GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE271nnn/GSE271705/primaryOK200TranscriptomicsHomo sapiensExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE271705GEOGSEfalseIntegrated ChIP-seq and Transcriptomic Profiling of Histone Modifications Across Breast Cancer Progression in MCF10A-Derived Cell LinesCancer arises from complex epigenetic mechanisms that drive tumorigenesis. Gene regulatory elements play a pivotal role in reprogramming gene expression patterns, facilitating tumor initiation, progression, and metastasis. However, a comprehensive characterization of epigenetic alterations across cancer development remains incomplete, particularly for the spectrum of post-translational histone modifications in the evolution of breast tumors. In this study, we explored the dynamic landscape of epigenetic changes using a breast cancer progression model based on the MCF10A cell line. We integrated ChIP-seq and transcriptomic profiling to investigate the epigenetic heterogeneity across four MCF10A-derived cancer cell lines: normal (MCF10A), HRAS G12V transformed, ductal carcinoma in situ (DCIS), and metastatic (CA1a). Our analysis revealed significant changes in chromatin patterns at regulatory elements, including stage-specific variability in H3K27me3 and H3K9me3-marked heterochromatin domains. These profiles underly the epigenomic changes in each of these cell states to provide insights into human breast cancer progression.2026/07/01GSE271705GSM8383045GSM8383046GSM8383043GSM8383044GSM8383049GSM8383039GSM8383047GSM8383048GSM8383041GSM8383042GSM8383050GSM838304016791271705Homo sapiens