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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profiling of the MV4-11 cell line treated with trabectidin or azacitidin

ABSTRACT: In order to study the effects of trabectedin in chronic myelomonocytic leukemia and in juvenile myelomonocytic leukemia, we performed whole genome transcriptional profiling of a model cell line treated under either the reference drug for CMML / JMML (Azacitidine) or trabectedin.

ORGANISM(S): Homo sapiens

SUBMITTER: Luca Beltrame

PROVIDER: E-MTAB-2978 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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miRNA profiling of the MV4-11 cell line treated with trabectidin or azacitidin

Project description:In order to study the effects of trabectedin in chronic myelomonocytic leukemia and in juvenile myelomonocytic leukemia, we performed whole genome transcriptional profiling of a model cell line treated under either the reference drug for CMML / JMML (Azacitidine) or trabectedin.

2017-04-30 | E-MTAB-2979 | biostudies-arrayexpress

Whole transcriptome profiling by microarray of monocytes stimulated with LPS and treated with trabectedin, lurbinectedin or doxorubicin

Project description:In order to assess the potential difference on the effect of lurbinectedin on monocytes compared to trabectedin, which has a selective killing effect (Germano et al., 2013), we performed a whole transcriptome assay on monocytes from healthy donors stimulated with LPS and with either trabectedin or lurbinectedin. Doxorubicin, an unrelated drug, was used as an internal control.

2018-01-15 | E-MTAB-5366 | biostudies-arrayexpress

Whole genome transcription profiling of the JN-DSCRT1 cell line treated with Trabectedin

Project description:The purpose of experiments consisted in studying the mode of action of Trabectedin in Desmoplastic Small Round Cell Tumor (DSRCT). In order to investigate the effects of Trabectedin in the expression of EWS-WT1 target genes in relation to the drug growth inhibitory effect, the JN-DSCRT-1 cell line was treated for 1 hour with 5 nM of Trabectedin. Samples were collected at 6, 12 and 24 hours after drug washout. Three biological replicates were used for each time point.

2017-01-27 | E-MTAB-4532 | biostudies-arrayexpress

Transcriptional profiling of human myxoid liposarcoma xenografts treated with trabectedin

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2013-12-10 | E-MTAB-1809 | biostudies-arrayexpress

Proteomic analysis of an induced pluripotent stem cell model reveals strategies to treat Juvenile Myelomonocytic Leukaemia

Project description:Juvenile myelomonocytic leukemia (JMML) is an aggressive myeloproliferative neoplasm of early childhood with a poor survival rate thus there is a requirement for improved treatment strategies. Induced pluripotent stem cells offer the ability to model disease and develop new treatment strategies. JMML is frequently associated with mutations in PTPN11. Children with Noonan syndrome, a development disorder, have an increased incidence of JMML associated with specific germline mutations in PTPN11. We undertook a proteomic assessment of myeloid cells derived from induced pluripotent stem cells obtained from Noonan syndrome patients with PTPN11 mutations, either associated or not associated with increased incidence of JMML. We report that the proteomic perturbations induced by the leukaemia-associated PTPN11 mutations are associated with TP53 and NF-ĸb signalling. We have previously shown that MYC is involved in the differential gene expression observed in Noonan syndrome patients associated with increased incidence of JMML. Thus, we employed drugs to target these pathways and demonstrate differentential effects on clonogenic hematopoietic cells derived from Noonan syndrome patients whom develop JMML and those who do not. Further, we demonstrated these small molecular inhibitors, JQ1 and CBL0137, preferentially extinguish primitive haematopoietic cells from sporadic JMML patients as opposed to cells from healthy individuals.

2019-10-30 | PXD014708 | Pride

Long-term proliferation of immature hypoxia-dependent JMML cells supported by a 3D in vitro system

Project description:Juvenile myelomonocytic leukemia (JMML) is a rare stem cell disorder occurring in early childhood and characterized by RAS pathway hyperactivation in 95% of patients. JMML is identified by a hyperproliferation of granulocyte and monocyte, and little is known about the heterogeneous nature of leukemia initiating cells as well as the cellular hierarchy of the JMML bone marrow (BM). In this study, we reported the generation and characterization of a novel patient-derived 3D in vitro JMML model (pd-JAO) sustaining long-term proliferation of JMML cells with stem cell features and patient specific hallmarks. JMML cells brewed in the 3D model under different microenvironmental conditions acquired a proliferative and survival advantage when placed at low oxygen tensions. Transcriptomic and microscopic analysis revealed the activation of specific metabolic energy pathways and the inactivation of processes leading to cell death. Furthermore, we demonstrated pd-JAO derived cells’ migratory, propagation and self-renewal capacities both in in vitro and in vivo mouse model. Our study contributed to the development of a robust JMML 3D in vitro model to study and comprehend the impact of microenvironment stimuli on JMML disease and the molecular mechanisms regulating JMML initiating and propagating cells. Pd-JAO may become a promising model for compound tests focusing on new therapeutic intervention aiming to eradicate JMML progenitors and control JMML disease. We defined a 3D in vitro model that under hypoxic conditions is able to sustain long-term propagation of JMML-patients cells with specific hallmarks. Different oxygen level enviroment drive specific metabolic switch that prompts JMML cells to self-renewal.

2023-04-03 | GSE188608 | GEO

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

Transcriptome and methylation analysis of JMML patients compare to healthy prenatal and postnatal samples.

Project description:JMML (Juvenile myelomonocytic leukaemia) is a leukaemia hat only develops in young children and is thought to have a prenatal initiation. To study the relationship between JMML and normal ontogeny we studied the transcriptome of HSPC (hematopoietic stem and progenitor cells) sorted from sporadic JMML patients, healthy prenatal samples and from healthy age matched donors. Bulk transcriptome of sorted HSPC reveals that some JMML samples cluster with prenatal samples whereas other from a distinct cluster apart from any healthy samples. Methylation profile on bulk mononucleated cell on theses JMML patients, 2 healthy postnatal and 2 healthy prenatal samples is also investigated. The results show a global hypermethylation in JMML samples compared to healthy samples and a specific JMML group with a hypermethylated profile compared to all JMML samples.

2022-12-31 | GSE198919 | GEO

TRAIL and taurolidine enhance the anticancer activity of doxorubicin, trabectedin and mafosfamide in human fibrosarcoma cells.

Project description:Microarray analysis revealed differential gene expression patterns of HT1080 cells treated with various chemical compounds alone and in combination (trabectedin, doxorubicin, mafosfamide, TRAIL, taurolidine) Microarray analysis of HT1080 cells treated with various chemical compounds alone and in combination (trabectedin, doxorubicin, mafosfamide, TRAIL, taurolidine)

2011-09-30 | E-GEOD-32441 | biostudies-arrayexpress

Identification of genes that may predict response to azacitidine treatment.

Project description:Azacitidine (AZA) is a hypomethylating drug used to treat disorders associated with myelodysplasia and related neoplasms. Approximately 50% of patients do not respond to AZA and have very poor outcomes. It is of great interest to identify predictive biomarkers for AZA responsiveness. Therefore, we searched for specific genes whose expression level was associated with response status.Using microarrays, we analyzed gene expression patterns in bone marrow CD34+ cells from 32 patients with myelodysplastic syndromes, chronic myelomonocytic leukemia, and acute myeloid leukemia with myelodysplasia-related changes before AZA therapy. Total RNA was isolated from bone marrow CD34+ cells obtained from myelodysplasia and related neoplasms patients who underwent treatment with 5-azacytidine (AZA, Vidaza). Using Illumina Human HT-12 v. 4 microarrays, we assayed gene expression profiles in patient CD34+ cells before AZA treatment in order to collect basic data for search for markers of the prediction of therapy response.

2016-02-10 | E-GEOD-77750 | biostudies-arrayexpress

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