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Journal: Clinical epigenetics
Article Title: Single-cell transcriptomics reveal the prognostic roles of epithelial and T cells and DNA methylation-based prognostic models in pancreatic cancer.
doi: 10.1186/s13148-024-01800-0
Figure Lengend Snippet: Fig. 6 Construction and Evaluation of Prognostic RiskScoreEpi Model and Nomogram Integrating Clinical Information. A, B For TCGA Train Set (A) and ICGC Validation Set (B): Top panel: Distribution plot of RiskScoreEpi in high- and low-risk groups. Middle panel: Distribution plot of survival time and survival status in high- and low-risk groups; X-axis represents patients with increasing RiskScoreEpi, and Y-axis represents survival time. Bottom panel: Beta values of the six CpG sites in high- and low-risk groups. C ROC curves and AUC analyses for 1-, 3-, and 5-year overall survival prediction of the RiskScoreEpi model in TCGA dataset. D Sankey diagram illustrating similarities and differences in sample composition before and after grouping based on two different criteria: TCGA DNAm subgroups (left) and RiskScoreEpi model (right). E, F Univariate E and Multivariate F Cox regression analysis of RiskScoreEpi and clinical information in TCGA dataset. G Heatmap of six CpG sites’ methylation levels, corresponding RiskScoreEpi, survival time, survival status, and risk groups of the 8 PDAC patients we collected. Color bar = β-value. H Nomogram for predicting 1-, 2-, and 3-year overall survival of PDAC patients based on RiskScoreEpi and prognostic factors. I Calibration curves of the nomogram at 1, 3, and 5 years. J DCA curves of the nomogram, RiskScoreEpi, and other prognostic factors. TCGA, The Cancer Genome Atlas Program; ICGC, International Cancer Genome Consortium; ROC, receiver operating characteristic; AUC, area under the curve; PDAC, pancreatic ductal adenocarcinoma; DCA, decision curve analysis
Article Snippet:
Techniques: Biomarker Discovery, Methylation
Journal: BMC Cancer
Article Title: Exploring DNA methylation changes in promoter, intragenic, and intergenic regions as early and late events in breast cancer formation
doi: 10.1186/s12885-015-1777-9
Figure Lengend Snippet: Example of how some gene regions were chosen for examination in this study on the basis of available RRBS DNA methylation profiles for breast cancer cell lines and normal cell cultures and tissues visualized in the UCSC Genome Browser . a The EN1 gene structure with exons as heavy horizontal bars; b , the aligned CpG islands in the illustrated region.; c , DNA methylation (ENCODE/RRBS/HudsonAlpha) profiles for the indicated cell cultures and normal tissues using an 11-color, semi-continuous scale (see color key) to indicate the average DNA methylation levels at each monitored CpG site; d , aligned transcription results indicating that the non-transformed breast cancer cell line is not transcribing this gene irrespective of its lack of DNA methylation. Paradoxically, normal myoblasts are transcribing it despite some upstream DNA methylation. All data are from ENCODE
Article Snippet: Using a candidate gene approach on a large, ethnically diverse set of subjects, we compared not only invasive breast cancer and adjacent histologically normal tissue (as in the TCGA Illumina HumanMethylation450 database [ ]), but also control samples of reductive mammoplasty tissue from non-cancer patients using a quantitative, gold-standard method for
Techniques: DNA Methylation Assay, Transformation Assay
Journal: BMC Cancer
Article Title: Exploring DNA methylation changes in promoter, intragenic, and intergenic regions as early and late events in breast cancer formation
doi: 10.1186/s12885-015-1777-9
Figure Lengend Snippet: Mean percent methylation by gene and tissue type from the Breast Cancer Care in Chicago study
Article Snippet: Using a candidate gene approach on a large, ethnically diverse set of subjects, we compared not only invasive breast cancer and adjacent histologically normal tissue (as in the TCGA Illumina HumanMethylation450 database [ ]), but also control samples of reductive mammoplasty tissue from non-cancer patients using a quantitative, gold-standard method for
Techniques: Methylation, Control
Journal: BMC Cancer
Article Title: Exploring DNA methylation changes in promoter, intragenic, and intergenic regions as early and late events in breast cancer formation
doi: 10.1186/s12885-015-1777-9
Figure Lengend Snippet: Mean percent methylation and 95 % error bars by gene and tissue type for the DNA regions listed in Table . a DNA methylation analysis of samples from the Breast Cancer Care in Chicago study (2005-2008) as determined by our bisulfite pyrosequencing. Control samples (reduction mammoplasty) from unaffected women are represented by green bars, cancer-adjacent, histologically normal samples by blue bars and cancer samples by red bars. b Bioinformatic analysis of DNA methylation of breast cancer samples and paired non-cancerous adjacent samples from The Cancer Genome Atlas (TCGA). Paired non-cancerous adjacent samples are represented by blue bars and cancer samples by red bars. In both panels, promoter sequences are displayed first, followed by upstream sequences, then introns and lastly, DNA repeats
Article Snippet: Using a candidate gene approach on a large, ethnically diverse set of subjects, we compared not only invasive breast cancer and adjacent histologically normal tissue (as in the TCGA Illumina HumanMethylation450 database [ ]), but also control samples of reductive mammoplasty tissue from non-cancer patients using a quantitative, gold-standard method for
Techniques: Methylation, DNA Methylation Assay, Control
Journal: BMC Cancer
Article Title: Exploring DNA methylation changes in promoter, intragenic, and intergenic regions as early and late events in breast cancer formation
doi: 10.1186/s12885-015-1777-9
Figure Lengend Snippet: Adjusted differences in mean % methylation comparing adjacent (referent) to cancer tissue, overall and stratified by ER/PR status
Article Snippet: Using a candidate gene approach on a large, ethnically diverse set of subjects, we compared not only invasive breast cancer and adjacent histologically normal tissue (as in the TCGA Illumina HumanMethylation450 database [ ]), but also control samples of reductive mammoplasty tissue from non-cancer patients using a quantitative, gold-standard method for
Techniques: Methylation