ReviewInternational journal of molecular sciences2023
Primary Liver Cancers: Connecting the Dots of Cellular Studies and Epidemiology with Metabolomics.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Global, regional, and national burden and changing trends of hepatoblastoma and retinoblastoma from 1990 to 2021, and projections until 2050: findings from the Global Burden of Disease Study 2021.Translational pediatrics · 2026Article
- HBx-mediated GPT2 suppression promotes liver cancer development by downregulating ADH1A.Cancer biology & medicine · 2026Article
- ALDH2 inhibits FASN stabilization via the E3 ligase CBL to suppress lipid accumulation and liver cancer development.Biology direct · 2026Article
- Burden of liver cancer and underlying etiologies in China from 1990 to 2021: A systematic analysis from the Global Burden of Disease Study 2021.Chinese medical journal · 2026Article
- Beyond the convergence of metabolic reprogramming in primary liver cancer: a comprehensive review on energy and lipids metabolism.Frontiers in cell and developmental biology · 2026Review
- Hepatitis B virus core protein promotes liver cancer progression by stabilizing CANX and suppressing IRF7 transcription.Acta pharmacologica Sinica · 2025Article
- Lipid Metabolism Reprogramming in Tumor-Associated Macrophages Modulates Their Function in Primary Liver Cancers.Cancers · 2025Review
- Hepatoblastoma: From Molecular Mechanisms to Therapeutic Strategies.Current oncology (Toronto, Ont.) · 2025Review
- Bidirectional regulation of the cyclic guanosine monophosphate-adenosine monophosphate synthase-stimulator of interferon gene pathway and its impact on hepatocellular carcinoma.World journal of gastrointestinal oncology · 2025Article
- Integrated Transcriptomic Analysis Leveraging Single-Cell and Bulk RNA Sequencing Data to Uncover Pyroptosis-Related Prognostic Signatures in HCC.Journal of hepatocellular carcinoma · 2025Article
- Identification of novel M2 macrophage-related molecule ATP6V1E1 and its biological role in hepatocellular carcinoma based on machine learning algorithms.Journal of cellular and molecular medicine · 2024Article
- Identifying Proteins and Amino Acids Associated with Liver Cancer Risk: A Study Utilizing Mendelian Randomization and Bulk RNA Sequencing Analysis.Journal of personalized medicine · 2024Article
- Transarterial Radioembolization for Management of Hepatocellular Carcinoma.The oncologist · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver cancers are rising worldwide. Between molecular and epidemiological studies, a research gap has emerged which might be amenable to the technique of metabolomics. This review investigates the current understanding of liver cancer's trends, etiology and its correlates with existing literature for hepatocellular carcinoma (HCC), cholangiocarcinoma (CCA) and hepatoblastoma (HB). Among additional factors, the literature reports dysfunction in the tricarboxylic acid metabolism, primarily for HB and HCC, and point mutations and signaling for CCA. All cases require further investigation of upstream and downstream events. All liver cancers reported dysfunction in the WNT/β-catenin and P13K/AKT/mTOR pathways as well as changes in FGFR. Metabolites of IHD1, IDH2, miRNA, purine, Q10, lipids, phosphatidylcholine, phosphatidylethanolamine, acylcarnitine, 2-HG and propionyl-CoA emerged as crucial and there was an attempt to elucidate the WNT/β-catenin and P13K/AKT/mTOR pathways metabolomically.
Indexed as
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.