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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

ABSTRACT: 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

PROVIDER: PRJNA1141902 | ENA |

REPOSITORIES: ENA

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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

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

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Affymetrix SNP array data for dic(1;7)(q10;p10) in Myelodysplastic Syndromes (MDS)

Project description:The unbalanced translocation t(1;7)(q10;p10), generating 1q trisomy and 7q monosomy, is due to centromere-centromere juxtaposition. This dicentric chromosome is a recurrent change in myelodysplastic syndromes (MDS), with half the cases arising after chemo/radio-therapy. To date, given the absence of genes within the centromeric regions, no specific molecular events have been identified in this cytogenetic subgroup. We first identified a comprehensive genetic and epigenetic landscape of MDS with dic(1;7)(q10;p10) and compared it to normal controls and other therapy-related Myeloid Neoplasms (t-MNs). RNA-seq showed a unique downregulated signature in dic(1;7) cases, affecting more than 80% of differentially expressed genes. As revealed by pathway and gene ontology analyses, downregulation of ATP-binding cassette (ABC) transporters and of genes related to lipid metabolism, and upregulation of p53 signaling were the most relevant biological features of dicentric-positive MDS. Despite 1q trisomy, more than 50% of 1q deregulated genes were downregulated. This partial gene dosage effect was clarified by epigenetic analysis, which highlighted the presence of a specific hypermethylated pattern on 1q. Furthermore, in a supervised analysis, hypermethylation in all dicentrics clustered at intronic enhancers and was enriched for Krüppel-like transcription factors binding sites. Low expression levels of enhancer putative target genes accounted for more than 30% of the downregulated signature. Our findings demonstrate that alteration of centromeric DNA in dic(1;7) cases imposes a specific transcriptional program, driven by a unique epigenomic signature.

2019-09-01 | GSE118477 | GEO

The National Myelodysplastic Syndromes (MDS) Study

Project description:The National Myelodysplastic Syndromes (MDS) Study

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Project description:The National Myelodysplastic Syndromes (MDS) Study

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Oxidative stress in myelodysplastic syndromes

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2019-10-30 | PXD013609 | Pride

A hypermethylated ALOX12 gene is highly susceptible to 5-azacytidine treatment in myelodysplastic syndromes

Project description:5-azacytidine (AZA) is widely used for treatment of myelodysplastic syndromes (MDS). However, identifying predictive factors for response to AZA remains challenging. The aim in present study was to identify the genes which are susceptible to AZA in MDS and investigate the possibility of the gene for predictor for response to AZA therapy. To identify AZA-susceptible genes, we compared the gene expression changes by AZA in MDS-L cells (AZA-sensitive) with those in MDS-L/CDA cells (AZA-resistant) in culture. Of 438 AZA-susceptible genes, we searched the genes which are hypermethylated in MDS patients as compared to healthy controls by analyzing public dataset GSE152710, and found ALOX12 gene. Analysis of public dataset GSE145733 and GSE58831 revealed that ALOX12 expression was suppressed in MDS classes with excess blasts but not in other classes, and were negatively and positively correlated with bone marrow blast counts and survival, respectively, in MDS patients. Analysis of public dataset GSE152710 revealed that the methylation level of ALOX12 gene was decreased in MDS patients with complete remission but not in those with partial response and progression disease after AZA therapy. Our retrospective clinical study in which nine AZA-treated patients were enrolled suggested that ALOX12 expression was increased in patients with favorable response, while decreased in patient with poor response after AZA therapy. In conclusion, ALOX12 gene could be tumor suppressive and promising marker for predicting the response to AZA therapy in MDS.

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Project description: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

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