AI Article Synopsis

  • Hepatocellular carcinoma (HCC) is a common cancer influenced by genetic factors, particularly polymorphisms in phase II enzymes like GSTP1 and GSTA1.
  • A study analyzed the relationship between these gene polymorphisms and HCC by using a sample of 386 healthy individuals and 177 HCC patients.
  • The findings indicated that while GSTA1 did not show any association with HCC risk, younger individuals (≤ 57 years) with certain GSTP1 alleles had a significantly increased risk of developing HCC.

Article Abstract

Background: Hepatocellular carcinoma (HCC) is one of the most frequent malignant neoplasms in the world. Genetic polymorphism has been reported to be a factor increasing the risk of HCC. Phase II enzymes such as glutathione s-transferases (GSTP1, GSTA1) play important roles in protecting cells against damage induced by carcinogens. The aim of this study was to estimate the relationship of the GSTP1 and GSTA1 gene polymorphisms to HCC risk and clinico-pathological status.

Methods: Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was used to measure GSTP1 (A-->G) and GSTA1 (C-->T) gene polymorphisms in 386 healthy controls and 177 patients with HCC.

Results: Neither gene polymorphism was associated with the clinico-pathological status of HCC and serum expression of liver-related clinico-pathological markers. No association between the GSTA1 gene polymorphism and HCC susceptibility was found. However, in the younger group, aged < or = 57 years, individuals with AG or GG alleles of GSTP1 had a 2.18-fold (95%CI = 1.09-4.36; p = 0.02) and 5.64-fold (95%CI = 1.02-31.18; p = 0.04) risk, respectively, of developing HCC compared to individuals with AA alleles, after adjusting for other confounders.

Conclusion: AG and GG alleles of GSTP1 gene polymorphisms may be considered as factors increasing the susceptibility to and risk of HCC in Taiwanese aged < or = 57 years.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2851593PMC
http://dx.doi.org/10.1186/1471-2350-11-46DOI Listing

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