ArticleGenome research2016
Three-dimensional disorganization of the cancer genome occurs coincident with long-range genetic and epigenetic alterations.
Article in Genome research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 1 of them a synthesis that pooled it.
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Who cites it
196 citing papers in PubMed, 1 synthesis or guideline pooled it, 368 citations in OpenAlex.
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- Rewiring cancer epigenome: lncRNA as modulator of chromatin architecture and neoplastic transformation.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- The urinary eccDNA landscape in prostate cancer reveals associations with genome instability and vital roles in cancer progression.Journal of advanced research · 2025Article
- Hi-C informed kernel association test: integrating 3-dimensional genome structure into variant-set association for whole-genome sequencing data.bioRxiv : the preprint server for biology · 2025Article
- TP63 mediates the generation of tumour-specific chromatin loops that underlie MYC activation in radiation-induced tumorigenesis.Nature communications · 2025Article
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- The Role of Non-Coding Regions in Breast Cancer: From Gene Regulation to Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The 3D genome of plasma cells in multiple myeloma.Scientific reports · 2025Article
- Estrogen-induced chromatin looping changes identify a subset of functional regulatory elements.Genome research · 2025Article
136 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A three-dimensional chromatin state underpins the structural and functional basis of the genome by bringing regulatory elements and genes into close spatial proximity to ensure proper, cell-type-specific gene expression profiles. Here, we performed Hi-C chromosome conformation capture sequencing to investigate how three-dimensional chromatin organization is disrupted in the context of copy-number variation, long-range epigenetic remodeling, and atypical gene expression programs in prostate cancer. We find that cancer cells retain the ability to segment their genomes into megabase-sized topologically associated domains (TADs); however, these domains are generally smaller due to establishment of additional domain boundaries. Interestingly, a large proportion of the new cancer-specific domain boundaries occur at regions that display copy-number variation. Notably, a common deletion on 17p13.1 in prostate cancer spanning the TP53 tumor suppressor locus results in bifurcation of a single TAD into two distinct smaller TADs. Change in domain structure is also accompanied by novel cancer-specific chromatin interactions within the TADs that are enriched at regulatory elements such as enhancers, promoters, and insulators, and associated with alterations in gene expression. We also show that differential chromatin interactions across regulatory regions occur within long-range epigenetically activated or silenced regions of concordant gene activation or repression in prostate cancer. Finally, we present a novel visualization tool that enables integrated exploration of Hi-C interaction data, the transcriptome, and epigenome. This study provides new insights into the relationship between long-range epigenetic and genomic dysregulation and changes in higher-order chromatin interactions in cancer.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.