway are present in over 50% of patients, thus defining Notch signaling as a central player in T-ALL onset and progression. Studies also defined an oncogenic c-MYC gene signature as a key characteristic of these T-ALL and connectivity map experiments implicated histone deacetylase inhibitors (HDACi) as potential modifiers of pathways de-regulated by Notch. Recently, studies have shown that panobinostat, an FDA-approved HDACi shows efficacy against human T-ALL cell lines in-vitro, but the molecular mechanism that underpin the therapeutic efficacy of panobinostat is poorly understood. To investigate this, we performed 3'mRNA-seq analysis on T-ALL cells treated for 2 hours with panobinostat in vitro.

2017-09-01 | GSE102757 | GEO

Effects of neonatal dosing of SERMs on CD1 mouse uterine gene expression at 3 months

Project description:Tamoxifen, a selective estrogen receptor modulator (SERM), is an effective treatment for breast cancers. In the CD-1 mouse model, neonatal oral dosing with tamoxifen leads to the development of adenomyosis. Both 4-hydroxyestradiol and tamoxifen can form DNA-reactive metabolites and may be involved in carcinogenesis of the uterus. After comparing the uterotrophic response of several SERMs the maximal uterotrophic doses of estradiol (100mg/kg) 4-hydroxyestradiol (385mg/kg) and tamoxifen (250mg/kg) were determined. Maximal uterotrophic doses were given orally to newborn CD-1 mice on days 1 â 4 after birth and gene and pathological changes examined in the uterus at 3 months after dosing. ERKOa knockout mice were dosed orally with tamoxifen (1mg/Kg) on days 1 â 4 after birth and uterine gene expression compared with CD-1 mice. Dosing groups: Estradiol (E2): 100mg/Kg 4-hydroxyestradiol (4OHE2): 385mg/Kg Tamoxifen : 250mg/Kg ERKO mice dosed with tamoxifen (1mg/Kg) 4 dosed animals and 4 controls for each treatment group. Uteri removed at 3 months after dosing and total RNA extracted. Controls were pooled. RNA labelling, hybridisation and analysis of fluorescence was carried out as described by Turton et al (2001). Cy3/Cy5 dye swap labelling was carried out on samples from each animal. Reference: Turton NJ et. al. (Oncogene (2001) 20, 1300-1306

2010-06-30 | E-GEOD-3625 | biostudies-arrayexpress

Differential gene expression in neuroblastoma cells after treatment with vehicle control, JQ1, panobinostat, or combination of JQ1 and panobinostat

Project description:The bromodomain inhibitor JQ1 and the histone deacetylase inhibitor panobinostat induce synergistic anticancer effects We analyzed whether JQ1 and panobinostat synergistically modulate gene expression Neuroblastoma SK-N-BE(2) cells were treated with vehicle control, 1 microM JQ1, 10 nM panobinostat, or combination of JQ1 and panobinostat for 6 hours, and subjected to differential gene expression studies with Affymetrix microarrays.

2015-12-31 | E-GEOD-68690 | biostudies-arrayexpress

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