Goat Anti-HBsAg protein Polyclonal antibody [HRP]

Background: Breast cancer and hepatitis B virus (HBV) infection are serious public health issues in China. But the effect of HBV infection on breast cancer remains unclear. The objective was to assess whether HBV infection was associated with prognosis of breast cancer. Methods: A retrospective database of 1,924 invasive breast cancer patients from Sun Yat-sen University Cancer Center from 2008 to 2010 was established. Propensity score matching method was applied to balance baseline parameters. Logistic regression was used for identifying the independent risk factors of liver metastasis. Prognostic outcomes were evaluated via Kaplan-Meier analysis and Cox model. Results: Primary evaluation of gross data suggested HBV infection was associated with much higher rate of liver metastasis. 642 patients were matched for analysis. The median follow-up time was about 69 months. Patients with HBV surface antigen (HBsAg) (+) had a specially higher risk of liver metastasis aside of other distant organs than those with HBsAg (-). HBsAg (-/+) was identified to be an independent risk factor of liver metastasis [odds ratio (OR), 2.651; 95% confidence intervals (CI), 1.213- 5.796; P=0.015]. HBsAg (+) was associated with liver metastasis significantly in stage III or in estrogen receptor (ER) (+) and/or progesterone receptor (PR) (+), human epidermal growth factor receptor-2 (HER-2) (-) subtype. Meanwhile, patients with HBsAg (+) had significant shorter liver metastasis-free survival (LMFS) compared with HBsAg (-) patients (P=0.041). But the difference of overall survival (OS) between the HBsAg (-) and HBsAg (+) groups reached statistically no significance (P=0.425).The multivariate analysis suggested HBsAg (+) could worsen the outcome of LMFS [hazards ratio (HR), 2.450; 95% CI, 1.169-5.135; P=0.018]. Conclusions: In breast cancer, HBsAg (+) was associated with specially a higher rate of liver metastasis and thus worsened the LMFS. HBsAg (-/+) was an independent risk factor of liver metastasis.

Objective The present study was undertaken to obtain data using the combination of SSc and lamivudine (LAM), entecavir (ETV) or telbivudine (LdT) in HepG2.2.15 cells to explore whether SSc acts as a potent adjuvant of nucleoside analogues in anti-HBV treatment. Methods HepG2.2.15 cells were incubated with either SSc combined with any one of three nucleoside analogues (NAs) LAM, ETV, LdT or only one of them for 48 h. The expression profiles of HBV DNA, HBsAg, HBeAg, and HBcAg were examined by real-time quantitative PCR, ELISA, and western blot. Results Compared with mono-drug treatment, the combination of SSc and any of the three nucleoside analogues significantly promoted additional reduction on HBV DNA level. Declined levels of HBsAg, HBeAg, and HBcAg were observed in SSc and LdT combination group. Conclusion These in vitro results indicated that SSc acted as a promising nucleoside analogue adjuvant, especially for telbivudine in the therapeutic strategies against HBV infection.