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replication timing and epigenomic data  (Epigenomics ag)

 
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    Epigenomics ag replication timing and epigenomic data
    a Quantile-quantile plot of fishHook p -values to assess significance of gene mutational burden after removing confounders. The p -values were obtained by comparing observed mutational rate to the right tail (one-sided) of the expected mutational rates derived from a gamma-Poisson model of genome-wide mutational density and the covariates replication timing, <t>epigenetic</t> state, and sequence context. In the first stage of CIRCLE, six significant genes were identified below a false-discovery threshold (FDR < 0.1). b Odds ratios (ORs) of response to ICB therapy in patients with a high or moderate impact mutation in the indicated gene as compared to patients that do not have a high or moderate mutation in the given gene ( n = 272 patients). Error bars indicate the 95% confidence interval of the odds ratio. ORs greater than one indicate enrichment in responders and ORs less than one indicate enrichment in non-responders. Statistical significance was tested using a two-sided Wald’s test of coefficients with multiple-hypothesis correction (FDR < 0.2).
    Replication Timing And Epigenomic Data, supplied by Epigenomics ag, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/replication+data+and+code/pmc09270330-217-3-12?v=Epigenomics+ag
    Average 90 stars, based on 1 article reviews
    replication timing and epigenomic data - by Bioz Stars, 2026-07
    90/100 stars

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    1) Product Images from "Recurrent somatic mutations as predictors of immunotherapy response"

    Article Title: Recurrent somatic mutations as predictors of immunotherapy response

    Journal: Nature Communications

    doi: 10.1038/s41467-022-31055-3

    a Quantile-quantile plot of fishHook p -values to assess significance of gene mutational burden after removing confounders. The p -values were obtained by comparing observed mutational rate to the right tail (one-sided) of the expected mutational rates derived from a gamma-Poisson model of genome-wide mutational density and the covariates replication timing, epigenetic state, and sequence context. In the first stage of CIRCLE, six significant genes were identified below a false-discovery threshold (FDR < 0.1). b Odds ratios (ORs) of response to ICB therapy in patients with a high or moderate impact mutation in the indicated gene as compared to patients that do not have a high or moderate mutation in the given gene ( n = 272 patients). Error bars indicate the 95% confidence interval of the odds ratio. ORs greater than one indicate enrichment in responders and ORs less than one indicate enrichment in non-responders. Statistical significance was tested using a two-sided Wald’s test of coefficients with multiple-hypothesis correction (FDR < 0.2).
    Figure Legend Snippet: a Quantile-quantile plot of fishHook p -values to assess significance of gene mutational burden after removing confounders. The p -values were obtained by comparing observed mutational rate to the right tail (one-sided) of the expected mutational rates derived from a gamma-Poisson model of genome-wide mutational density and the covariates replication timing, epigenetic state, and sequence context. In the first stage of CIRCLE, six significant genes were identified below a false-discovery threshold (FDR < 0.1). b Odds ratios (ORs) of response to ICB therapy in patients with a high or moderate impact mutation in the indicated gene as compared to patients that do not have a high or moderate mutation in the given gene ( n = 272 patients). Error bars indicate the 95% confidence interval of the odds ratio. ORs greater than one indicate enrichment in responders and ORs less than one indicate enrichment in non-responders. Statistical significance was tested using a two-sided Wald’s test of coefficients with multiple-hypothesis correction (FDR < 0.2).

    Techniques Used: Derivative Assay, Genome Wide, Sequencing, Mutagenesis



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