ReviewCancers2023
Chromatin and Cancer: Implications of Disrupted Chromatin Organization in Tumorigenesis and Its Diversification.
Review in Cancers, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed, 27 citations in OpenAlex.
- The evolving global landscape of first-in-class oncology drug innovation.Signal transduction and targeted therapy · 2026Review
- Material-Induced Nuclear Deformation Controls Chromatin Architecture in Adipose Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The Future of Epigenetics: Emerging Technologies and Clinical Applications.ACS pharmacology & translational science · 2026Review
- Cancer cell identification in tissue imaging via phasor map analysis in polarization-resolved two-photon excitation fluorescence microscopy.Biomedical optics express · 2026Article
- Article
- Quantum annealing for enhanced feature selection in single-cell RNA sequencing data analysis.Quantum machine intelligence · 2025Article
- Integrative proteo-genomic profiling uncovers key biomarkers of lapatinib resistance in HER2-positive breast cancer.British journal of cancer · 2025Article
- Enhancer regulation in cancer: from epigenetics to mArchives of pharmacal research · 2025Review
- Unveiling Epigenetic Regulatory Elements Associated with Breast Cancer Development.International journal of molecular sciences · 2025Article
- Integration of multi-source gene interaction networks and omics data with graph attention networks to identify novel disease genes.Bioinformatics (Oxford, England) · 2025Article
- Multiclassification of Colorectal Polyps from Colonoscopy Images Using AI for Early Diagnosis.Diagnostics (Basel, Switzerland) · 2025Article
- The SWI/SNF PBAF complex facilitates REST occupancy at repressive chromatin.Molecular cell · 2025Article
- RID is required for both repeat-induced point mutation and nucleation of a novel transitional heterochromatic state for euchromatic repeats.Nucleic acids research · 2025Article
- RNA Binding Proteins are Pivotal Regulators of Cancer Radioresistance and Potential Targets for Preventing Tumor Recurrence.Current radiopharmaceuticals · 2025Review
- Plasma Cell-Free DNA Concentration and Fragmentomes Predict Neoadjuvant Chemotherapy Response in Cervical Cancer Patients.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- An oncogene regulating chromatin favors response to immunotherapy: Oncogene CHAF1A and immunotherapy outcomes.Oncoimmunology · 2024Article
- Article
- The Regenerative Power of Stem Cells: Treating Bleomycin-Induced Lung Fibrosis.Stem cells and cloning : advances and applications · 2023Review
- Mitochondria in Cancer Stem Cells: From an Innocent Bystander to a Central Player in Therapy Resistance.Stem cells and cloning : advances and applications · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A hallmark of cancers is uncontrolled cell proliferation, frequently associated with an underlying imbalance in gene expression. This transcriptional dysregulation observed in cancers is multifaceted and involves chromosomal rearrangements, chimeric transcription factors, or altered epigenetic marks. Traditionally, chromatin dysregulation in cancers has been considered a downstream effect of driver mutations. However, here we present a broader perspective on the alteration of chromatin organization in the establishment, diversification, and therapeutic resistance of cancers. We hypothesize that the chromatin organization controls the accessibility of the transcriptional machinery to regulate gene expression in cancerous cells and preserves the structural integrity of the nucleus by regulating nuclear volume. Disruption of this large-scale chromatin in proliferating cancerous cells in conventional chemotherapies induces DNA damage and provides a positive feedback loop for chromatin rearrangements and tumor diversification. Consequently, the surviving cells from these chemotherapies become tolerant to higher doses of the therapeutic reagents, which are significantly toxic to normal cells. Furthermore, the disorganization of chromatin induced by these therapies accentuates nuclear fragility, thereby increasing the invasive potential of these tumors. Therefore, we believe that understanding the changes in chromatin organization in cancerous cells is expected to deliver more effective pharmacological interventions with minimal effects on non-cancerous cells.
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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.