ReviewNPJ precision oncology2019
Accumulation of genetic and epigenetic alterations in normal cells and cancer risk.
Review in NPJ precision oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 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
157 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Association Between Anti-Neoplastic Effects of Curcumin and Urogenital Cancers: A Systematic Review.BioMed research international · 2024Pooled it
- Tuning epigenetics to enhance cancer virotherapy.Acta pharmaceutica Sinica. B · 2026Review
- Rethinking Oxidative Stress inLife (Basel, Switzerland) · 2026Review
- Methylation profiling of normal tissue adjacent to breast tumors reveals two distinct groups with divergent tumor microenvironment features.NPJ breast cancer · 2026Article
- Metachronous Primary Pancreatic Neuroendocrine Tumor and Adenocarcinoma: A Case Report.Cancer reports (Hoboken, N.J.) · 2026Article
- Reactivation ofInternational journal of molecular sciences · 2026Article
- Article
- A liquid biopsy-based multi-methylation marker panel for minimally invasive gastric cancer screening.Clinical epigenetics · 2026Article
- The extracellular matrix in inflammation and cancer.Molecular biomedicine · 2026Review
- Mutational Signatures and Clonal Hematopoiesis in Intestinal Metaplasia across Countries with Varying Stomach Cancer Incidence.Cancer discovery · 2026Article
- Proteomic analysis across Healthy-NAT-Tumor tissues uncovers clinically relevant biological events in esophageal squamous cell carcinoma.Briefings in bioinformatics · 2026Article
- Epigenetic modulation of CTCs as a novel therapeutic target in oncology.Molecular and cellular biochemistry · 2026Review
- UpregulatedImmunoTargets and therapy · 2026Article
- IFN-γ-driven UBE2D3 upregulation impairs antigen presentation pathways and anti-tumor immunity in pancreatic cancer.Nature communications · 2025Article
- Quinoline-Based DNA Methyltransferase Inhibitors Featuring Basic Side Chains: Design, Synthesis, and Insight in Biochemical and Anticancer Cell Properties.Journal of medicinal chemistry · 2025Article
- Precision Oncology: Current Landscape, Emerging Trends, Challenges, and Future Perspectives.Cells · 2025Review
- Unravelling the genetics and epigenetics of the ageing tumour microenvironment in cancer.Nature reviews. Cancer · 2025Review
- Review
- Immune System-Tumor Crosstalk Under Microgravity: Mechanistic Insights, Challenges, and Translational Perspectives.Cancers · 2025Review
- Clonal Hematopoiesis and Solid Cancers.Cancer science · 2025Review
97 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancers develop due to the accumulation of genetic and epigenetic alterations. Genetic alterations are induced by aging, mutagenic chemicals, ultraviolet light, and other factors; whereas, epigenetic alterations are mainly by aging and chronic inflammation. The accumulation and patterns of alterations in normal cells reflect our past exposure levels and life history. Most accumulated alterations are considered as passengers, but their accumulation is correlated with cancer drivers. This has been shown for aberrant DNA methylation but has only been speculated for genetic alterations. However, recent technological advancements have enabled measurement of rare point mutations, and studies have shown that their accumulation levels are indeed correlated with cancer risk. When the accumulation levels of aberrant DNA methylation and point mutations are combined, risk prediction becomes even more accurate. When high levels of alterations accumulate, the tissue has a high risk of developing cancer or even multiple cancers and is considered as a "cancerization field", with or without expansion of physiological patches of clonal cells. In this review, we describe the formation of a cancerization field and how we can apply its detection in precision cancer risk diagnosis.
Identifiers
What OpenQuestion holds
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.