ReviewInternational journal of cancer2026
Genetic variants underlying precancerous conditions of hepatocellular carcinoma.
Review in International journal of cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Super-enhancer-driven KIAA1522 upregulation suppresses ferroptosis in hepatocellular carcinoma.Clinical and translational medicine · 2026Article
- Cabozantinib activates TFEB-mediated autophagy to exert anti-tumor effects in hepatocellular carcinoma.In vitro cellular & developmental biology. Animal · 2026Article
- Development of a triplex FMCA assay for genotyping three genes, ADH1B, ADH1C, and ALDH2, involved in alcohol metabolism.Scientific reports · 2026Article
- Genetic variants underlying precancerous conditions of hepatocellular carcinoma.International journal of cancer · 2026Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Hepatocellular carcinoma (HCC) is the most common form of liver cancer, accounting for 80% of cases worldwide. While chronic hepatitis B and C infections remain primary risk factors, emerging evidence highlights the increasing contributions of metabolic dysfunction-associated steatotic liver disease (MASLD) and alcohol-associated liver disease (ALD) to HCC development. Genetic predispositions play a crucial role in modulating individual susceptibility to HCC, particularly through variants affecting viral persistence, lipid metabolism, and fibrogenesis. This review aims to summarize key genetic variants associated with precancerous conditions leading to HCC. The genetic risk factors, such as TP53 R249S mutant, TERT promoter mutations, and Wnt/B-catenin pathway alterations, influence disease progression and treatment response in HCC subjects with chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. In MASLD-related HCC, variants in PNPLA3, TM6SF2, and MBOAT7 modulate hepatic lipid metabolism and fibrosis. ALD-associated HCC is influenced by polymorphisms in ADH1B, ADH1C, and ALDH2, which affect alcohol metabolism and oxidative stress. Additionally, inherited metabolic disorders, including Wilson's disease and hemochromatosis, further contribute to HCC susceptibility. Despite previous insights into HCC-related genetic cues, challenges such as limited population-specific data, lack of genetic screening programs, and ethical concerns regarding genetic tests hinder the translation of genetic discoveries into personalized HCC prevention strategies. Expanding population-specific studies, improving genetic screening accessibility, and developing standardized risk prediction models will be crucial in shifting traditional medications toward a precision medicine setting for HCC management.
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What 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.