{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["72"],"submitter":["Gonye AL"],"funding":["National Institutes of Health National Cancer Institute","US Department of Defense Prostate Cancer Research Program"],"pubmed_abstract":["Chemotherapy resistance remains a critical barrier in cancer treatment, partly driven by polyploid cells that survive therapy and contribute to tumor recurrence. Here, we investigated epigenomic and transcriptional changes associated with cisplatin-surviving polyploid cells compared to parental cancer cells in prostate cancer (PC3) and triple-negative breast cancer (MDA-MB-231) cell lines. We observed persistent dysregulation of chromatin compaction and altered nuclear structure in polyploid cells following cisplatin treatment. Genome-wide chromatin accessibility profiling via ATAC-seq revealed significant remodeling, notably decreased promoter accessibility at proliferation-associated loci and increased accessibility of distal regulatory elements linked to inflammation and stress response"],"journal":["Neoplasia (New York, N.Y.)"],"pagination":["101268"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12857548"],"repository":["biostudies-literature"],"pubmed_title":["Polyploid cisplatin-resistant cancer cells have altered nuclear organization and epigenomic status."],"pmcid":["PMC12857548"],"pubmed_authors":["Cherry C","Orzolek L","Butler G","Pienta KJ","Amend SR","Gonye AL","Truskowski K","Loftus LV","Patatanian M"],"additional_accession":[]},"is_claimable":false,"name":"Polyploid cisplatin-resistant cancer cells have altered nuclear organization and epigenomic status.","description":"Chemotherapy resistance remains a critical barrier in cancer treatment, partly driven by polyploid cells that survive therapy and contribute to tumor recurrence. Here, we investigated epigenomic and transcriptional changes associated with cisplatin-surviving polyploid cells compared to parental cancer cells in prostate cancer (PC3) and triple-negative breast cancer (MDA-MB-231) cell lines. We observed persistent dysregulation of chromatin compaction and altered nuclear structure in polyploid cells following cisplatin treatment. Genome-wide chromatin accessibility profiling via ATAC-seq revealed significant remodeling, notably decreased promoter accessibility at proliferation-associated loci and increased accessibility of distal regulatory elements linked to inflammation and stress response","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Feb","modification":"2026-06-10T08:53:44.741Z","creation":"2026-06-10T03:12:18.535Z"},"accession":"S-EPMC12857548","cross_references":{"pubmed":["41570447"],"doi":["10.1016/j.neo.2025.101268"]}}