AI Article Synopsis
- Elevated serum alpha-fetoprotein (AFP) levels in chronic hepatitis C patients indicate a higher risk for developing hepatocellular carcinoma (HCC) and suggest potential gene expression changes in the liver.
- A study of liver samples from 48 patients showed distinct gene expression patterns tied to AFP levels, with AKR1B10 identified as the most significantly up-regulated gene in patients with elevated AFP.
- The research concluded that higher levels of AKR1B10 are independently linked to an increased risk of HCC development, highlighting its role in early liver cancer progression.
Article Abstract
Background: Elevated serum alpha-fetoprotein (AFP) is not only a diagnostic marker for hepatocellular carcinoma (HCC), but is also a risk factor for HCC in chronic hepatitis C patients who do not have HCC.
Aim: The aim was to analyse the hepatic gene expression signature in chronic hepatitis C patients with elevated AFP, who were at high risk for HCC.
Methods: Liver tissue samples from 48 chronic hepatitis C patients were stratified by their serum AFP levels and analysed for gene expression profiles. The association between aldo-keto reductase family 1 member B10 (AKR1B10) expression and serum AFP was confirmed by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemical analyses. A matched case-control study was performed to evaluate the risk of AKR1B10 expression for HCC development.
Results: Distinct hepatic gene expression patterns were demonstrated in patients with elevated AFP (≥10 ng/mL) and normal AFP (<10 ng/mL). Of the 627 differently expressed genes, the most abundantly expressed gene in patients with elevated AFP was AKR1B10 (fold change, 26.2; P < 0.001), which was originally isolated as an overexpressed gene in human HCC. The qRT-PCR and immunohistochemical studies confirmed a proportional correlation between AKR1B10 expression and serum AFP. A matched case-control study identified that AKR1B10 up-regulation (>6%) was an independent risk factor for HCC development (hazard ratio, 21.4; P = 0.001).
Conclusion: AKR1B10 was up-regulated in association with serum AFP, and was an independent risk factor for HCC in chronic hepatitis C patients, suggesting its possible involvement at a very early stage of hepatocarcinogenesis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3466415 | PMC |
| http://dx.doi.org/10.1111/j.1478-3231.2012.02827.x | DOI Listing |
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