24 In this study, we evaluated the AFB1 exposure levels according

24 In this study, we evaluated the AFB1 exposure levels according to AFB1 DNA adduct levels of DNA samples from all subjects’ peripheral blood leukocytes for the following reasons: DNA samples of liver tissue were impossible to obtain from the controls, but according to our previous

study,7 AFB1 DNA adduct levels of HCC cancerous tissue, although higher, are positively and linearly related to peripheral blood leukocyte adduct levels. Therefore, it was feasible to elucidate Ceritinib mw the AFB1 exposure status by means of an analysis of AFB1 DNA adduct levels of peripheral blood leukocytes in the case-control study. In this study, the effects of possible confounders, such as HBV and HCV infection status, were controlled with an individually matched design. Actually, no significant interactive effects were found in the stratified analysis, and this implied that these factors should be effectually manipulated and not modify the correlation between the XPC codon 939 polymorphism and HCC related to AFB1 exposure. To the best of our knowledge, this is the first report investigating an association between XPC codon 939

polymorphisms and the risk and prognosis of HCC in Guangxi patients. We have found evidence suggesting that the genotypes of XPC with codon http://www.selleckchem.com/products/atezolizumab.html 939 Gln alleles may be correlated with increased risk and poor prognosis for AFB1-related HCC, and the NER pathway may play an important role in the mechanism of action of this genotoxin. However, there were several limitations to our study. Potential selection bias might have occurred because the selection of control subjects in our study was hospital-based. There may have been a biased distribution of liver disease severity (e.g., the HBV DNA level). The increased risk with AFB1 exposure

status seen in this study was probably underestimated because the liver disease itself may affect the metabolism of AFB1 and modify the levels of AFB1 DNA adducts. Despite the analysis of the XPC codon 939 polymorphism, Etoposide ic50 we did not analyze other polymorphisms of this gene11, 12 possibly able to modify the risk of AFB1 for HCC. Therefore, more genes deserve further elucidation based on a large sample and the combination of genes and AFB1 exposure. The authors thank Dr. Qiu-Xiang Liang, Dr. Yun Yi, and Dr. Min-Fa Wang for sample collection and management and Dr. Yong-Zhi Huang and Dr. Hua Huang for molecular biochemical techniques. They also thank all members of the Department of Medical Testing and Infection Control, Affiliated Hospital of Youjiang Medical College for Nationalities, for their help. Additional Supporting Information may be found in the online version of this article. “
“It has been difficult to prove that hepatitis B virus (HBV) treatment reduces the incidence of hepatocellular carcinoma (HCC).

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