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Tumor eQTM screening reveals distinct CpG panels for deconvolving cancer immune signatures

ABSTRACT: Tumor eQTM screening reveals distinct CpG panels for deconvolving cancer immune signatures

PROVIDER: PRJNA798830 | ENA |

REPOSITORIES: ENA

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Tumor eQTM screening reveals distinct CpG panels for deconvolving cancer immune signatures

Project description:Genome-wide DNA methylation profiling of melanoma samples. The Illumina Infinium Human DNA methylation EPIC Beadchip Kit was used to obtain DNA methylation profiles across approximately 850,000 CpGs.

2022-01-28 | GSE194042 | GEO

Tumor Expression Quantitative Trait Methylation Screening Reveals Distinct CpG Panels for Deconvolving Cancer Immune Signatures.

Project description:DNA methylation signatures in tumors could serve as reliable biomarkers that are accessible in archival tissues for tracking the epigenetic dynamics shaped by both cancer cells and the tumor microenvironment. However, given the ultrahigh dimensionality and noncollapsible nature of the data, it remains challenging to screen all CpG sites to identify the most promising marker panels. In this article, we introduce the concept of tumor-based expression quantitative trait methylation (eQTM) for the prioritization and systematic mining of predictive biomarkers. In melanoma as a disease model, eQTM CpGs and genes represent new and efficient candidate targets to be investigated for both prognostic and immune status monitoring purposes. Three cis-eQTM CpGs (cg07786657, cg12446199, and cg00027570) were strongly associated with and can serve as surrogate biomarkers for the tumor immune cytolytic activity score (CYT). In addition, multiple eQTM genes could be further exploited for predicting immunoregulatory phenotypes. A targeted gene panel analysis identified one eQTM in TCF7 (cg25947408) as a novel candidate biomarker for uncoupling overall T-cell differentiation and exhaustion status in a tumor. The prognostic significance of this eQTM as an independent signature to CYT was validated by both The Cancer Genome Atlas and Moffitt melanoma cohort data. Overall, eQTMs represent a mechanistically distinct class of potential biomarkers that can be used to predict patient prognosis and immune status.SignificanceThis study provides a novel and promising approach to identify targeted epigenetic biomarkers in cancer and will spur further analysis in tumor immune phenotyping.

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Project description:We assayed CpG methylation in cerebral cortex of neurologically and psychiatrically normal human postmortem specimens, as well as mouse forebrain specimens. Cross-species human-mouse DNA methylation conservation analysis shows that DNA methylation is not correlated with sequence conservation. Instead, greater DNA methylation conservation is correlated with increasing CpG density. We identified key genomic features that can be targeted for identification of epigenetic loci that may be developmentally and evolutionarily conserved and wherein aberrations in DNA methylation patterns can confer risk for disease. Characterization of evolutionary signatures of DNA methylation in the brain

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Project description:Cytosine (C) modifications within CpG dyads are central regulatory elements of mammalian genomes. In addition to 5-methylcytosine (mC), genomes can also contain high levels of 5-hydroxymethylcytosine (hmC) that is read differently by nuclear proteins than mC. However, hmC can co-exist with C and mC in different combinations in the two strands of CpG dyads, and it is poorly understood, how these combinatorial marks differ in their protein interactomes and regulatory functions. To identify nuclear binding proteins, we employed DNA promoter probes with differentially modified CpG dyads in pulldown experiments. The datasets comprise three biological replicates of HEK293T nuclear proteins binding to a VEGFA promoter sequence with differentially modified CpG dyads. Each biological replicate contains five technical replicates per modified CpG dyad, resulting in a total of 15 replicates for C/C, mC/mC and hmC/mC, and 10 replicates for hmC/C and hmC/hmC.

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Binding proteins of Hydroxymethylcytosine-modified CpG dyads from mouse brain tissue

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