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Unknown,Transcriptomics,Genomics,Proteomics

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MiRNA 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-2979 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional 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.

2016-12-14 | E-MTAB-2978 | 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

Kinome profiling of patient JMML samples pre- and post-trametinib treatment

Project description:Juvenile myelomonocytic leukemia (JMML) is an aggressive cancer of young children initiated by mutations in NRAS, KRAS and other genes encoding proteins that modulate Ras signal output. Hematopoietic stem cell transplantation (HSCT) is the only curative treatment and patients with relapsed and refractory disease have dismal outcomes. This trial evaluated the safety and efficacy of trametinib in advanced JMML. Kinase enrichment proteomic analysis was performed using available patient samples pre- or post-treatment with trametinib (NCT03190915) to evaluate the effects on the functional kinome.

2024-04-23 | PXD042328 | Pride

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

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

Transcriptional profiling of human myxoid liposarcoma xenografts treated with trabectedin

Project description:To elucidate the mechanisms behind the high sensitivity of myxoid/round cell liposarcoma (MRCL) to trabectedin and the suggested selectivity for specific subtypes we have developed and characterized two MRCL xenografts differing for the breakpoint of the fusion gene FUS- HOP, respectively of type II and III. Transcription profiling experiments were carried out after trabectidin treatment in four separate time points (control, 24h after the first dose, 24h after the third dose, and 15 days after the third dose) for both types of xenografts in order to identify genes and pathways involved with the mechanisms of action of trabectedin in MRCL.

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

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

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

Project description:JMML (Juvenile myelomonocytic leukaemia) is a leukaemia that 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 HPC (hematopoietic progenitor cells) sorted from sporadic JMML patients, healthy prenatal samples and from healthy age matched donors. Bulk transcriptome of sorted HPC reveals that some JMML samples cluster with prenatal samples whereas other from a distinct cluster apart from any healthy samples.

2024-05-16 | GSE267628 | GEO

Prototypical innate immune mechanism hijacked by leukemia-initiating mutant stem cells for selective advantage and immune evasion in Ptpn11 mutation-associated juvenile myelomonocytic leukemia

Project description:Juvenile myelomonocytic leukemia (JMML), a clonal hematologic malignancy, originates from mutated hematopoietic stem cells (HSCs) with genetic alterations in the Ras signaling pathway. The mechanism sustaining the persistence of these mutant stem cells leading to leukemia development remains poorly understood. In this study, we conducted comprehensive examination of gene expression profiles, transcriptional factor regulones, and cell compositions throughout various stages of tumor cell development in a mouse model of Ptpn11 mutation-associated JMML. Our analyses unveiled that leukemia-initiating Ptpn11E76K/+ mutant stem cells exhibited de novo activation of the myeloid transcriptional program and aberrant developmental trajectories. Intriguingly, these mutant stem cells displayed significantly elevated expression levels of anti-microbial molecules and pro-inflammatory proteins, particularly S100a9 and S100a8. These proteins conferred a selective advantage to leukemia-initiating cells through autocrine effects and facilitated immune evasion by recruiting and promoting immune suppressive myeloid-derived suppressor cells (MDSCs) to the microenvironment. Importantly, pharmacological inhibition of S100a9/S100a8 signaling effectively impeded leukemia development from Ptpn11E76K/+ mutant stem cells. These findings collectively suggest that JMML tumor-initiating cells exploit evolutionarily conserved innate immune and inflammatory mechanism to establish clonal dominance.

2024-09-12 | GSE266821 | GEO

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

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