Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA293703 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:DNA methylation-based immune response signature improves patient diagnosis in multiple cancers (TOP Cohort)
| PRJNA293702 | ENA
Project description:DNA methylation-based immune response signature improves patient diagnosis in multiple cancers (Cohort 1)
| PRJNA293704 | ENA
Project description:DNA methylation-based immune response signature improves patient diagnosis in multiple cancers
| PRJNA293700 | ENA
Project description:Here we characterize an association between disease progression and DNA methylation in Diffuse Large B cell Lymphoma (DLBCL). By profiling genome-wide DNA methylation at single base-pair resolution in thirteen DLBCL diagnosis-relapse sample pairs, we show DLBCL patients exhibit heterogeneous evolution of tumor methylomes during relapse. We identify differentially methylated regulatory elements and determine a relapse–associated methylation signature converging on key pathways such as transforming growth factor beta (TGF-beta) receptor activity. We also observe decreased intra-tumor methylation heterogeneity from diagnosis to relapsed tumor samples. Relapse-free patients display lower intra-tumor methylation heterogeneity at diagnosis compared to relapsed patients in an independent validation cohort. Furthermore, intra-tumor methylation heterogeneity is predictive of time to relapse. Therefore, we propose that epigenomic heterogeneity may support or drive the relapse phenotype and can be used to predict DLBCL relapse. Using ERRBS, we profiled genome-wide DNA methylation patterns of non-relapse DLBCL tumor samples at diagnosis, relaspe DLBCL patient samples at diagnosis and relaspe.
2015-04-14 | E-GEOD-66329 | biostudies-arrayexpress
Project description:Background an Aim: Epigenetics are thought to play a major role in the carcinogenesis of patients that develop multiple colorectal cancers (CRC) in the non-hereditary setting. Previous studies have suggested concordant DNA hypermethylation between tumor pairs. However, only a few methylation markers have been analyzed. This study was aimed at describing the underlying epigenetic signature that differentiates multiple from solitary colorectal cancer tumors using a genome-scale DNA methylation profiling. Patients and Methods: We used a population-based cohort (EPICOLON II) of 12 patients with synchronous CRC and 29 age- sex- and tumor location-paired solitary CRC patients. DNA methylation profiling was performed using the Illumina Infinium HM27 DNA methylation assay. The most significantly hypermethylated CpG sites results were validated by Methylight. Tumors samples were also analyzed for the CpG Island Methylator Phenotype (CIMP) using the Infinium DNA methylation data; KRAS and BRAF mutations; microsatellite instability; and immunohistochemistry for MLH1/MSH2/MSH6/PMS2. Functional annotation clustering of differentially methylated genes between multiple and solitary CRCs was performed. Results: We identified 102 CpG sites that showed significant DNA hypermethylation in multiple versus solitary tumors (difference in M-NM-2 value >0.1 and p<0.05). Methylight assays validated the array results for 4 selected significantly hypermethylated genes (MAP1B, HTRA1, ALOX15, TIMP3) identified in the profiling (p=0.0002). Based on the Infinium data, 8/12 (66.6%) of multiple tumors were classified as CIMP-high, as compared to 5/29 (17%) solitary tumors (p=0.004). CIMP-high tumors displayed significant hypermethylation in 301 CpG sites (difference in M-NM-2 value >0.1; p value <0.05). Interestingly, 76/102 (74.5%) of the hypermethylated CpG sites found in multiple vs. solitary tumors were also seen to be hypermethylated in CIMP-H tumors. Functional analysis of hypermethylated genes found in multiple vs. solitary tumors showed the presence and enrichment of genes involved in different tumorigenic functions. Conclusions: Multiple colorectal cancers are associated with a distinct methylation phenotype, with a close association between tumor multiplicity and CIMP-high. Our results may be important to unravel the underlying mechanism of tumor multiplicity in the non-hereditary scenario, and provide novel potential biomarkers for identifying high-risk patients and tailoring surveillance strategies. We used a population-based cohort (EPICOLON II) of 12 patients with synchronous CRC and 29 solitary CRC patients. DNA methylation profiling was performed using the Illumina Infinium HM27 DNA methylation assay.
2014-09-01 | E-GEOD-52573 | biostudies-arrayexpress
Project description:Patient with multiple sclerosis improves during pregnancy while temporarily worsening post-partum. The reasons behind the disease modulation during pregnancy remain unknown. In this study, we have investigated the effect of pregnancy on circulating CD4+ and CD8+ T cells from patients with multiple sclerosis and healthy controls to gain a deeper understanding why patients with multiple sclerosis improves during pregnancy. We assessed epigenome-wide DNA methylation in CD4+ and CD8+ T cells obtained during (1st, 2nd and 3rd trimester) and after pregnancy (6 weeks post-partum), using the Infinium MethylationEPIC 850K array.
2023-09-23 | E-MTAB-12250 | biostudies-arrayexpress
Project description:Triple-Negative Breast Cancer (TNBC) is a heterogeneous collection of cancers where personalized treatment is difficult and chemotherapy and immunotherapy combinations are the main treatment options. Many attempts to tackle patient heterogeneity have focused on defining cancer-intrinsic subtypes based on differential tumor mRNA-expression across patient cohorts. While these multi-gene diagnostics have shown success in hormone receptor- positive cancers (e.g. OncotypeDX), no TNBC classifiers have shown clinical utility in predicting patient survival or treatment response. We hypothesize that TNBC-infiltrating immune-cells both affect mRNA-based classification and contribute to treatment response variability. To evaluate this hypothesis, we benchmarked the performance of common TNBC-classification (TNBC-type) and infiltrating immune (CIBERSORT) algorithms on the same underlying datasets. Encouragingly, we found that – as with OncotypeDx– highly proliferative TNBC-subtypes (BL1) show the strongest evidence of response to cytotoxic chemotherapies. Interestingly, this cancer-proliferative signature (BL1) is strongly correlated with enrichment in tumor-infiltrating lymphocyte signatures (TIL) which show superior prognostic and predictive power. In addition, Tumor Associated Macrophage (TAM) signatures show independent predictive and prognostic power for both patient survival and response to anthracycline- and taxane-based chemotherapies. These gene signature-based correlations were validated in a new independent cohort of 67 TNBC-patients treated with neoadjuvant chemotherapy. Overall, these results argue for the independent contributions of both cancer-intrinsic and -extrinsic factors in predicting treatment response in the neoadjuvant setting.
2024-03-20 | GSE260693 | GEO
Project description:Colorectal polyp is known a precursor of colorectal cancer (CRC) that holds an increased risk for progression to CRC. Circulating cell-free DNA(cfDNA) methylation has shown favorable performance in the detection and monitoring the malignant progression in a variety of cancers. Here, we conducted a study to discovery cfDNA methylation markers for the diagnosis of CRC. We first performed a genome-wide analysis using the Infinium HumanMethylationEPIC BeadChip array to identify differentially methylated CpGs (DMCs) between 8 CRC and 8 polyp tissues. Then, we validated DMCs in a larger tissue cohort and four methylation markers (cg04486886, cg06712559, cg13539460 and cg27541454) were selected as the methylation markers in tissue by LASSO and random forest models. A diagnosis prediction model was bulit based on the four markers and the methylaion diagnosis score (md-score) can effectively discriminate patients with CRC from polyp tissues. Finally, a single cfDNA methylation marker, cg27541454, was confirmed hypermethylated in CRC in the plasma validation cohort. Together, our findings suggested that the md-score derived from tissue could robustly detect CRC from polpy patients, and cg27541454 may be a promising candidate non-invasive biomarker for CRC early diagnosis.
2024-01-01 | GSE220160 | GEO
Project description:Less than half of all patients with advanced-stage high-grade serous ovarian cancers (HGSC) survive more than five years post-diagnosis but those who have an exceptionally long survival could provide new insights into tumor biology and therapeutic approaches. We analyzed 60 patients with advanced-stage, HGSC who survived more than 10 years after diagnosis using whole-genome sequencing, transcriptome, and methylome profiling of their primary tumor samples, comparing this data to 66 short- or moderate-term survivors. Tumors of long-term survivors were more likely to have multiple alterations in genes associated with DNA repair, and more frequent somatic variants resulting in an increased predicted neoantigen load. Patients clustered into survival groups based on genomic and immune cell signatures, including three subsets of patients with BRCA1 alterations with distinctly different outcomes. Specific combinations of germline and somatic gene alterations, tumor cell phenotypes, and differential immune responses appear to contribute to long-term survival in HGSC. Methylation profiling was done on 58 high grade serous ovarian cancer samples, 53 of which were primary tumors and and 5 were relapse tumors. 73 primary tumors from GSE65820 were also used as part of the cohort.
2022-08-26 | GSE211686 | GEO
Project description:A Methylation-Based Signature Predicts Survival In Hepatocellular Carcinoma Patient
| PRJNA244008 | ENA