ArticleNature communications2024
Pervasive structural heterogeneity rewires glioblastoma chromosomes to sustain patient-specific transcriptional programs.
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 24 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Unlocking glioblastoma: breakthroughs in molecular mechanisms and next-generation therapies.Medical oncology (Northwood, London, England) · 2025Pooled it
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Peptides from the Shadows: Molecular Depth Insights and Clinical Horizons of Circular RNA-encoded Peptides in Gliomas.Neuromolecular medicine · 2026Review
- Enhancer-dependent gene regulation in space, time, and malignancies.International journal of cancer · 2026Review
- Structural variation drives enhancer hijacking via 3D genome disruption in ccRCC.NPJ digital medicine · 2026Article
- FKBP9 enhances IGF2BP1-mediated mJHEP reports : innovation in hepatology · 2025Article
- Do Glioma Cells Rewire Neural Circuits through Epigenetic Changes? DNA Methylation Analysis of Genes Involved in Neuron-Glioma Communication in the Human Frontal Cortex.Journal of molecular neuroscience : MN · 2025Article
- Structural variants in the 3D genome as drivers of disease.Nature reviews. Genetics · 2025Review
- Cracking glioblastoma core regulatory codes.Nature cell biology · 2025Article
- A 3D genome compendium of breast cancer progression.iScience · 2025Article
- Perturbing neural stem cell fate in glioblastoma heterogeneity and beyond.Stem cell reports · 2025Article
- What Epigenetics Teaches Us About Neuron-Glioma Interactions.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Regulation of the brain tumor microenvironment by focused ultrasound.Molecular therapy. Oncology · 2025Review
- Enhancer RNA-mediated transcriptional regulatory programs reveal the malignant progression of glioma.Science advances · 2025Article
- [New methods at the transition from research to routine diagnostics].Pathologie (Heidelberg, Germany) · 2025Article
- Three-dimensional regulatory hubs support oncogenic programs in glioblastoma.Molecular cell · 2025Article
- Spatial 3D genome organization reveals intratumor heterogeneity in primary glioblastoma samples.Science advances · 2025Article
- Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025Review
- Three-dimensional regulatory hubs support oncogenic programs in glioblastoma.bioRxiv : the preprint server for biology · 2024Article
- The genome in space and time comes of age.Nucleus (Austin, Tex.) · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
Abstract
Glioblastoma multiforme (GBM) encompasses brain malignancies marked by phenotypic and transcriptional heterogeneity thought to render these tumors aggressive, resistant to therapy, and inevitably recurrent. However, little is known about how the spatial organization of GBM genomes underlies this heterogeneity and its effects. Here, we compile a cohort of 28 patient-derived glioblastoma stem cell-like lines (GSCs) known to reflect the properties of their tumor-of-origin; six of these were primary-relapse tumor pairs from the same patient. We generate and analyze 5 kbp-resolution chromosome conformation capture (Hi-C) data from all GSCs to systematically map thousands of standalone and complex structural variants (SVs) and the multitude of neoloops arising as a result. By combining Hi-C, histone modification, and gene expression data with chromatin folding simulations, we explain how the pervasive, uneven, and idiosyncratic occurrence of neoloops sustains tumor-specific transcriptional programs via the formation of new enhancer-promoter contacts. We also show how even moderately recurrent neoloops can relate to patient-specific vulnerabilities. Together, our data provide a resource for dissecting GBM biology and heterogeneity, as well as for informing therapeutic approaches.
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Registered trials
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.