Aflatoxin B1 (AFB1) is the most common carcinogen of aflatoxin, which contaminates many agricultural products in the daily diet of humans. More than 50% of patients with developing hepatocellular carcinoma (HCC) feature AFB1 exposure due to their shared consumption of contaminated food. One of the main mechanisms of AFB1-induced liver carcinogenesis is its biological activation and its interaction with DNA to produce AFB1-E-N7-dG adduct. This product may result in the formation of DNA damage and the mutations of tumor-associated genes such as TP53 and ras. In human, several pathways involving in AFB1 detoxification, including I-and II-type detoxification, DNA repair, have been reported. This study reviewed the detoxification mechanisms of AFB1 in human as well as AFB1 occurrence and toxification. Additionally, we also discussed prevention methods for AFB1 exposure.

Background: Previous studies have shown that chromobox 4 (CBX4) expression may involve in the progression of liver cancer, however, it is unclear whether it affects the prognosis of hepatocellular carcinoma (HCC) related to aflatoxin B1 (AFB1). Methods: A retrospective study was conducted in the high AFB1 exposure areas and a total of 428 patients with HCC were included in the final survival analyses. AFB1 exposure levels and CBX4 expression in the tumor tissues were tested using enzyme-linked immunosorbent assay and immunohistochemistry, respectively. The effects of AFB1 and CBX4 on HCC outcome were elucidated by Kaplan-Meier survival method and Cox regression model. Results: We found that the levels of AFB1 exposure and CBX4 expression in tumor tissues were significantly associated with some clinicopathological features such as microvessel density and tumor stage. Furthermore, both AFB1 and CBX4 significantly modified overall survival and tumor reoccurrence-free survival status of HCC. Additionally, some evidence of CBX4-AFB1 interaction affecting HCC prognosis was observed, with an interactive value of 1.98 for overall survival and 1.94 for tumor reoccurrence-free survival, respectively. Conclusion: These results suggest that CBX4 expression might be a useful marker for AFB1related HCC prognosis.

Diabetes was associated with the primary liver cancer, most likely is one of the causes of primary liver cancer.

Introduction 3. Materials and methods 3.1 Study design and subjects 3.2 AFB1 exposure data 3.3 SNPs selection and genotyping 3.4 Immunochemistry 3.5 Statistical analysis 4. Results 4.1 The demographic and clinicopathological features and the survival of HCC patients 4.2 Univariable analyses indicating CBX4 SNPs as significant prognostic biomarker for HCCs' survival 4.3 The effects of CBX4 rs77447679 SNP on survival stratified by the clinicopathological features of HCC patients 4.4 Multivariable analyses indicating CBX4 rs77447679 SNP as an independent prognostic factor for patients with HCC 4.5 CBX4 rs77447679 but not rs2289728 SNP significantly linking with CBX4 protein expression 4.6 CBX4 rs77447679 SNP differently regulating the therapeutic effects of pa-TACE on HCC 5. Discussion 6. Conclusions 7. Author contributions 8. Ethics approval and consent to participate 9. Acknowledgment 10. Funding 11. Conflict of interest 12. References

Objectives CDGSH iron sulfur domain 2 (CISD2) is essential to maintain iron (Fe) and reactive oxygen species (ROS) homeostasis, and ferroptosis suppressor protein 1 (FSP1) can protect cells from ferroptosis by inhibiting lipid peroxidation. Here, we investigate the role and potential mechanism of CISD2 and FSP1 in ferroptosis of hepatocellular carcinoma (HCC). Methods Human HCC cells were exposed to ferroptosis inducer Erastin, and the expression changes of CISD2 and FSP1 during ferroptosis were detected. Subsequently, we investigated the effect of overexpression of CISD2 on ferroptosis and FSP1 expression in HCC cells. Finally, we also investigated the effect of overexpression of FSP1 on ferroptosis in HCC cells. Results Erastin induced ferroptosis in hepatoma cells, and HepG2 cells were sensitive to Erastin. In addition, it was found that the expression of CISD2 was significantly upregulated and the expression of FSP1 was significantly downregulated in Erastin treated HepG2 cells. Subsequently, CISD2 was found to be highly expressed in HCC tissues, and overexpression of CISD2 reversed ferroptosis induced by Erastin in HepG2 cells and upregulated the expression of FSP1. Meanwhile, FSP1 showed a low expression level in HCC tissues and cells, and overexpression of FSP1 could reverse the ferroptosis induced by Erastin in HepG2 cells. Conclusion CISD2 and FSP1 are involved in the ferroptosis process of HCC induced by Erastin. CISD2 protects against the ferroptosis of HCC induced by Erastin by upregulating the expression of FSP1.