ArticleMolecular cancer2015
TP53 R72P polymorphism modulates DNA methylation in hepatocellular carcinoma.
Article in Molecular cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Trends of genetic contributions on epigenetic clocks and related methylation sites with aging: A population-based adult twin study.Aging cell · 2025Article
- Identification of novel germline and somatic mutations associated with hepatocellular carcinoma by next-generation sequencing.Frontiers in pharmacology · 2025Article
- Pegylated Interferon-α-Induced Functional Cure for Special Populations with Chronic Hepatitis B Virus Infection: Current Trends, Challenges and Prospection.Drug design, development and therapy · 2025Review
- Comprehensive Genomic Profiling IdentifiesJournal of hepatocellular carcinoma · 2023Article
- Association of TP53 gene polymorphisms with the risk of acute lymphoblastic leukemia in Moroccan children.Molecular biology reports · 2022Article
- DNA Methylation Haplotype Block Markers Efficiently Discriminate Follicular Thyroid Carcinoma from Follicular Adenoma.The Journal of clinical endocrinology and metabolism · 2021Article
- Article
- Frequency of somatic mutations inOncology letters · 2020Article
- TP53 codon 72 Polymorphism and bladder cancer risk: a meta-analysis and emphasis on the role of tumor or smoking status.Journal of Cancer · 2018Article
- Variants of ubiquitin-specific peptidase 24 play a crucial role in lung cancer malignancy.Oncogene · 2016Article
- Association of p53 rs1042522, MDM2 rs2279744, and p21 rs1801270 polymorphisms with retinoblastoma risk and invasion in a Chinese population.Scientific reports · 2015Article
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) is characterized by widespread epidemiological and molecular heterogeneity. Previous work showed that in the western part of North Africa, a region of low incidence of HCC, mutations are scarce for this tumor type. As epigenetic changes are considered possible surrogates to mutations in human cancers, we decided, thus, to characterize DNA methylation in HCC from North-African patients.
methodsA set of 11 loci was investigated in a series of 45 tumor specimens using methylation-specific and combined-bisulfite restriction assay PCR. Results obtained on clinical samples were subsequently validated in liver cancer cell lines.
resultsDNA methylation at tumor suppressor loci is significantly higher in samples displaying chromosome instability. More importantly, DNA methylation was significantly higher in Arg/Arg when compared to Pro/Pro genotype carriers at codon 72 rs1042522 of TP53 (65% vs 20% methylated loci, p = 0.0006), a polymorphism already known to affect somatic mutation rate in human carcinomas. In vitro experiments in cell lines indicated that enzymes controlling DNA methylation were differentially regulated by codon 72 Arg or Pro isoforms of p53. Furthermore, the Arg72-carrying version of p53 was shown to re-methylate DNA more rapidly than the pro-harboring isoform. Finally, Pro-carrying cell lines were shown to be significantly more resistant to decitabine treatment (two-fold, p = 0.005).
conclusionsOur data suggest that Arg72Pro polymorphism in a WT p53 context may act as a primary driver of epigenetic changes in HCC. It suggests, in addition, that rs1042522 genotype may predict sensitivity to epigenetic-targeted therapy. This model of liver tumorigenesis that associates low penetrance genetic predisposition to epigenetic changes emerges from a region of low HCC incidence and it may, therefore, apply essentially to population living in similar areas. Surveys on populations submitted to highly mutagenic conditions as perinatally-acquired chronic hepatitis B or aflatoxin B1 exposure remained to be conducted to validate our observations as a general model.
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