Project description:To investigate ferroptosis-dependent changes in DNA methylation, a genome wide DNA methylation profiling of ferroptotic (RSL3-treated) multiple myeloma cells (MM1S & MM1R) was performed using the 850K MethylationEPIC BeadChip Array. The ferroptotic DNA methylation signature was compared to myeloma cells pre-treated with the ferroptosis inhibitor ferrostatin-1 (FRSL3), which served as a negative control. In total, three biological replicates per treatment per cell line were included.
Project description:We performed genome-wide DNA methylation profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to identify methylation changes distinct to each cell line Three multiple myeloma cell lines (KMS11, MM.1S, and RPMI8226) with two replicates each
Project description:We performed genome-wide DNA methylation profiling of KMS11, MM.1S, and RPMI8226 multiple myeloma cell lines to identify methylation changes distinct to each cell line
Project description:Genome wide DNA methylation profiling of bone marrow-derived mesenchymal stromal cells from healthy donors (n=11), monoclonal gammopathy of undetermined significance (MGUS) (n=10), smoldering myeloma (SMM) (n=8), multiple myeloma (MM) (n=9) patients, and healthy donors exposed to the MM.1S cell line (n=3). The Illumina Infinium MethylationEPIC Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in this cell type.
Project description:Genome wide DNA methylation profiling of bone marrow-derived mesenchymal stromal cells from healthy donors (n=11), monoclonal gammopathy of undetermined significance (MGUS) (n=10), smoldering myeloma (SMM) (n=8), multiple myeloma (MM) (n=9) patients, and healthy donors exposed to the MM.1S cell line (n=3). The Illumina Infinium MethylationEPIC Beadchip was used to obtain DNA methylation profiles across approximately 850,000 CpGs in this cell type.
Project description:Methylation data on 442 multiple myeloma patients. Multiple myeloma cells from patient bone marrow aspirates were obtained at diagnosis and purified (>95%) using immune-magnetic CD138-cell sorting. RNA and DNA were extracted using RNA/DNA mini kit or Allprep kits (QIAGEN) according to manufacturers’ instructions. The EZ DNA Methylation kit (Zymo Research) was used for bisulfite conversion of genomic DNA. Tumor DNA methylation was profiled using Illumina Infinium HumanMethylation450 (450k).
Project description:Multiple myeloma (MM) remains incurable despite the introduction of novel agents and a relapsing course is observed in the majority of patients. Although the development of genomic technologies has greatly improved our understanding of MM pathogenesis, the mechanisms underlying relapse have been less investigated. In this study, an integrative analysis of DNA copy number, DNA methylation and gene expression was conducted in matched diagnosis and relapse samples from 17 MM patients. Overall, the acquisition of abnormalities at relapse was much more frequent than the lost of lesions present at diagnosis, and DNA losses were significantly more frequent at relapse than in diagnosis samples. Interestingly, copy number abnormalities involving more than 100 Mb of DNA at relapse significantly impact the gene expression of these samples, provoking a particular deregulation of IL-8 pathway. On the contrary, no relevant modifications of gene expression were observed in those samples with less than 100 Mb affected by chromosomal changes. Although different statistical approaches were used to uncover genes whose abnormal expression at relapse was regulated by DNA methylation, only two genes significantly deregulated in relapse samples (SORL1 and GLT1D1) showed a negative methylation-expression correlation. A deeper analysis demonstrated that DNA methylation was involved in regulation of SORL1 expression in MM. Finally, relevant changes in gene expression observed in relapse samples, such us downregulation of CD27 and P2RY8, were not apparently preceded by alterations in corresponding DNA. Taken together, these results showed that genomic heterogeneity, both at the DNA and RNA level, is a hallmark of MM transition from diagnosis to relapse. Please note that an a first step all analyses were carried out independently in each series, being the number of samples of 40 in methylation, 38 in SNP and 34 in expression series. In the next step, association studies were performed only in the overlapping samples, being 34 matching samples between expression and methylation and 32 samples between expression and SNP data.