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Whole exome sequencing of human MDS/AML OCI-M2 and patient-derived bone marrow cell lines treated with 5-azacytidine

ABSTRACT: Whole exome sequencing of human MDS/AML OCI-M2 and patient-derived bone marrow cell lines treated with 5-azacytidine

PROVIDER: PRJEB48883 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR7385080_1.fastq.gz	Fastqsanger.gz
	ERR7385080_2.fastq.gz	Fastqsanger.gz
	ERR7385075_1.fastq.gz	Fastqsanger.gz
	ERR7385075_2.fastq.gz	Fastqsanger.gz
	ERR7385076_1.fastq.gz	Fastqsanger.gz

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Whole exome sequencing of human MDS/AML OCI-M2 and patient-derived bone marrow cell lines treated with 5-azacytidine

Project description:The whole exome sequencing experiment is part of the study: “Analysis of 5-azacytidine resistance models reveals a set of targetable pathways”. In the study we generated myelodysplastic syndrome/acute myeloid leukemia (MDS/AML) OCI-M2 cell lines as well as patient-derived bone marrow cell lines that are resistant to hypomethylating therapy by 5-azacytidine (AZA). By integrated analysis of expression and mutation data obtained from these samples we have identified multiple signaling pathways whose modulation by specific small molecule inhibitors significantly block proliferation of AZA-resistant cell lines without increasing their sensitivity to AZA. The understanding of the molecular mechanisms which characterize the AZA-R phenotype can be used for broadening therapeutic options at progressing states during AZA therapy.

2022-05-02 | E-MTAB-11172 | biostudies-arrayexpress

RNA-seq of human MDS/AML cell line OCI-M2 treated with 5-azacytidine and sulforaphane

Project description:The RNA sequencing experiment is part of the study: “Modulating Redox Balance Restores Azacytidine Efficacy in Hypomethylating Agent Resistant Disease.” In the study we generated myelodysplastic syndrome/acute myeloid leukemia (MDS/AML) OCI-M2 cell line that is resistant to hypomethylating therapy by 5-azacytidine (AZA). By modulation of the redox environment via modification of redox sensor KEAP1 using sulforaphane (SFN) in these cells we were able to restore sensitivity to AZA. We used RNA sequencing to define transcriptomic differences between AZA sensitive (AZA-S) and AZA resistant (AZA-R) cells and to characterize how the transcriptome is changing upon treatment of these cells with AZA, SFN and combination of both.

2021-07-16 | E-MTAB-10635 | biostudies-arrayexpress

RNA-seq of human MDS/AML cell line OCI-M2 treated with 5-azacytidine and sulforaphane

Project description:RNA-seq of human MDS/AML cell line OCI-M2 treated with 5-azacytidine and sulforaphane

| PRJEB46095 | ENA

Genome-wide DNA methylation in MDS/secondary AML and de novo AML

Project description:An increasing body of work reveals aberrant hypermethylation of genes occurring in and potentially contributing to the pathogenesis of myeloid malignancies. Several of these diseases, such as myelodysplastic syndromes (MDS), are responsive to DNA methyltransferase inhibitors. In order to determine the extent of promoter hypermethylation in such tumors we compared the distribution of DNA methylation of 14,000 promoters in MDS and secondary AML patients enrolled in a phase I trial of 5-azacytidine and the histone deacetylase inhibitor entinostat against de novo AML patients and normal CD34+ bone marrow cells. The MDS and secondary AML patients displayed more extensive aberrant DNA methylation involving thousands of genes than did the normal CD34+ bone marrow cells or de novo AML blasts. Aberrant methylation in MDS and secondary AML tended to affect particular chromosomal regions, occurred more frequently in Alu poor genes, and included prominent involvement of genes involved in the WNT and MAPK signaling pathways. DNA methylation was also measured at days 15 and 29 after the first treatment cycle. DNA methylation was reversed at day 15 in a uniform manner throughout the genome, and this effect persisted through day 29, even without continuous administration of the study drugs. Keywords: DNA methylation profiling Direct comparison of DNA methylation in bone marrow samples from patients with Myelodysplastic syndrome or secondary Acute Myeloid Leukemia (AML) at baseline and after in vivo treatment with 5-azacytidine + etinostat. A comparison to de novo normal karyotype AML was also performed. Two control groups were included: one consisting of 8 CD34+ bone marrow samples from healthy donors and a second one consisting of matched CD34+ and CD34- fractions from the bone marrows of 4 healthy donors.

2010-05-15 | E-GEOD-17328 | biostudies-arrayexpress

Affymetrix SNP array data for longitudinal analysis of adult Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukemia (AML) with 1q jumping translocation after 5'-azacytidine treatment

Project description:Jumping translocations are cytogenetic abnormalities associated with poor clinical outcome and progression in Myelodysplastic Syndromes/Acute Myeloid Leukemia (MDS/AML).Typically a donor chromosome, often a trisomic 1q, is transferred onto 2 or more recipient chromosomes. Previous studies have demonstrated the crosstalk between DNA hypomethylation and 1q trisomy. Here, we used an epi-genomic approach in sequential samples from a cohort of MDS and AML with the appearance of 1q jumping translocations after 5’-azacytidine (AZA) treatment.

2025-07-01 | GSE272012 | GEO

5-azacytidine and entinostat treatment of patients with MDS, chronic myelomonocytic leukemia (CMMoL), and high risk AML

2009-06-20 | GSE16625 | GEO

Multiplex Enhanced Reduced Representation Bisulfite Sequencing (mERRBS) longitudinal analysis of adult Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukemia (AML) with 1q jumping translocation after 5'-azacytidine treatment compared to controls

2025-07-01 | GSE271912 | GEO

Genome-wide DNA methylation in MDS/secondary AML and de novo AML

2009-08-05 | GSE17328 | GEO

5-azacytidine and entinostat treatment of patients with MDS, chronic myelomonocytic leukemia (CMMoL), and high risk AML

Project description:Early epigenetic changes and DNA damage do not predict clinical response in an overlapping schedule of 5-azacytidine and entinostat in patients with myeloid malignancies. The patients with MDS, chronic myelomonocytic leukemia (CMMoL), and high risk AML were treated with sequential administration of methylation inhibitor drugs (5AC and entinostat). To study gene expresion regulation in treated patients, microarray analysis was done on RNA samples extracted from CD34+ cells from 18 patients before and 15 days after treatment using Affymetrix U133Plus2.0. 18 enrolled patients were treated with sequential administration of 5AC and entinostat and microarray analysis were done on RNA samples from CD34+ cells before and 15 days after treatment using Affymetrix U133Plus2.0. One chip was used for one sample and there was no technical replicates. Twelve pairs of day 0 and day 15 specimens passed quality control for hybridization and RNA integrity. A list of differentially regulated genes was created after GC-RMA normalization by t-test paired using a 1.5 fold cut-off with p<0.005.

2009-06-20 | E-GEOD-16625 | biostudies-arrayexpress

Microarray transcription analysis of MDS/MPN leukocyte samples with and without EZH2 mutations (n = 12, each) and EZH2-downregulated F-36P, MOLM-13 and OCI-M2 cell lines, using 2 shRNAs targeting EZH2 and a non-targeting control shRNA, each

Project description:The aim of this study was to identify EZH2 targets in myeloid malignancies. RNA samples from control F-36P, MOLM-13 and OCI-M2 cells (secondary AML after MDS; EZH2 wild type) treated with random shRNA (n = 4, each) and test F-36P, MOLM-13 and OCI-M2 cells treated with either one of two EZH2-targeting shRNAs (n = 4, each) were screened for differential gene expression. RNA from EZH2 wild type (n = 12) and mutant (n = 12) MDS/MPN patients was also analyzed by microarray transcriptome analysis.

2017-06-15 | E-MTAB-5766 | biostudies-arrayexpress

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