Of the 185 patients, 89 had serum samples stored in the serum bank. These samples were retrieved for virological analysis. Regression analysis indicated that the HBV-DNA levels derived from liver samples were significantly correlated with those from serum samples (regression coefficient 0.0439; 95% CI 0.0391-0.0487; P < 0.001) (Fig. 5). In a subgroup of patients, a large amount of HBV-DNA was found in the liver tissue, but a relatively lower HBV-DNA concentration was detected in the serum sample (Fig. 5, squares [n = 8]), suggesting a defect of viral secretion. In another subgroup of patients, a small amount of

HBV-DNA Epacadostat in vitro was found in the liver tissue, but a high HBV-DNA concentration click here was detected in the serum sample (Fig. 5, circles [n = 5]), indicating an extraordinarily high efficiency of viral secretion. Using cases without abnormal secretion efficiency, a regression equation was obtained to convert tissue to serum HBV-DNA levels for practical

application (Fig. 5). Sequence analysis for precore stop codon mutation, BCP mutation, and genotype revealed discrepancies between serum-derived and tissue-derived data in 11 patients, including eight and seven discrepancies for precore stop codon mutation and BCP mutation, respectively. Interestingly, of these 11 patients, six were in either of the two abnormal subgroups (Fig. 5, solid squares and circles). Discrepancies in the detection selleck chemicals llc of large fragment pre-S mutants occurred in 18 patients. The mutants were detected in the serum but not the tissue samples in 11 of them, whereas in the remaining seven patients, the mutants were detected in the tissue but not the serum samples. Five of these seven patients were in the subgroup with secretion defect (Fig. 5, asterisks).

Of the 89 patients with available serum samples, short fragment pre-S deletion mutants were detected in the liver tissues in nine of them (PSMUT 1-8 and 11). Of these mutants, seven were also detected in the serum samples (PSMUT 1-5, 7, 8). The remaining two were in the subgroup with secretion defect (Fig. 5, pound symbols). Despite HCC’s multifactorial etiology, HBV remains the major causative factor in Southeast Asia, where HBV is highly prevalent.26 By characterizing the HBV genome sequences derived from patients’ serum, several studies have illustrated that various virological factors are closely associated with hepatocarcinogenesis, including serum HBV-DNA concentration, genotype, and the presence of a basal core promoter mutation.27 Furthermore, by performing cell-based and animal-based experiments, several viral proteins have been shown to be implicated in the oncogenesis of liver cancer, including X proteins, large surface proteins, and pre-S deletion mutants.