ReviewSeminars in cancer biology2013
Higher order chromatin organization in cancer.
Review in Seminars in cancer biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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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.
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Who cites it
57 citing papers in PubMed, 99 citations in OpenAlex.
- SMARCA4 activation engages FOSL1 to drive enhancer reprogramming and tumorigenic phenotypes in SMARCA4-deficient LUAD cells.Cell death discovery · 2026Article
- Chromatin Remodeling in VSMC Phenotype Switching During Vascular Remodeling: From Mechanism to Therapeutic Potential.Biomolecules · 2026Review
- The isoflavone genistein selectively stimulates major satellite repeat transcription in mouse heterochromatin.Epigenetics & chromatin · 2025Article
- High Mobility Group A1 Chromatin Keys: Unlocking the Genome During MPN Progression.International journal of molecular sciences · 2025Review
- HMGA1 acts as an epigenetic gatekeeper of ASCL2 and Wnt signaling during colon tumorigenesis.The Journal of clinical investigation · 2025Article
- Review
- Review
- Chromatin as an old and new anticancer target.Trends in cancer · 2024Review
- Epigenetic regulation in cancer.MedComm · 2024Review
- Neutrophil nucleus: shaping the past and the future.Journal of leukocyte biology · 2023Article
- Super-resolution microscopy reveals the nanoscale cluster architecture of the DEK protein cancer biomarker.iScience · 2023Article
- Review
- HMGA1 induces FGF19 to drive pancreatic carcinogenesis and stroma formation.The Journal of clinical investigation · 2023Article
- Chromatin and Cancer: Implications of Disrupted Chromatin Organization in Tumorigenesis and Its Diversification.Cancers · 2023Review
- Low lamin A levels enhance confined cell migration and metastatic capacity in breast cancer.Oncogene · 2022Article
- Review
- Article
- 3D chromatin architecture and transcription regulation in cancer.Journal of hematology & oncology · 2022Review
- To be or not be (in the LAD): emerging roles of lamin proteins in transcriptional regulation.Biochemical Society transactions · 2022Review
- Epigenetic-Mediated Regulation of Gene Expression for Biological Control and Cancer: Cell and Tissue Structure, Function, and Phenotype.Results and problems in cell differentiation · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
In spite of our increased understanding of how genomes are dysregulated in cancer and a plethora of molecular diagnostic tools, the front line and 'gold standard' detection of cancer remains the pathologist's detection of gross changes in cellular and tissue structure, most strikingly nuclear dis-organization. In fact, for over 140 years it has been noted that nuclear morphology is often disrupted in cancer. Even today, nuclear morphology measures include nuclear size, shape, DNA content (ploidy) and 'chromatin organization'. Given the importance of nuclear shape to diagnoses of cancer phenotypes, it is surprising and frustrating that we currently lack a detailed understanding to explain these changes and how they might arise and relate to molecular events in the cell. It is an implicit hypothesis that perturbation of chromatin and epigenetic signatures may lead to alterations in nuclear structure (or vice versa) and that these perturbations lie at the heart of cancer genesis. In this review, we attempt to synthesize research leading to our current understanding on how chromatin interactions at the nuclear lamina, epigenetic modulation and gene regulation may intersect in cancer and offer a perspective on critical experiments that would help clarify how nuclear architecture may contribute to the cancerous phenotype. We also discuss the historical understanding of nuclear structure in normal cells and as a diagnostic in cancer.
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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.