Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA183086 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data of multiple sclerosis patients receiving subcutaneous Interferon-beta-1a therapy [U133 Plus 2.0]
| PRJNA148781 | ENA
Project description:The purpose of this study was to analyze the transcriptional effects induced by glatiramer acetate treatment (GA; Copaxone, 20 mg injected subcutaneously once daily) in blood monocytes of patients with relapsing-remitting form of multiple sclerosis (MS). By using Affymetrix DNA microarrays, we obtained genome-wide expression profiles of monocytes from 8 MS patients within the first two months of GA administration. EDTA blood samples were taken from all patients immediately before first and second GA injection as well as after 1 week, 1 month and 2 months. Total RNA of CD14+ monocytes isolated by magnetic-activated cell sorting (MACS) from each sample was extracted, labeled and hybridized to Affymetrix Human Genome U133 Plus 2.0 arrays to quantify the mRNA levels. This GEO entry provides the U133 Plus 2.0 microarray data.
2012-12-07 | E-GEOD-42763 | biostudies-arrayexpress
Project description:DNA methylation changes in PBMCs of multiple sclerosis patients on glatiramer acetate therapy
| PRJNA1367033 | ENA
Project description:Glatiramer Acetate (GA) has provided safe and effective treatment for multiple sclerosis (MS) patients for two decades. It acts as an antigen, yet the precise mechanism of action remains to be fully elucidated, and no validated pharmacokinetic or pharmacodynamic biomarkers exist. In order to better characterize GA’s biological impact, genome-wide expression studies were conducted with a human monocyte (THP-1) cell line. Consistent with previous literature, branded GA upregulated antiinflammatory markers (e.g. IL10), and modulated multiple immune-related pathways. Despite some similarities, significant differences were observed between expression profiles induced by branded GA and Probioglat, a differently-manufactured glatiramoid purported to be a generic GA. Cells from a human monocyte cell line (THP-1) were stimulated with either branded GA, purported generics from several manufacturers including Probioglat by ProbioMed, or vehicle control (mannitol) for 6, 12, or 24h. RNA was extracted and expression profiled genome-wide using the Affymetrix U133 Plus 2.0 chip. Four batches of GA and one batch of Probioglat were comparatively tested in six biological replicates each.
2015-05-22 | E-GEOD-68527 | biostudies-arrayexpress
Project description:DNA methylation is a universal epigenetic mechanism involved in the regulation of gene expression in both normal physiological conditions and various pathologies. It has been demonstrated that the development of multiple sclerosis (MS) is accompanied by significant alterations in DNA methylation profiles in the blood immune cells of patients. Studies investigating genome-wide DNA methylation changes during therapy for MS patients using immunomodulatory drugs are limited, and for glatiramer acetate (GA), such investigations have not been conducted at all.
2026-06-03 | GSE310754 | GEO
Project description:RNA was isolated from fresh cerebrospinal fluid samples of multiple sclerosis and control patients and analyzed by hybridization of HG U133 plus 2.0 arrays in order to investigate disease mechanisms of multiple sclerosis and to identify transcriptional biomarker
2014-06-01 | E-MTAB-2374 | biostudies-arrayexpress
Project description:The purpose of this study was to analyze the transcriptional effects induced by glatiramer acetate treatment (GA; Copaxone, 20 mg injected subcutaneously once daily) in blood monocytes of patients with relapsing-remitting form of multiple sclerosis (MS). By using Affymetrix DNA microarrays, we obtained genome-wide expression profiles of monocytes from 8 MS patients within the first two months of GA administration.
2012-12-07 | GSE42763 | GEO
Project description:Glatopa is a generic glatiramer acetate recently approved for the treatment of patients with relapsing forms of multiple sclerosis. Gene expression profiling was performed as a means to evaluate equivalence of Glatopa and Copaxone. Microarray analysis containing 39,429 unique probes across the entire genome was performed in murine glatiramer acetate–responsive Th2-polarized T cells, a test system highly relevant to the biology of glatiramer acetate. A closely related but nonequivalent glatiramoid molecule was used as a control to establish assay sensitivity. Multiple probe-level (Student’s t-test) and sample-level (principal component analysis, multidimensional scaling, and hierarchical clustering) statistical analyses were utilized to look for differences in gene expression induced by the test articles. The analyses were conducted across all genes measured, as well as across a subset of genes that were shown to be modulated by Copaxone. The following observations were made across multiple statistical analyses: the expression of numerous genes was significantly changed by treatment with Copaxone when compared against media-only control; gene expression profiles induced by Copaxone and Glatopa were not significantly different; and gene expression profiles induced by Copaxone and the nonequivalent glatiramoid were significantly different, underscoring the sensitivity of the test system and the multiple analysis methods. Comparative analysis was also performed on sets of transcripts relevant to T-cell biology and antigen presentation, among others that are known to be modulated by glatiramer acetate. No statistically significant differences were observed between Copaxone and Glatopa in the expression levels (magnitude and direction) of these glatiramer acetate-regulated genes. In conclusion, multiple methods consistently supported equivalent gene expression profiles between Copaxone and Glatopa.
2015-09-26 | GSE73465 | GEO
Project description:Expression data of multiple sclerosis patients receiving subcutaneous Interferon-beta-1b therapy [U133 A and B]
| PRJNA132617 | ENA
Project description:Expression data of multiple sclerosis patients receiving intramuscular Interferon-beta-1a therapy [U133 A and B]
| PRJNA120367 | ENA