ReviewCancers2018
Lipid Metabolic Reprogramming in Hepatocellular Carcinoma.
Review in Cancers, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 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
95 citing papers in PubMed, 171 citations in OpenAlex.
- Trial
- Review
- Research progress and therapeutic strategies in hepatocellular carcinoma metabolic reprogramming.Journal of advanced research · 2026Review
- GPD1L supports glycerol-3-phosphate and triacylglycerol synthesis and promotes tumor progression in HCC.Hepatology (Baltimore, Md.) · 2026Article
- Crosstalk BetweenCancers · 2026Review
- MicroRNA-21 promotes dysregulated lipid metabolism and hepatocellular carcinoma.Disease models & mechanisms · 2026Article
- Exploratory Analysis of Gut Microbiome and Metabolic Profile Changes Following Lenvatinib and Anti-PD-1 Combination Therapy in Liver Cancer.Metabolites · 2026Article
- Metabolic reprogramming in cardiac fibrosis: mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.Molecular and cellular biochemistry · 2025Review
- Stabilization of FASN by USP5-mediated deubiquitination promotes hepatocellular carcinoma progression.Oncogenesis · 2025Article
- Differential Metabolic Dysregulations in Hepatocellular Carcinoma and Cirrhosis: Insights into Lipidomic Signatures.Biomolecules · 2025Article
- APOA2 mediates immune therapy tolerance in hepatocellular carcinoma by inhibiting the antigen-presenting function of dendritic cells through the PPAR signaling pathway.Translational cancer research · 2025Article
- Mendelian randomization analysis reveals no causal association between non-alcoholic fatty liver disease and hepatocellular carcinoma: implications for lipid metabolomics and shared pathophysiological mechanisms.Discover oncology · 2025Article
- Lipogenesis and MASLD: re-thinking the role of SREBPs.Archives of toxicology · 2025Review
- Dysregulation of the SREBP pathway is associated with poor prognosis and serves as a potential biomarker for the diagnosis of hepatocellular carcinoma.Molecular medicine reports · 2025Article
- IRX5 Promoted SREBP1-Mediated de Novo Fatty Acid Synthesis via HMGN4 in Hepatocellular Carcinoma.Journal of cellular and molecular medicine · 2025Article
- Deciphering the metabolic landscape of colorectal cancer through the lens of AhR-mediated intestinal inflammation.Discover oncology · 2025Review
- Construction of a prognostic signature for breast cancer based on genes involved in unsaturated fatty acid biosynthesis.Translational cancer research · 2025Article
- The association between Clonorchis sinensis seropositivity and hepatocellular carcinoma in an endemic area: a study in Guangxi, China.BMC infectious diseases · 2025Article
- MyD88 orchestrates fatty acid metabolism in tumor-associated macrophages and non-alcoholic fatty liver disease-related hepatocarcinogenesis.Frontiers in immunology · 2025Article
35 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
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming for adaptation to the local environment has been recognized as a hallmark of cancer. Although alterations in fatty acid (FA) metabolism in cancer cells have received less attention compared to other metabolic alterations such as glucose or glutamine metabolism, recent studies have uncovered the importance of lipid metabolic reprogramming in carcinogenesis. Obesity and nonalcoholic steatohepatitis (NASH) are well-known risk factors of hepatocellular carcinoma (HCC), and individuals with these conditions exhibit an increased intake of dietary FAs accompanied by enhanced lipolysis of visceral adipose tissue due to insulin resistance, resulting in enormous exogenous FA supplies to hepatocytes via the portal vein and lymph vessels. This "lipid-rich condition" is highly characteristic of obesity- and NASH-driven HCC. Although the way in which HCC cells adapt to such a condition and exploit it to aid their progression is not understood, we recently obtained new insights into this mechanism through lipid metabolic reprogramming. In addition, accumulating evidence supports the importance of lipid metabolic reprogramming in various situations of hepatocarcinogenesis. Thus, in this review, we discuss the latest findings regarding the role of FA metabolism pathways in hepatocarcinogenesis, focusing on obesity- and NASH-driven lipid metabolic reprogramming.
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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.