ReviewInternational journal of molecular sciences2013
Cancer development, progression, and therapy: an epigenetic overview.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 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
151 citing papers in PubMed, 374 citations in OpenAlex.
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- Association between the traditional Chinese diet, non-communicable diseases and all-cause mortality: a longitudinal study based on China Health and Nutrition Survey (CHNS).European journal of nutrition · 2026Article
- An Overview of the Antioxidant, Anti-inflammatory, and Anticancer Effects of Statins.Anti-cancer agents in medicinal chemistry · 2026Review
- Cannabis sativa phytochemicals in cancer therapy: molecular mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Recent Advances in Nanocarrier-mediated Combination Drug Therapy for Tackling Solid-resistant Tumors.Current drug delivery · 2026Review
- Computational characterization and machine learning analysis of quantum optimized marine fungal metabolites targeting PD-L1 in cancer immunotherapy.Journal of computer-aided molecular design · 2025Article
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- Exploring Artificial Intelligence's Potential to Enhance Conventional Anticancer Drug Development.Drug development research · 2025Review
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- Loss of PCAF in proximal tubular cells exacerbates renal fibrosis by promoting partial epithelial-to-mesenchymal transition.Experimental & molecular medicine · 2025Article
- Effect of pyrogallol nanocomposite on miRNA and its associated pathways during radiation-induced toxicity in small intestine of irradiated Balb/C mice.Medical oncology (Northwood, London, England) · 2025Article
- Genetic and computational analysis of AKR1C4 gene rs17134592 polymorphism in breast cancer among the Bangladeshi population.Scientific reports · 2025Article
- Enhanced Anticancer Potential of Pd(II)-Thiosemicarbazone Complexes: Selectivity, Mechanisms, and 3D Models.Pharmaceutics · 2025Article
- An Insight into Cancer Cells and Disease Progression Through the Lens of Mathematical Modeling.Current issues in molecular biology · 2025Review
- hsa-miR-5688 inhibits FOXC1-OCT4/SOX2 feedforward loop that drives chemoresistance in breast cancer stem cells.Molecular therapy. Oncology · 2025Article
- Epigenomic insights and computational advances in hematologic malignancies.Molecular cytogenetics · 2025Review
- Facilitators and Barriers to Cancer Screening Participation Across Southeastic Asia: A Scoping Review.Psycho-oncology · 2025Article
- Interplay Between Traditional and Scientific Knowledge: Phytoconstituents and Their Roles in Lung and Colorectal Cancer Signaling Pathways.Biomolecules · 2025Review
91 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Carcinogenesis involves uncontrolled cell growth, which follows the activation of oncogenes and/or the deactivation of tumor suppression genes. Metastasis requires down-regulation of cell adhesion receptors necessary for tissue-specific, cell-cell attachment, as well as up-regulation of receptors that enhance cell motility. Epigenetic changes, including histone modifications, DNA methylation, and DNA hydroxymethylation, can modify these characteristics. Targets for these epigenetic changes include signaling pathways that regulate apoptosis and autophagy, as well as microRNA. We propose that predisposed normal cells convert to cancer progenitor cells that, after growing, undergo an epithelial-mesenchymal transition. This process, which is partially under epigenetic control, can create a metastatic form of both progenitor and full-fledged cancer cells, after which metastasis to a distant location may occur. Identification of epigenetic regulatory mechanisms has provided potential therapeutic avenues. In particular, epigenetic drugs appear to potentiate the action of traditional therapeutics, often by demethylating and re-expressing tumor suppressor genes to inhibit tumorigenesis. Epigenetic drugs may inhibit both the formation and growth of cancer progenitor cells, thus reducing the recurrence of cancer. Adopting epigenetic alteration as a new hallmark of cancer is a logical and necessary step that will further encourage the development of novel epigenetic biomarkers and therapeutics.
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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.