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An epigenetic gene signature underlies phenotype switching in early stage melanomas [ChIP-seq]

GSE197235 Homo sapiens Genome binding/occupancy profiling by high throughput sequencing 8 samples Submitted 2024/05/08 Platform GPL18573
Summary
A 122-epigenetic gene signature distinguished low- versus high-risk early stage melanomas. We sought to validate the signature, examined clinical correlates in a cohort of primary melanomas of the skin, and studied the underlying transcriptomic aberrations and changes in chromatin in cell lines representing these two groups. H3K27Ac ChipSeq profiles of primary human melanoma cell lines (n=4) as well as corresponding input samples were generated by deep sequencing using Illumina NextSeq500. Purpose: The goals of this study are to identify H3K27Ac differential peak expression between two groups of melanoma cell lines (Epgn1 and Epgn3) and relate this data to RNASeq. Methods: H3K27Ac ChipSeq was performed on 4 melanoma cell lines by deep sequencing 75bp single end reads using Illumina NextSeq500. Reads were aligned and counts called using____. The sequence reads that passed quality filters were analyzed. Results: Using an optimized data analysis workflow, we mapped about 40 million reads per Chip sample and 60 million reads per input sample to the human genome (build _____). Conclusions: Our study allowed us to identify differentially expressed peaks between two classes of melanoma cell lines and relate this information to differential gene expression. Further in vitro and in vivo assays using some of the candidate genes identified will allow us to more fully understand primary melanoma progression.
Published in
Differential histone acetylation and super-enhancer regulation underlie melanoma cell dedifferentiation
Mendelson K, Martin TC, Nguyen CB et al. · JCI insight 2024 · PMID 38319712 · doi:10.1172/jci.insight.166611
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Also filed as BioProject PRJNA809401 and SRA study SRP360984. Searching any of these in the dataset finder brings you back here.

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