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Currently, the systematized nomenclature of medicine (SNOMED) of liver cancer is confusing, and it is mixed with the SNOMED of cholangiocarcinoma. We hereby presented our own points, hoping to provide a reference for standardizing the nomenclatures and classifications of liver cancer in future clinical studies. The preface of Chinese Guidelines of Primary Liver Cancer Diagnosis and Treatment (2019 Edition) indicated that primary liver cancer mainly includes three different pathological types, hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC), and mixed-type carcinoma of both HCC and ICC. These three types of carcinoma show great differences in terms of pathogenesis, biological behavior, histological morphology, treatment methods, and prognosis, among which, HCC accounts for 85% to 90%. Therefore, this study is a detailed analysis of the above-mentioned related SNOMED and proposes suggestions for corrections.

Objective: Liver cancer is a common malignant tumor in the digestive system. Curcumin is a kind of phenolic pigment, which is extracted from herbage and has a plenty of physiological roles in anti-inflammation, anti-oxidation and anti-tumor. In our study, human hepatoma SMMC-7721 cell lines were selected and treated with curcumin to detect its effects on the apoptosis and AMPK signaling pathway., Materials and Methods: Human liver cancer cell strain SMMC-7721 was cultured and treated with different curcumin concentrations for different times followed by measuring the changes of cell proliferation activity and cycle by MTT and flow cytometry, respectively. Protein expression of Bcl-2, Bax and Caspase-3 were tested by Western blot, and the activation level of AMPK was also detected., Results: Different concentrations of curcumin could inhibit the proliferation of tumor cells in a dose-dependent manner. After 48 h inhibition by curcumin with a concentration of 40 mmol/L, the inhibitory effect was more obvious with statistically significant (p<0.05). The number of human liver cancer SMMC-7721 cells increased in G1 stage and decreased in S stage after treated with different concentrations of curcumin. During the G1 stage to the S stage, inhibition occurred and the effect of curcumin intervention group with 40 mmol/L was more evident than that of 10 mmol/L group, 20 mmol/L group and the control group with statistically significant (p<0.05). SMMC-7721 cell stains had been intervening by curcumin with concentrations of 10 mmol/L, 20 mmol/L and 40 mmol/L for 12 h, 24 h and 48 h, as the drug concentration increased, the reaction time prolonged, the protein expressions of Bcl-2 and Survivin were significantly decreased and Bax protein expression was significantly increased (p<0.05)., Conclusions: Curcumin decreased the proliferation activity of tumor cells, increased the cell quantities in G1 stage and decreased the cell numbers in S stage in human liver cancer SMMC-7721 cells. The Bcl-2 and Survivin proteins were downregulated and Bax protein was upregulated; furthermore, the AMPK signaling pathway was activated.

Aim: To evaluate the efficacy of combined PET/CT in the detection of viable tumour in patients with hepatocellular carcinoma (HCC) after transcatheter arterial chemoembolization (TACE). The correlation between 2-[(18)F]-fluoro-2-deoxy-d-glucose (FDG) uptake during PET and prognosis was evaluated., Materials and Methods: Seventy-three patients with 91 HCCs who had undergone TACE with lipiodol before (18)F-FDG PET/CT were retrospectively reviewed. The pattern of lipiodol deposition in the tumour was divided into three groups: grade I, lipiodol remaining in ≥60% of the tumour; grade II, 20-60%; and grade III, ≤20%. The performance of (18)F-FDG PET/CT in evaluating the viability of HCC was assessed and compared with that of contrast-enhanced CT (CECT). The predictive value of maximal tumoural standardized uptake value (SUV) to mean liver SUV (TSUVmax/LSUVmean) ratio was tested., Results: Comparing the receiver-operating characteristic area, (18)F-FDG-PET/CT was found to be superior to CECT for the detection of viable tumour in patients with HCC after TACE (p = 0.04). A high SUV ratio (TSUVmax/LSUVmean ≥1.65) correlated significantly with tumour size (p = 0.0096), the grade of lipiodol deposition (p = 0.0387) and serum α-foetoprotein (AFP) level (p = 0.0142), but did not correlate with pathological grade (p = 0.2626). The overall survival rate was significantly higher in the low SUV ratio (TSUVmax/LSUVmean<1.65) group (p = 0.024)., Conclusion: (18)F-FDG-PET/CT is efficient in assessing the viability of HCC after TACE and is superior to CECT in grades I and II, and similar in grade III. It provides valuable information for prediction of prognosis and may aid decisions regarding treatment strategy., (Copyright © 2014 The Royal College of Radiologists. Published by Elsevier Ltd. All rights reserved.)

Objectives: The purpose of this study was to identify featured miRNAs of hepatocellular carcinoma (HCC) by comparing normal and cancer cell line samples and find potential utility as biomarkers for early diagnosis and treatment of HCC., Materials and Methods: We downloaded the gene expression profile GSE41077 from Gene Expression Omnibus database which included 6 HCC cell lines samples and 2 controls. Differentially expressed miRNAs were identified by multtest package in R language after the data normalization. The selected differentially expressed miRNAs were further analyzed using bioinformatics methods. Target genes of these miRNAs were predicted using miRTarBase and miRecords databases. STRING software was used to construct the interaction network of target genes. Finally, we made module analysis by using Cytoscape software and its plugins--MCODE and BiNGO., Results: A total of 40 differentially expressed miRNAs were identified and the remarkably down-regulated miRNA was hsa-miR-122 which included 29 high confident target genes. The interaction network of target genes was constructed among 629 interaction pairs. Four functional modules in the network were obtained, from which EGLN3, ALDOA, NCAM1 and AACS were the high confident target genes, respectively. Genes in the modules most related to biological functions of signal transmission, regulation of macromolecule metabolic process., Conclusions: Low level of expression of hsa-miR-122 in HCC cell line is consistent with the existed previous studies. It is not only confirm the importance role of such miRNA in HCC cells, but also provide important help in identifying specific biomarker of HCC cells.

Background and Purpose: Reactivation of hepatitis B virus (HBV) happens after systemic chemotherapy, transarterial chemoembolization (TACE) or hepatic resection for HBV-related hepatocellular carcinoma (HCC) patients. The incidence and risk factors of HBV reactivation after radiofrequency ablation (RFA) are unclear., Patients and Methods: From August 2006 to August 2011, 218 consecutive patients with HBV-related small HCC treated with RFA (n = 125) or hepatic resection (n = 93) were retrospectively studied. The incidence of HBV reactivation and risk factors were analyzed., Results: HBV reactivation developed in 20 (9.2%) patients after treatment. The incidence of HBV reactivation was significantly lower in the RFA group (5.6%, 7/125) than the hepatic resection group (14.0%, 13/93, P = 0.034). On univariate and multivariate analyses, no antiviral therapy (OR 11.7; 95% CI 1.52-90.8, P = 0.018) and treatment with RFA/hepatic resection (OR3.36; 95% CI 1.26-8.97, P = 0.016) were significant risk factors of HBV reactivation. On subgroup analysis, the incidence of HBV reactivation was lower in patients who received antiviral therapy than those who did not receive antiviral therapy in both the hepatic resection group (2.9% vs. 20.7%, P = 0.027) and the RFA group (0% vs. 7.6%, P = 0.188), although the difference was not significant in the latter group., Conclusion: The incidence of HBV reactivation after RFA was relatively low when compared with hepatic resection. Prophylactic antiviral therapy is recommended, especially for patients who are going to receive hepatic resection for HBV-related HCC to decrease the incidence of post-treatment HBV reactivation., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Aims: To evaluate long-term results of patients with small solitary hepatocellular carcinoma (HCC) and well-preserved liver function who received radiofrequency ablation (RFA) as first-line treatment., Materials and Methods: Between November 1999 and June 2007, 247 patients with solitary HCC ≤5 cm and liver status scored as Child-Pugh class A were enrolled. RFA was performed in 224 patients as first-line treatment; 23 patients excluded from RFA because of unfavorable tumor location or their unwillingness, and all of these patients converted to surgical resection., Results: In the 224 patients treated with RFA, the overall 5-, 7-, 10-year survival rates were 59.8%, 55.2%, 33.9%, respectively, and the median of overall survival was 76.1 months. Complete ablation was achieved in 216 patients (96.4%). Major complications occurred in two patients (0.9%), with no treatment-related death or needle track seeding. Indocyanine green retention rate in 15 min (ICGR15) (P = 0.014) and prothrombin activity (P = 0.004) were associated with overall survival. A subgroup of patients with ICGR15 ≤ 10% and prothrombin activity >75% had 5-, 7-, 10-year survival rates of 67.1%, 64.2%, 57.1%, respectively, with a median survival of 87.7 months. The 10-year recurrence-free, tumor-free survival rates were 17.5%, 28.2%, respectively. Serum albumin was the only factor that significantly impacted recurrence-free and tumor-free survival (P = 0.008, 0.002, respectively)., Conclusion: RFA is considered to be the treatment of first choice for patients with solitary HCC ≤5 cm and well-preserved liver function. Surgery can be used as second-line therapy for few patients if RFA is unfeasible., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Aims: To assess whether combining percutaneous radiofrequency ablation (PRFA) with transcatheter arterial chemoembolization (TACE) was better than PRFA alone for hepatocellular carcinoma (HCC)., Materials and Methods: One hundered twenty patients (with a solitary HCC5.0 cm (p=.031) and for multiple tumors (p=.032), but not for tumors 5 cm or multiple tumors., (Copyright (c) 2009 Elsevier Ltd. All rights reserved.)

Aims: This study aimed to evaluate the efficacy and safety of percutaneous radiofrequency ablation (PRFA) for hepatocellular carcinoma (HCC) in the caudate lobe., Patients and Methods: Between January 2001 and December 2006, 17 patients (twelve males and five females) who were between 33 and 68years old (mean 54.3), with caudate lobe HCC [2.0-6.5cm in diameter (mean 3.1)] were treated with either PRFA alone (n=14), or PRFA with percutaneous ethanol injection (n=3) under ultrasound guidance. The right or the anterior approach was used in 12 and 5 patients, respectively., Results: All procedures were performed successfully. There was no mortality and major morbidity due to PRFA. Fourteen tumors (82%) were completely ablated after one to two sessions of treatment. During follow-up (range 3-60, mean 29.1months), two (14%) developed local recurrence. Intrahepatic metastases developed in 9 of 17 patients (53%). No distant metastasis was found. Four patients died (24%), 3 from tumor progression and 1 from hepatic failure. The 1-, 2-, and 4-year overall survivals were 88%, 80%, and 72%, respectively, and the progress free survivals were 47%, 20%, and 10%, respectively., Conclusions: PRFA is efficacious and safe for patients with HCC in the caudate lobe.

To elucidate the molecular mechanisms involved in the action of common carcinogens, which can act as important cofactors in modulating hepatitis B virus-mediated hepatocellular carcinogenesis, we have investigated the influence of aflatoxin B(1) (AFB), a potent liver carcinogen, as well as benzo[a]pyrene (BP) and 4-aminobiphenyl (4-ABP), carcinogens in cigarette smoke, on the induction of various transcription factors in human hepatoblastoma HepG2 cells. DNA electrophoretic mobility shift assays were performed with nuclear extracts from HepG2 cells treated with 10 micromol/L AFB, 40 micromol/L BP, or 300 micromol/L 4-ABP for 6 and 24 hours. Eight- and 6-fold increases in nuclear transcription factor kappaB (NF-kappaB), and 5- and 10-fold increases in activated protein (AP-1) transcription factor were observed with 24 hours AFB and BP treatments, respectively, whereas 4-ABP treatment resulted in an approximately 4-fold induction of both NF-kappaB and AP-1. Moreover, 4-ABP gave the strongest NF-kappaB activation in 6 hours of treatment. Four- and 10-fold activation of stress protein was detected by a consensus heat shock factor (HSF) sequence binding probe, with AFB and BP treatments, respectively. DNA adducts were observed by immunoassays in HepG2 cells treated with AFB and BP but not with 4-ABP. Increased human hepatitis B virus (HBV) surface antigen (HBsAg) synthesis was detected in AFB- and BP-treated HepG2 cells following transfection with recircularized HBV DNA. These data suggest that certain carcinogen-induced transcription factors may influence viral carcinogenesis and initiate hepatocellular carcinomas (HCC).

Previous research showed that risk factors associated with hepatocellular carcinoma (HCC) include infection with hepatitis B (HBV) and hepatitis C (HCV) viruses, exposure to aflatoxin B1 (AFB1), and liver cirrhosis, due primarily to alcohol consumption. To determine whether AFB1 may play a role in HCC in the United States, a search for AFB1 adducts and p53 alterations, potentially induced by AFB1, was conducted in the United States in 23 HCC patients with available tissue samples. The presence of AFB1 tumor-DNA and -serum lysine adducts and mutant p53 product was determined by immunoassays and codon 249 p53 mutation by restriction enzyme analysis. HBV and HCV serology and serum HBV-DNA were also determined. Thirteen patients were positive for HBV by HBs antigen or anti-HBc antigen or by polymerase chain reaction for HBV-DNA sequences. Nine patients were free of HBV and HCV markers; 5 of 22 sera tested were anti-HCV positive. p53 Protein expression, determined by immunohistochemical staining, was present in 5 of the 23 tumor tissues, whereas p53 codon 249 mutations were not observed in the 5 cases in which tissue was available for study. AFB1 tumor-DNA adducts were present in 3 of 19 tumor tissues, and in 1 of these 3 samples p53 protein was also detected. Sera from only 5 of the patients were tested for AFB1-lysine adducts, and all were positive. In these five patients, neither p53 protein nor a mutation on codon 249 was detected. The demonstration that AFB1-DNA and -lysine adducts are present in HCC patients in the United States is intriguing but requires further substantiation because of the small number of subjects in this pilot study. To elucidate the pathogenetic significance of these findings, further investigation, including studies in larger patient cohorts and properly selected controls, is warranted.

Epidemiologic studies have suggested that cigarette smoking is a risk factor for the development of hepatocellular carcinoma (HCC). To further investigate this relation, the authors measured levels of 4-aminobiphenyl-DNA adducts by an immunoperoxidase method in surgical liver tissues obtained between 1984 and 1995 from 105 Taiwanese patients with histologically confirmed HCC and 37 Taiwanese patients with metastatic liver tumors or intrahepatic stones. Information on clinicopathologic characteristics, cigarette smoking, and alcohol drinking was abstracted from hospital charts. Mean relative staining intensity for 4-aminobiphenyl-DNA was slightly higher in tumor tissues than in nontumor tissues obtained from HCC patients. Both mean intensities were significantly higher than the mean intensity of control tissues taken from non-HCC patients. However, no difference in mean relative staining intensity was found between smokers and nonsmokers in tissues obtained from non-HCC patients, or in tumor or nontumor tissues taken from HCC cases. After stratification of the relative staining intensities of 4-aminobiphenyl-DNA adduct levels into tertiles according to the total numbers of control tissues analyzed, there was a monotonically increasing risk of HCC. Odds ratios were 4.14 (95% confidence interval (CI) 1.15-15.50) and 9.71 (95% CI 2.82-34.86) for medium and high adduct levels compared with low adduct levels, respectively. The linear relation between adduct levels in liver tissue and HCC risk was also significant after adjustment for covariates, including hepatitis B surface antigen (HBsAg) status. The multivariate adjusted odds ratios were 3.41 (95% CI 0.82-14.25) and 6.48 (95% CI 1.59-26.50) for medium and high adduct levels, respectively. Moreover, there were monotonically increasing HCC risks for higher adduct levels in both HBsAg carriers and noncarriers. The increased risk ratios were more pronounced in noncarriers than in carriers. However, because of the small numbers of subjects, especially controls positive for HBsAg, the interaction between HBsAg status and 4-aminobiphenyl-DNA adduct level was not significant. Among HCC cases, none of the clinicopathologic characteristics were associated with relative staining intensity. These results indicate that 4-aminobiphenyl exposure, which is primarily a result of cigarette smoking, plays a role in the development of HCC in humans.

Recent studies have implicated aflatoxin B1 (AFB1) exposure as an etiological agent in hepatocellular carcinoma (HCC) and suggested an interaction with chronic hepatitis B virus (HBV) infection. Worldwide AFB1 exposure correlates with a specific mutation at codon 249 in the p53 tumor suppressor gene in liver tumors. This study investigated the roles of HBV and AFB1 in the HCC carcinogenic pathway involving p53 mutations. In cases and controls, chronic HBV infection was assessed by serum hepatitis B surface antigen (HBsAg) and AFB1 exposure by immunohistochemical detection of AFB1-DNA adduct in liver tissue. p53 protein mutations in tumor tissues of HCC cases were identified by immunohistochemistry and DNA mutations by single-stranded conformational polymorphism and sequencing analysis. Both chronic HBsAg carrier status and liver AFB1-DNA adducts were significantly higher in cases than in controls with odds ratios (OR) of 8.4 and 3.9, respectively (P < 0.01). Moreover, HCC risk was greatest in individuals with both AFB1-DNA adducts and HBsAg, suggesting a viral-chemical interaction. Mutant p53 protein, mutations in the p53 gene, and specific codon 249 mutations were detected in 37, 29, and 13%, respectively, of the HCC cases. Most of the DNA mutations were transversions, and the only major clustering site for mutations was codon 249. AFB1-DNA adducts were associated with p53 protein (OR = 2.9, P = 0.054) and DNA mutations (OR = 2.9, P = 0.082) but with borderline significance. All of the codon 249 mutations (n = 12) occurred in HBsAg-seropositive carriers, resulting in an OR of 10.0 (P < 0.05), suggesting that HBV may be involved in the selection of these mutations. The ORs between HBsAg and p53 DNA and protein mutations were 2.6 (P = 0.077) and 1.8 (P > 0.05), respectively. Both p53 DNA and protein mutations were related to tumor stage, suggesting that they are late events. These studies provided further support for the role of aflatoxin exposure in HCC in Taiwan and insight into viral-chemical interactions and molecular pathogenesis.

To elucidate the importance of aflatoxin in the etiology of hepatocellular carcinoma (HCC), a community-based cohort study combined with molecular dosimetry of aflatoxin exposure was performed in the Penghu Islets where the HCC mortality rate is highest in Taiwan. A total of 6,487 residents aged 30 to 65 years were recruited in the two-stage screening survey and underwent regular follow-up examination. Among 33 newly diagnosed HCC cases, 31 (94%) were chronic hepatitis B surface antigen (HBsAg) carriers and 3 (9%) were positive for antibodies against hepatitis C virus (HCV). Among 20 HCC patients and 86 matched healthy controls whose serum samples were tested for aflatoxin B1 (AFB1)-albumin adducts by competitive enzyme-linked immunosorbant assay (ELISA), 13 (65%) HCC patients and 32 (37%) matched controls were seropositive, showing a statistically significant multivariate-adjusted odds ratio of 5.5 with a 95% confidence interval of 1.2 to 24.5. The results imply the elevated risk of HCC among Penghu residents may be attributable to their heavy exposure to aflatoxins and high HBsAg carrier rate.

Copper contents (Cu) in bodies and serum ceruloplasmin (Cp) were assayed in patients with liver cirrhosis (LC) and hepatocarcinoma (HCC) with atomic absorption and other methods. The results were shown as follows: 1. The mean levels of serum Cp and urine Cu in LC were higher than those of normal (P < 0.05 and 0.01). 2. Serum Cu and Cp levels were consistently high in HCC. Urine Cu level was also elevated and had positive correlation with that of serum Cu (r = 0.567, P < 0.01). 3. Cirrhotic liver Cu content was almost the same as that of pericarcinomatous liver Cu, being higher than that of normal and carcinomatous liver. 4. Hair Cu level in both LC and HCC was apparently lower than that of normal subjects. 5. Serum Cu level in patients with tumor more than 5 cm in size was higher than that in patients with tumor less than 5 cm (P < 0.05). 6. Serum Cu level decreased along with the reduction of tumor size after treatment. 7. Serum Cu and Cp levels may be used as markers for detection of HCC, especially for AFP-negative HCC. Serum Cu estimation is valuable in assessment of the therapeutic effect and prognosis in patients with HCC.

Amplification of the chromosome 11q13 region occurs in several types of human cancer including esophageal, breast, lung, bladder and hepatocellular carcinoma (HCC). The gene cyclin D1 maps to this region in close proximity to two proto-oncogenes hst-1 and int-2. We previously demonstrated that cyclin D1 was not only amplified but also overexpressed in about 30% of human esophageal cancers. To investigate the role of cyclin D1 in human hepatocellular carcinoma (HCC), DNA from 30 HCC and 5 control liver tissues from Taiwan and also the HCC cells lines HepG2 and Hep3B, were examined for amplification of the cyclin D1 gene. A 3 to 20-fold amplification was found in 4 of the 30 (13%) HCC samples but not in any of the 5 control tissues or the 2 cell lines. Immunohistochemical analysis of cyclin D1 indicated overexpression of this protein in tumors that displayed gene amplification. Weak or negative staining was observed in the other HCC samples as well as in the control tissues and cell lines. These data suggest that increased expression of cyclin D1 may play an important role in the development of a subset of human HCC, perhaps by perturbing normal control of the cell cycle.

Monoclonal antibodies recognizing the stable imidazole ring-opened form of the major N7-guanine aflatoxin B1-DNA adduct have been used in competitive enzyme-linked immunosorbent assays (ELISA) and indirect immunofluorescence assays to quantitate adduct levels in liver tissue. Methods were developed in AFB1-treated animals, then applied to paired tumor and nontumor liver tissues of hepatocellular carcinoma patients from Taiwan. An avidin-biotin complex staining method was also used for of the detection of hepatitis B surface (HBsAg) and X (HBxAg) antigens in liver sections. A total of 8 (30%) hepatocellular carcinoma (HCC) samples and 7 (26%) adjacent nontumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent nontumorous liver samples were positive, and 9 (33%) HCC samples and 11 (41%) adjacent nontumor liver samples were HBxAg positive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These methods should be useful in determining the role of exposure in the induction of HCC in Taiwan.

Aflatoxins are well-known animal hepatocarcinogens, but the association between aflatoxins and human hepatocellular carcinoma remains to be elucidated. A study method consisting of indirect immunofluorescence assay combined with densitometry was developed to quantitate aflatoxin B1 DNA adducts in smeared liver tissue obtained at the time of biopsy for diagnosis in 50 hepatocellular carcinoma patients in Taiwan. Monoclonal antibody 6A10, generated against the persistent form of the major N7 guanine adduct of aflatoxin B1, was used for detection of adduct. Thirty-five (70%) of the hepatocellular carcinoma samples had detectable levels of aflatoxin B1 DNA adducts (> or = 1/10(6) nucleotides). The detection rate was slightly lower in men (69%) than in women (75%), and younger patients had a significantly higher rate of adducts (83%) than did older ones (58%). Carriers of both HBsAg and HBeAg, carriers of HBsAg only and noncarriers had different rates of detection: 29%, 74% and 82%, respectively. Patients with family histories of hepatocellular carcinoma had a higher detection rate (100%) than did those patients without such histories (67%). No association was found between aflatoxin B1 DNA adducts in liver tissue and Child's score for severity of liver disease. The results suggest that aflatoxin B1 may be involved in the pathogenesis of hepatocellular carcinoma in Taiwan. Our immunohistochemical method for analysis of adducts in small numbers of cells from the target organ should improve results of monitoring for the biologically effective dose of aflatoxin.

Studies were carried out to test the hypothesis that exposure to aflatoxin B1 (AFB1) is common among individuals with hepatocellular carcinoma (HCC) who are also chronically infected with hepatitis B virus (HBV). Experiments were also carried out to determine whether there is a close association between the presence of AFB1-DNA adducts and the expression of one or more HBV antigens in the tumor or non-tumor regions of the liver. Twenty-seven paired tumor and non-tumor liver tissues of HCC patients from Taiwan were analyzed. Monoclonal antibody 6A10, generated against the imidazole ring-opened persistent form of the major N-7 guanine adduct of AFB1, was used for adduct detection by both indirect immunofluorescence and competitive enzyme-linked immunosorbent assay. An avidin-biotin complex staining method was used for the detection of HBsAg and HBxAg in liver sections. A total of 8 (30%) HCC samples and 7 (26%) adjacent non-tumor liver tissue samples from Taiwan were positive for AFB1-DNA adducts. For HBsAg, 10 (37%) HCC samples and 22 (81%) adjacent non-tumorous liver samples were positive while 9 (33%) HCC samples and 11 (41%) adjacent non-tumor liver samples were HBxAg-positive. No association with AFB1-DNA adducts was observed for HBsAg and HBxAg. These results suggest that both AFB1 exposure and carrier status of HBsAg/HBxAg may be involved in the induction of HCC in Taiwan.