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| EWAS ID | EWAS1296 |
| GSE ID | GSE112596 |
| EWAS Title | DNA Methylation Signatures of Crohn's disease Largely a Consequence of Inflammation |
| Disease/Phenotype | multiple sclerosis |
| Group1 | multiple sclerosis patients treated with fumaric acid esters(FAE) |
| Group2 | untreated/treatment naive multiple sclerosis patients(Naive) |
| Group1 Sample Size | 42 |
| Group2 Sample Size | 54 |
| Summary | Crohn’s disease is a relapsing inflammatory disorder with a variable clinical course. While most patients present with purely an inflammatory phenotype (B1) at diagnosis, a subgroup (~20%) rapidly progresses to complicated disease manifestations that include stricturing (B2) within 5 years. DNA methylation is a key epigenetic mechanism that can regulate gene expression and thereby influence the development and progression of complex diseases. Site-specific DNA methylation differences have been reported in peripheral blood of patients with Crohn’s disease, but investigation of the temporal relationship between methylation and disease is required to establish whether the methylome plays a causal role and can be leveraged for therapeutic benefits. To this end, we conducted an epigenome-wide study of methylation (~850K sites) in peripheral blood at diagnosis and during follow-up from the RISK pediatric Crohn’s disease inception cohort. While some methylation changes associated with Crohn’s disease might be causal, in peripheral blood the vast majority are found to be a transient consequence of inflammation and thus a symptom of disease. |
| Contributor | Somineni HK, Venkateswaran S, Kilaru V, Marigorta UM, Mo A, Okou DT, Kellermayer R, Mondal K, Cobb D, Walters TD, Griffiths A, Noe JD, Crandall WV, Rosh JR, Mack DR, Heyman MB, Baker SS, Stephens MC, Baldassano RN, Markowitz JF, Dubinsky MC, Cho J, Hyams JS, Denson LA, Gibson G, Cutler DJ, Conneely KN, Smith AK, Kugathasan S |
| Public date | Public on Apr 03, 2018 |
| Citation (PubMed ID) | - |
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