ArticleNature communications2024
3D genomic analysis reveals novel enhancer-hijacking caused by complex structural alterations that drive oncogene overexpression.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- scAmp enables focal gene amplification analysis from single-cell data.Nature communications · 2026Article
- Telomere-driven replicative crisis is driven by large-scale changes in genomic architecture.Genome research · 2026Article
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- Oncogene amplification of CCND1 via extrachromosomal DNA impacts overall survival in head and neck squamous cell carcinoma.Discover oncology · 2026Article
- 3D chromatin architecture in cancer: mechanisms of dysregulation and emerging therapeutic strategies.Experimental & molecular medicine · 2026Review
- Histone mark remodeling in cancer: an enhancer-centered perspective.Genes & genomics · 2026Review
- Hi-C for genome-wide detection of enhancer-hijacking rearrangements in routine lymphoid cancer biopsies.Cell genomics · 2026Article
- Machine learning-predicted chromatin organization landscape across pediatric tumors.Scientific reports · 2026Article
- Chromatin Accessibility in Cancer: Biological Functions, Mechanisms, Therapeutic Potential, and Future Directions.MedComm · 2026Review
- Enhancer-dependent gene regulation in space, time, and malignancies.International journal of cancer · 2026Review
- Deregulated enhancer-promoter communication in cancer through altered nuclear architecture.International journal of cancer · 2026Review
- Mechanisms of enhancer-driven oncogene activation.International journal of cancer · 2026Review
- Extrachromosomal DNA in Solid Tumors-Landscape, Immune Effects, and Resistance to Targeted Therapy.Oncology research · 2026Review
- Engineering the Link: From Genome Interaction Maps to Functional Insight.Advanced biology · 2025Review
- Direction and modality of transcription changes caused by TAD boundary disruption in Slc29a3/Unc5b locus depends on tissue-specific epigenetic context.Epigenetics & chromatin · 2025Article
- HiC4D-SPOT: a spatiotemporal outlier detection tool for Hi-C data.Briefings in bioinformatics · 2025Article
- Modern biology of extrachromosomal DNA: A decade-long voyage of discovery.Cell research · 2025Review
- The role of extrachromosomal DNA in tumorigenesis and progression.Frontiers in oncology · 2025Review
- Article
- Role of Harmaline in Inhibiting c-Myc, Altering Molecular Typing, and Promoting Apoptosis in Triple-Negative Breast Cancer.Breast cancer (Dove Medical Press) · 2024Article
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10 authors.
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Abstract
Cancer genomes are composed of many complex structural alterations on chromosomes and extrachromosomal DNA (ecDNA), making it difficult to identify non-coding enhancer regions that are hijacked to activate oncogene expression. Here, we describe a 3D genomics-based analysis called HAPI (Highly Active Promoter Interactions) to characterize enhancer hijacking. HAPI analysis of HiChIP data from 34 cancer cell lines identified enhancer hijacking events that activate both known and potentially novel oncogenes such as MYC, CCND1, ETV1, CRKL, and ID4. Furthermore, we found enhancer hijacking among multiple oncogenes from different chromosomes, often including MYC, on the same complex amplicons such as ecDNA. We characterized a MYC-ERBB2 chimeric ecDNA, in which ERBB2 heavily hijacks MYC's enhancers. Notably, CRISPRi of the MYC promoter led to increased interaction of ERBB2 with MYC enhancers and elevated ERBB2 expression. Our HAPI analysis tool provides a robust strategy to detect enhancer hijacking and reveals novel insights into oncogene activation.
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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.