Methylation_PBL_UC_Tofacitinib
Ontology highlight
ABSTRACT:
PROVIDER: EGAD00010002590 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Whole-genome DNA methylation profiling of PBL obtained from male patients with PSC-UC, or UC alone, or healthy individuals.
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Project description:A gene expression profiling sub-study was conducted in which colonic biopsy samples were collected for RNA extraction and hybridization to microarrays from 48 patients with UC who were participating in ACT 1, a placebo-controlled study of infliximab. Gene expression profiles from infliximab responders were compared with those of baseline and infliximab non-responder samples. Infliximab had a significant effect on mRNA expression in treatment responders, with both infliximab dose and duration of treatment having an effect. Genes affected are primarily involved with inflammatory response, cell-mediated immune responses, and cell-to-cell signaling. Infliximab non-responders had a molecular phenotype that closely resembled that of untreated patients with UC. Unlike responders, non-responders do not effectively modulate TH1, TH2, and TH17 pathways. Gene expression can differentiate placebo and infliximab responders. Patients with moderate-to-severe, active UC were treated with infliximab or placebo at weeks 0, 2, 6 and every 8 weeks thereafter. Biopsy samples (n=113) were collected from 48 patients at baseline, weeks 8 and 30 for RNA extraction and microarray analysis.
2011-07-21 | E-GEOD-23597 | biostudies-arrayexpress
Project description:Ulcerative colitis is heritable disorder with variable clinical outcome but to date only less than 10% of the disease susceptibility and the disease outcome is explained by IBD (inflammatory bowel disease) associated genetic loci. This missing heritability lay fertile grounds for investigating epigenetics as possible explanation. The aims of the study were to investigate genome-wide DNA methylation of the rectal tissue in an inception cohort of UC at two time points, once at baseline (treatment naïve) and at follow-up to explore how longitudinal DNA methylation influences the disease onset, disease progression and outcome. For this purpose, we profiled DNA methylation within rectal mucosal biopsies of pediatric UC (n=211) and non-IBD control patients (n=85) to perform epigenome-wide association studies (EWAS) of specific cell types (i.e epithelial, immune, and fibroblast), to identify UC specific differences. We have also performed longitudinal analysis on follow-up samples (n =73), and also additional comparisons were made between patients eventually undergoing colectomy versus those who did not.
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Project description:Despite the increasing of available drugs in RA, the overall rate of non response is 30 to 40% of treated patients. To optimize the drug prescription and better elaborate the therapeutic strategies, gene profiling in PBMCs was used to predict the responsiveness to anakinra. Thirty two patients treated by anakinra (100mg/day s.c.) and méthotrexate, were categorized as responders whenever a change of Disease Activity Score 28 > 1.2 was obtained at 3 months. Blood from treated patients was collected at baseline. In 7 responders and 7 non responders, 51 mRNAs identified by microarray were expressed as a function of the response to treatment and an unsupervised hierarchical clustering perfectly separated responders from non responders. Keywords: anakinra effect PBMC then RNA were extracted from blood samples of 7 anakinra responders, 7 anakinra non responders and 1 pool of healthy subjects used as control. Each sample was hybridized twice in different nylon membrane. The control sample was hybridized twice in each nylon membrane.
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Project description:Myelodysplastic syndromes and chronic myelomonocytic leukemia (CMML) are characterized by mutations in epigenetic modifiers and aberrant DNA methylation. DNA methyltransferase inhibitors (DMTis) are used to treat these disorders, but response is highly variable with few means to predict which patients will benefit. To develop a molecular means of predicting response at diagnosis, we examined baseline differences in mutations, DNA methylation, and gene expression in 40 CMML patients responsive and resistant to decitabine (DAC). While somatic mutations did not differentiate responders and non-responders, we were able to identify for the first time 158 differentially methylated regions (DMRs) at baseline between responders and non-responders using next-generation sequencing. These DMRs were primarily localized to non-promoter regions and overlapped with distal regulatory enhancers. Using the methylation profiles, we developed an epigenetic classifier that accurately predicted DAC response at the time of diagnosis. We also found 53 differentially expressed genes between responders and non-responders. Genes up-regulated in responders were enriched in the cell cycle, potentially contributing to effective DAC incorporation. Two chemokines overexpressed in non-responders -- CXCL4 and CXCL7 -- were able to block the effect of DAC on normal CD34+ and primary CMML cells in vitro, suggesting their up-regulation contributes to primary DAC resistance. DNA methylation profiling in bone marrow mononuclear cells (BM MNC) from 39 CMML patients (19 decitabine responders vs. 20 non-responders).
2015-03-31 | E-GEOD-61161 | biostudies-arrayexpress
Project description:Myelodysplastic syndromes and chronic myelomonocytic leukemia (CMML) are characterized by mutations in epigenetic modifiers and aberrant DNA methylation. DNA methyltransferase inhibitors (DMTis) are used to treat these disorders, but response is highly variable with few means to predict which patients will benefit. To develop a molecular means of predicting response at diagnosis, we examined baseline differences in mutations, DNA methylation, and gene expression in 40 CMML patients responsive and resistant to decitabine (DAC). While somatic mutations did not differentiate responders and non-responders, we were able to identify for the first time 158 differentially methylated regions (DMRs) at baseline between responders and non-responders using next-generation sequencing. These DMRs were primarily localized to non-promoter regions and overlapped with distal regulatory enhancers. Using the methylation profiles, we developed an epigenetic classifier that accurately predicted DAC response at the time of diagnosis. We also found 53 differentially expressed genes between responders and non-responders. Genes up-regulated in responders were enriched in the cell cycle, potentially contributing to effective DAC incorporation. Two chemokines overexpressed in non-responders -- CXCL4 and CXCL7 -- were able to block the effect of DAC on normal CD34+ and primary CMML cells in vitro, suggesting their up-regulation contributes to primary DAC resistance. mRNA profiling in bone marrow mononuclear cells (BM MNC) from 14 CMML patients (8 decitabine responders vs. 6 non-responders).
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