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Romidepsin and azacitidine synergize in their epigenetic modulatory effects to induce apoptosis in CTCL

ABSTRACT: We demonstrate that the combination of the HDAC inhibitor, romidepsin, and the demethylating agent, azacitidine, exerts synergistic anti-proliferative effects and induction of apoptosis involving activation of the caspase cascade in CTCL cell lines as well as CD4+ T cells derived from patients with Sézary Syndrome (SS) with high tumor burden. We identified genes that were selectively induced by the combination treatment, such the tumor suppressor gene RhoB.

ORGANISM(S): Homo sapiens

PROVIDER: GSE66732 | GEO | 2016/03/30

SECONDARY ACCESSION(S): PRJNA277836

REPOSITORIES: GEO

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Romidepsin and azacitidine synergize in their epigenetic modulatory effects to induce apoptosis in CTCL

Project description:We demonstrate that the combination of the HDAC inhibitor, romidepsin, and the demethylating agent, azacitidine, exerts synergistic anti-proliferative effects and induction of apoptosis involving activation of the caspase cascade in CTCL cell lines as well as CD4+ T cells derived from patients with SÃ©zary Syndrome (SS) with high tumor burden. We identified genes that were selectively induced by the combination treatment, such the tumor suppressor gene RhoB. We performed global CpG methylation-sequencing in a CTCL cell line and in patient cells. Results showed a subset of genes with a unique change in methylation profile in the combination treatment as compared to single drugs.

2016-03-30 | E-GEOD-66732 | biostudies-arrayexpress

Romidepsin and afatinib combination treatment induce synergistic anti-lymphoma effect in CTCL

Project description:Cutaneous T-cell lymphomas (CTCL) are an aggressive group of T-cell lymphomas that present in the skin and are associated with dismal prognosis. Romidepsin is a histone deacetylase (HDAC) inhibitor that is an FDA approved systemic therapeutic indicated for the treatment of CTCL in patients who have received at least one prior systemic therapy. Romidepsin demonstrates promising single agent activity in patients with advanced stages of CTCL, however response is typically low and not durable. One method of overcoming resistance to romidepsin and improving response is through combination therapies. Here, we demonstrate that romidepsin in combination with the epidermal growth factor receptor (EGFR) inhibitor afatinib and afatinib dimaleate produce strongly synergistic anti-tumor effects in CTCL cell lines and an in vivo model of CTCL. Gene expression and western blot analysis further identifies the decreased activation of the JAK-STAT signalling pathway as a key driver of synergy in this combination. These results suggest a potential indication for FDA-approved EGFR inhibitors previously unrecognized in CTCLs as a combination therapeutic with HDAC inhibitors that can be rapidly adopted in the clinic.

2024-07-12 | GSE237167 | GEO

Romidepsin and afatinib combination treatment induce synergistic anti-lymphoma effect in CTCL

Project description:Romidepsin and afatinib combination treatment induce synergistic anti-lymphoma effect in CTCL

| PRJNA994103 | ENA

Quantitative RNAseq Analysis of Treatment Outcomes with Talazoparib, Romidepsin or Combination in MBL2 cell line

Project description:To explore the molecular mechanisms by which romidepsin potentiates the effect of talazoparib, RNA sequencing analysis of MBL2 cell lines treated with talazoparib, romidepsin, or talazoparib plus romidepsin was performed. 40% of the 2023 genes in combination were from talazoparib, whereas only 5.9% of the genes deregulated during the treatment with the combination of talazoparib plus romidepsin were from the effect of romidepsin. 94 genes were presented in all three treatment groups and included upregulation of Prdm1, Dusp5, and CD74, among others. Analysis of genes responsible for DNA repair, cell cycle arrest and apoptosis demonstrated the contribution of romidepsin to downregulation of DNA repair, the synergistic effect of romidepsin and talazoparib on downregulation of genes of cell cycle leading to cell cycle arrest, and activation of apoptosis by talazoparib predominantly.

2020-09-04 | GSE157434 | GEO

Gene expression profiling of cutaneous T cell lymphoma cell lines and primary tumor samples treated with mechlorethamine and romidepsin.

Project description:In this study, we demonstrated the synergistic effect of the mechlorethamine-romidepsin combination in cutaneous T cell lymphoma cell lines and CD4+ T cells derived from patients with Sezary Syndrome. We identify the signaling pathways specifically perturbed under treatment with mechlorethamine-romidepsin combination.

2018-12-10 | GSE110248 | GEO

Targeting T-cell Lymphoma Epigenome Induces Cell Death, Cancer Testes Antigens, Immune Modulatory Signaling Pathways

Project description:We perform expression analysis on a panel of four T-cell lymphoma lines exposed to romidepsin and 5-azacytidine as single agent and combination.

2020-04-04 | GSE148069 | GEO

Expression data of Panc1 cells treated with romidepsin and tamoxifen

Project description:Tamoxifen enhances romidepsin-induced senescence in pancreatic cancer cells. We compared gene-expression profile among untreated control, romidepsin-treated, tamoxifen-treated, and romidepsin plus tamoxifen-treated Panc1 cells.

2021-08-21 | GSE182526 | GEO

Gene expression profiles of MV-4-11 AML cells treated HDAC1/2 -selective inhibitor and Azacitidine

Project description:Determine the differences in gene expression profiles of MV-4-11 AML cells treated with HDAC1/2-selective inhibition, azacitidine, or the combination of the two agents. Acute myeloid leukemia (AML) is a heterogeneous group of hematopoietic stem cell disorders characterized by defects in myeloid differentiation and increased proliferation of neoplastic hematopoietic precursor cells. Outcomes for patients with AML remain poor, highlighting the need for novel treatment options. Aberrant epigenetic regulation plays an important role in the pathogenesis of AML, and inhibitors of DNA methyltransferase or histone deacetylase (HDAC) enzymes have exhibited activity in preclinical AML models. Combination studies with HDAC inhibitors plus DNA methyltransferase inhibitors have suggested beneficial clinical activity in AML, however the toxicity profiles of non-selective HDAC inhibitors in the combination setting limit their clinical utility. In this work, we describe the preclinical development of selective inhibitors of HDAC1 and HDAC2, which are hypothesized to have improved safety profiles, for combination therapy in AML. We demonstrate that selective inhibition of HDAC1 and HDAC2 is sufficient to achieve efficacy both as a single agent and in combination with azacitidine in preclinical models of AML, including established AML cell lines, leukemia cells from AML patient bone marrow samples and in vivo xenograft models of human AML. Gene expression profiling of AML cells treated with either an HDAC1/2 inhibitor, azacitidine, or the combination of both have identified a list of genes involved in transcription and cell cycle regulation as potential mediators of the combinatorial effects of HDAC1/2 inhibition with azacitidine. Together, these findings support the clinical evaluation of selective HDAC1/2 inhibitors in combination with azacitidine in AML patients.

2017-03-08 | GSE84440 | GEO

Expression data of MOLT-4 cells treated with romidepsin and tamoxifen

Project description:Tamoxifen enhaces romidepsin-induced apoptosis in T-cell malignant cells. We compared gene-expression profile among untreated control, romidepsin-treted,

2020-02-21 | GSE145606 | GEO

ChIP-seq. analysis of pan-histone 3 acetylation in Romidepsin treated TCam-2

Project description:ChIP-seq. analysis of TCam-2 16 h after 10 nanomolar Romidepsin application. DMSO treated cells were used as controls. For ChIP, an antibody against histone H3 pan-acetylation was used. These data are part of the article 'The Histone Deacetylase Inhibitor Romidepsin Efficiently Targets Cisplatin-resistant Germ Cell Cancer Cells via Downregulation of the SWI/SNF-Complex Member ARID1A' (Nettersheim et al., 2016). TCam-2 cells treated for 16h with romidepsin or the solvent were fixed by formaldehyde solution and further processed by Active Motif, including DNA shearing by sonication, chromatin-immunoprecipitaion, library generation and sequencing (NextSeq 500, Illumina). Pooled input DNA of each sample including spike-in Drosophila DNA was used as controls and for normalization. The 75-nt sequence reads were mapped against the genome using BWA algorithm. Duplicate reads were removed. Only peaks that align with no more than 2 mismatches and map uniquely to the genome were used for further analysis. Intervals / peaks were identified by the MACS peak finding algorithm (cutoff p-value 1x10-7) including ENCODE blacklist filtering

2016-09-01 | E-GEOD-78262 | biostudies-arrayexpress

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