{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yost KE"],"funding":["U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI)","Cancer Research UK","NHLBI NIH HHS","U.S. Department of Health & Human Services | NIH | National Human Genome Research Institute (NHGRI)","NHGRI NIH HHS","NCI NIH HHS","National Science Foundation (NSF)","NINDS NIH HHS","U.S. Department of Health & Human Services | National Institutes of Health (NIH)","NIGMS NIH HHS"],"pagination":["1189-1200"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12081301"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["57(5)"],"pubmed_abstract":["Genome conformation underlies transcriptional regulation by distal enhancers, and genomic rearrangements in cancer can alter critical regulatory interactions. Here we profiled the three-dimensional genome architecture and enhancer connectome of 69 tumor samples spanning 15 primary human cancer types from The Cancer Genome Atlas. We discovered the following three archetypes of enhancer usage for over 100 oncogenes across human cancers: static, selective gain or dynamic rewiring. Integrative analyses revealed the enhancer landscape of noncancer cells in the tumor microenvironment for genes related to immune escape. Deep whole-genome sequencing and enhancer connectome mapping provided accurate detection and validation of diverse structural variants across cancer genomes and revealed distinct "],"journal":["Nature genetics"],"pubmed_title":["Three-dimensional genome landscape of primary human cancers."],"pmcid":["PMC12081301"],"funding_grant_id":["U24 CA264032","F99 CA274692","RM1-HG007735","DP1HG013599","R01HL171611","U24 CA264379","OT2 CA278635","R01 NS128028","OT2CA278635","R01 HL171611","R01CA218668","1U24CA264029-01","1U24CA264023-01","CGCATF-2021/100025","U24 CA264021","U24CA264032","CGCSDF-2021\\100007","F99 CA253729","RM1 HG007735","U24 CA264029","NIH F99CA274692","R01 CA218668","R01 GM114362","R01NS128028","R01GM114362","U24CA264379","U24 CA264023","DGE-1656518","U24 CA264009","R35-CA209919","DP1 HG013599","R35 CA209919","NIH F99CA253729"],"pubmed_authors":["Sundaram L","Zenklusen JC","Cancer Genome Atlas Analysis Network","Shams S","Doane AS","Greenleaf WJ","Clarke S","Khurana E","Zhao Y","Louie BH","Granja JM","Bafna V","Sarmashghi S","Curtis C","Chang HY","Felau I","Xu D","Choudhry H","Cherniack AD","Laird PW","Zhu K","Luebeck J","Yost KE","Imielinski M","Hung KL","Corces MR"],"additional_accession":[]},"is_claimable":false,"name":"Three-dimensional genome landscape of primary human cancers.","description":"Genome conformation underlies transcriptional regulation by distal enhancers, and genomic rearrangements in cancer can alter critical regulatory interactions. Here we profiled the three-dimensional genome architecture and enhancer connectome of 69 tumor samples spanning 15 primary human cancer types from The Cancer Genome Atlas. We discovered the following three archetypes of enhancer usage for over 100 oncogenes across human cancers: static, selective gain or dynamic rewiring. Integrative analyses revealed the enhancer landscape of noncancer cells in the tumor microenvironment for genes related to immune escape. Deep whole-genome sequencing and enhancer connectome mapping provided accurate detection and validation of diverse structural variants across cancer genomes and revealed distinct ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-01T05:51:21.06Z","creation":"2026-04-08T09:44:21.321Z"},"accession":"S-EPMC12081301","cross_references":{"pubmed":["40355593"],"doi":["10.1038/s41588-025-02188-0"]}}