ArticleNature cancer2024
Global loss of promoter-enhancer connectivity and rebalancing of gene expression during early colorectal cancer carcinogenesis.
Article in Nature cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.
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
19 citing papers in PubMed.
- Review
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Promoter reinforcement supports transcriptional resilience in drug-resistant cancer.Nature structural & molecular biology · 2026Article
- BRD2 upregulation as a pan-cancer adaptive resistance mechanism to BET inhibition.Cellular & molecular biology letters · 2026Article
- NanoLoop: A Deep Learning Framework Leveraging Nanopore Sequencing for Chromatin Loop Prediction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Review
- Enhancer-dependent gene regulation in space, time, and malignancies.International journal of cancer · 2026Review
- Organoids glimpse: the nexus for diverse tumor heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Tumor heterogeneity as a driver of drug resistance and its implications for personalized therapy.Cancer drug resistance (Alhambra, Calif.) · 2026Review
- Bioinformatics combined with machine learning for the identification of malignant transformation markers in colorectal polyps.Frontiers in molecular biosciences · 2026Article
- Pan-cancer 3D genomic analysis revealed extremely long Polycomb loops as the biomarker for sensitivity to Polycomb inhibition.bioRxiv : the preprint server for biology · 2025Article
- BRD2 Upregulation as a Pan-Cancer Adaptive Resistance Mechanism to BET Inhibition.bioRxiv : the preprint server for biology · 2025Article
- Redefining familial adenomatous polyposis: competition, cooperation, and the path to monoclonality.Familial cancer · 2025Review
- Unravelling tumour spatiotemporal heterogeneity using spatial multimodal data.Clinical and translational medicine · 2025Review
- Environmental Drivers of Malignant Clonal Selection in Precancerous Lesion Evolution.Cell proliferation · 2025Review
- 3D genome landscape of primary and metastatic colorectal carcinoma reveals the regulatory mechanism of tumorigenic and metastatic gene expression.Communications biology · 2025Article
- Global chromatin reorganization and regulation of genes with specific evolutionary ages during differentiation and cancer.Nucleic acids research · 2025Article
- Machine learning tools for deciphering the regulatory logic of enhancers in health and disease.Frontiers in genetics · 2025Review
- A 3D genome view of colon cancer initiation.Nature cancer · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
26 authors.
Funding
Abstract
Although three-dimensional (3D) genome architecture is crucial for gene regulation, its role in disease remains elusive. We traced the evolution and malignant transformation of colorectal cancer (CRC) by generating high-resolution chromatin conformation maps of 33 colon samples spanning different stages of early neoplastic growth in persons with familial adenomatous polyposis (FAP). Our analysis revealed a substantial progressive loss of genome-wide cis-regulatory connectivity at early malignancy stages, correlating with nonlinear gene regulation effects. Genes with high promoter-enhancer (P-E) connectivity in unaffected mucosa were not linked to elevated baseline expression but tended to be upregulated in advanced stages. Inhibiting highly connected promoters preferentially represses gene expression in CRC cells compared to normal colonic epithelial cells. Our results suggest a two-phase model whereby neoplastic transformation reduces P-E connectivity from a redundant state to a rate-limiting one for transcriptional levels, highlighting the intricate interplay between 3D genome architecture and gene regulation during early CRC progression.
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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 Socratic graph.