Carriage of the PNPLA3 rs738409 C >G polymorphism confers an increased risk of non-alcoholic fatty liver disease associated hepatocellular carcinoma
Abstract
Background & aims Subtle inter-patient genetic variation and environmental factors combine to determine disease progression in non-alcoholic fatty liver disease (NAFLD). Carriage of the PNPLA3 rs738409 c.444C >G minor allele (encoding the I148M variant) has been robustly associated with advanced NAFLD. Although most hepatocellular carcinoma (HCC) is related to chronic viral hepatitis or alcoholic liver disease, the incidence of NAFLD-related HCC is increasing. We examined whether rs738409 C >G was associated with HCC-risk in patients with NAFLD.Methods PNPLA3 rs738409 genotype was determined by allelic discrimination in 100 European Caucasians with NAFLD-related HCC and 275 controls with histologically characterised NAFLD.Results Genotype frequencies were significantly different between NAFLD-HCC cases (CC=28, CG=43, GG=29) and NAFLD-controls (CC=125, CG=117, GG=33) (p=0.0001). In multivariate analysis adjusted for age, gender, diabetes, BMI, and presence of cirrhosis, carriage of each copy of the rs738409 minor (G) allele conferred an additive risk for HCC (adjusted OR 2.26 [95% CI 1.23-4.14], p=0.0082), with GG homozygotes exhibiting a 5-fold [1.47-17.29], p=0.01 increased risk over CC. When compared to the UK general population (1958 British Birth Cohort, n=1476), the risk-effect was more pronounced (GC vs. CC: unadjusted OR 2.52 [1.55-4.10], p=0.0002; GG vs. CC: OR 12.19 [6.89-21.58], p<0.0001).Conclusions Carriage of the PNPLA3 rs738409 C >G polymorphism is not only associated with greater risk of progressive steatohepatitis and fibrosis but also of HCC. If validated, these findings suggest that PNPLA3 genotyping has the potential to contribute to multi-factorial patient-risk stratification, identifying those to whom HCC surveillance may be targeted.
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Overall evidence suggests that PNPLA3 p.I148M and TM6SF2 p.E167K variants are major risk factors for progressive MASLD, and genotyping helps to noninvasively predict progressive MASH, cirrhosis and HCC when considered alongside clinical factors, but accuracy is suboptimal for prediction of liver disease severity and progression at the individual level.
“Overall evidence suggests that the PNPLA3 p.I148M and TM6SF2 p.E167K variants are major risk factors for progressive MASLD, and genotyping helps to noninvasively predict progressive MASH, cirrhosis and HCC when considered alongside clinical factors, 194 -196 but accuracy is suboptimal for prediction of liver disease severity and progression at the individual level.”
From EASL-EASD-EASO Clinical Practice Guidelines on the management of metabolic dysfunction-associated steatotic liver disease (MASLD). (2024) · cites this paper as [195]
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- Authors
- Liu, Y.-L., Patman, G. L., Leathart, J. B. S., Piguet, A.-C., Burt, A. D., Dufour, J.-F., Day, C. P., Daly, A. K., Reeves, H. L., & Anstee, Q. M.
- Affiliations
- Newcastle University (GB)
- University Hospital of Bern (CH)
- Corresponding author
- Reeves, H.L.
- Venue
- Journal of Hepatology
- Publisher
- Elsevier BV
- Published
- 2014-07
- Volume
- 61
- Issue
- 1
- Pages
- 75-81
- ISSN
- 0168-8278 (ISSN-L)
- OpenAlex
- W2060278601
- Cited by
- 549
- References
- 46
- Citations by year
- 2026: 25 · 2025: 39 · 2024: 49 · 2023: 53 · 2022: 50 · 2021: 63 · 2020: 59 · 2019: 41 · 2018: 34 · 2017: 40 · 2016: 52 · 2015: 36 · 2014: 7
- FWCI
- 34.09
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Hepatology › Hepatocellular Carcinoma Treatment and Prognosis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- PNPLA3 I148M variant, non-alcoholic fatty liver disease, hepatocellular carcinoma, genetic susceptibility, liver fibrosis, steatohepatitis, genetic polymorphism, cancer risk, liver cirrhosis, diabetes mellitus, body mass index, alcohol consumption
- MeSH terms
- Acyltransferases, Adult, Aged, Female, Gene Frequency, Carcinoma, Hepatocellular, Homozygote, Humans, Lipase, Liver Neoplasms, Male, Membrane Proteins, Middle Aged, Risk Factors, Cohort Studies, Case-Control Studies, Disease Progression, Polymorphism, Single Nucleotide, White People, Phospholipases A2, Calcium-Independent, Genetic Association Studies, Non-alcoholic Fatty Liver Disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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