ArticleGenome medicine2012
From hepatitis to hepatocellular carcinoma: a proposed model for cross-talk between inflammation and epigenetic mechanisms.
Article in Genome medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- The role of LINE-1 methylation in predicting survival among colorectal cancer patients: a meta-analysis.International journal of clinical oncology · 2017Pooled it
- The STING in Non-Alcoholic Fatty Liver Diseases: Potential Therapeutic Targets in Inflammation-Carcinogenesis Pathway.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Crosstalk Between Inflammatory Signaling and Methylation in Cancer.Frontiers in cell and developmental biology · 2021Review
- Epstein-Barr Virus Promotes B Cell Lymphomas by Manipulating the Host Epigenetic Machinery.Cancers · 2020Review
- Whole Genome 5'-Methylcytosine Level Quantification in Cirrhotic HCV-Infected Egyptian Patients with and without Hepatocellular Carcinoma.International journal of genomics · 2020Article
- Prognostic value of combined preoperative gamma-glutamyl transpeptidase to platelet ratio and fibrinogen in patients with HBV-related hepatocellular carcinoma after hepatectomy.American journal of translational research · 2020Article
- Interleukin-6 polymorphisms in HCC patients chronically infected with HCV.Infectious agents and cancer · 2020Article
- Predicting the impact of non-coding variants on DNA methylation.Nucleic acids research · 2017Article
- Macrolide antibiotics differentially influence human HepG2 cytotoxicity and modulate intrinsic/extrinsic apoptotic pathways in rat hepatocellular carcinoma model.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- Hepatitis viruses exploitation of host DNA methyltransferases functions.Clinical and experimental medicine · 2016Review
- Tumorigenic potential is restored during differentiation in fusion-reprogrammed cancer cells.Cell death & disease · 2016Article
- The Liver MicroRNA Expression Profiles Associated With Chronic Hepatitis C Virus (HCV) Genotype-4 Infection: A Preliminary Study.Hepatitis monthly · 2016Article
- Chronic liver inflammation modifies DNA methylation at the precancerous stage of murine hepatocarcinogenesis.Oncotarget · 2015Article
- The Role of Reactive Oxygen Species in Myelofibrosis and Related Neoplasms.Mediators of inflammation · 2015Review
- Dynamic imbalance between cancer cell subpopulations induced by transforming growth factor beta (TGF-β) is associated with a DNA methylome switch.BMC genomics · 2014Article
- Effect of estrogen receptor α binding on functional DNA methylation in breast cancer.Epigenetics · 2014Article
- STAT3 in hepatocellular carcinoma: new perspectives.Hepatic oncology · 2014Review
- A model for the epigenetic switch linking inflammation to cell transformation: deterministic and stochastic approaches.PLoS computational biology · 2014Article
- SAMD9L inactivation promotes cell proliferation via facilitating G1-S transition in hepatitis B virus-associated hepatocellular carcinoma.International journal of biological sciences · 2014Article
- Insight into the impact of diabetes mellitus on the increased risk of hepatocellular carcinoma: mini-review.Journal of diabetes and metabolic disorders · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation represents the body's natural response to tissue damage; however, chronic inflammation may activate cell proliferation and induce deregulation of cell death in affected tissues. Chronic inflammation is an important factor in the development of hepatocellular carcinoma (HCC), although the precise underlying mechanism remains unknown. Epigenetic events, which are considered key mechanisms in the regulation of gene activity states, are also commonly deregulated in HCC. Here, we review the evidence that chronic inflammation might deregulate epigenetic processes, thus promoting oncogenic transformation, and we propose a working hypothesis that epigenetic deregulation is an underlying mechanism by which inflammation might promote HCC development. In this scenario, different components of the inflammatory response might directly and indirectly induce changes in epigenetic machineries ('epigenetic switch'), including those involved in setting and propagating normal patterns of DNA methylation, histone modifications and non-coding RNAs in hepatocytes. We discuss the possibility that self-reinforcing cross-talk between inflammation and epigenetic mechanisms might amplify inflammatory signals and maintain a chronic state of inflammation culminating in cancer development. The potential role of inflammation-epigenome interactions in the emergence and maintenance of cancer stem cells is also discussed.
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.