ReviewJournal of clinical medicine2018
Molecular Targets in Hepatocarcinogenesis and Implications for Therapy.
Review in Journal of clinical medicine, 2018. 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, 42 citations in OpenAlex.
- Research progress on the protective effect and oxidative stress mechanism of rutin against liver injury (Review).Molecular medicine reports · 2026Review
- Insights into oncovirus-driven tumor dynamics: a perspective from intravital imaging.Frontiers in cell and developmental biology · 2026Review
- Gut Microbiota and Primary Liver Cancer: Mendelian Randomization and Network Pharmacology Used to Predict Potential Therapeutic Intervention With Traditional Chinese Medicine.International journal of genomics · 2026Article
- Research trends and visualization analysis of autoimmune disease-related liver cancer from 2004 to 2024: a bibliometric study.Discover oncology · 2025Article
- Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025Review
- BRAP Promotes the Tumorigenesis of Hepatocellular Carcinoma by Corrupting Cancer Cell Cycle Regulation and Enhancing Immune Evasion.Journal of hepatocellular carcinoma · 2025Article
- Immune cell metabolic reprogramming in hepatocellular carcinoma: mechanisms, tumor microenvironment, and future immunotherapeutic directions.Frontiers in immunology · 2025Review
- Dual role of ANGPTL8 in promoting tumor cell proliferation and immune escape during hepatocarcinogenesis.Oncogenesis · 2023Article
- DNA methylation in cell plasticity and malignant transformation in liver diseases.Pharmacology & therapeutics · 2023Review
- JAK/STAT Signaling: Molecular Targets, Therapeutic Opportunities, and Limitations of Targeted Inhibitions in Solid Malignancies.Frontiers in pharmacology · 2022Review
- SLC39A1 Overexpression is Associated with Immune Infiltration in Hepatocellular Carcinoma and Promotes Its Malignant Progression.Journal of hepatocellular carcinoma · 2022Article
- Modulation of SCD1 activity in hepatocyte cell lines: evaluation of genomic stability and proliferation.Molecular and cellular biochemistry · 2021Article
- Chemopreventive Effect ofMolecules (Basel, Switzerland) · 2021Article
- Molecular pathways in viral hepatitis-associated liver carcinogenesis: An update.World journal of clinical cases · 2021Review
- Modulation of the TGF-β signaling pathway by long noncoding RNA in hepatocellular carcinoma.Biomarker research · 2020Review
- The Role of Autophagy in Liver Cancer: Crosstalk in Signaling Pathways and Potential Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2020Review
- The Molecular Mechanism of Epithelial-Mesenchymal Transition for Breast Carcinogenesis.Biomolecules · 2019Review
- Overexpression of LGR-5 as a Predictor of Poor Outcome in Patients with Hepatocellular Carcinoma.International journal of environmental research and public health · 2019Article
- The Toxicity Of Metallic Nanoparticles On Liver: The Subcellular Damages, Mechanisms, And Outcomes.International journal of nanomedicine · 2019Review
- Demystifying the manipulation of host immunity, metabolism, and extraintestinal tumors by the gut microbiome.Signal transduction and targeted therapyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocarcinogenesis comprises of multiple, complex steps that occur after liver injury and usually involve several pathways, including telomere dysfunction, cell cycle, WNT/β-catenin signaling, oxidative stress and mitochondria dysfunction, autophagy, apoptosis, and AKT/mTOR signaling. Following liver injury, gene mutations, accumulation of oxidative stress, and local inflammation lead to cell proliferation, differentiation, apoptosis, and necrosis. The persistence of this vicious cycle in turn leads to further gene mutation and dysregulation of pro- and anti-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, IL-10, IL-12, IL-13, IL-18, and transforming growth factor (TGF)-β, resulting in immune escape by means of the NF-κB and inflammasome signaling pathways. In this review, we summarize studies focusing on the roles of hepatocarcinogenesis and the immune system in liver cancer. In addition, we furnish an overview of recent basic and clinical studies to provide a strong foundation to develop novel anti-carcinogenesis targets for further treatment interventions.
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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.