ReviewCurrent oncology reports2026
Reprogrammed Lipid Metabolism as a Gatekeeper of Hepatocarcinogenesis: from Enzyme Regulation to Precision Therapy.
Review in Current oncology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
purpose of reviewHepatocellular carcinoma (HCC), a lethal malignancy with rising global incidence, is characterized by profound metabolic reprogramming, particularly in lipid metabolism. This process, orchestrated by specialized lipid transporters and key metabolic enzymes, drives tumorigenesis, therapeutic resistance, and immune evasion. The purpose of this review is to integrate the latest mechanistic insights into how these lipid-handling proteins rewire tumor biology and reshape clinical outcomes. RECENT
findingsLipid accumulation in hepatocytes serves as a critical driver of hepatocarcinogenesis through the pathological continuum of metabolic-associated fatty liver disease (MAFLD) and steatohepatitis (MASH). These effects are mediated through coordinated pathways: the SEC63-ACLY axis enhances metastasis, FASN confers therapy resistance and immune evasion, and CD36 triggers T cell dysfunction, collectively fueling HCC progression. Notably, the novel anti-CD36 antibody PLT012 demonstrates substantial therapeutic efficacy, highlighting the clinical potential of targeting metabolic-immune crosstalk in HCC. Collectively, these findings establish the hepatic lipid metabolic network as a druggable hub and advocate for synergistic targeting strategies in HCC. This review systematically delineates the lipid transporter and key metabolic enzymes driving hepatic lipid reprogramming in HCC, integrating mechanistic and translational evidence to redefine lipid metabolism as a central therapeutic target. It further evaluates their druggability, proposing precision oncology frameworks to guide HCC treatment strategies.
Indexed as
Identifiers
41642507What Socratic 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 Socratic graph.