Abstract 3820: Hepatitis B virus gene pre-S2 mutant as a high risk serum marker for hepatoma recurrence after a hepatic resection

Abstract

Abstract Background: Chronic hepatitis B virus (HBV) infection is the major cause of hepatocellular carcinoma (HCC). The pre-S2 mutant large HBV surface antigen (LHBS) is highly associated with HCC. This study aimed to evaluate the serum pre-S2 mutant LHBS as a high-risk recurrence marker in HCC patients after a hepatic resection. Methods: The pre-S gene chip was used to analyze 175 patients with HBV-related HCC who underwent a hepatic resection between 2008 and 2012. Thirty independent pre-S clones in every patient were analyzed for a semi-quantitative detection. Results: Multivariate regression analysis showed that the serum pre-S2 mutant level (≥ 5%) and the American Joint Committee on Cancer (AJCC) tumor stage were two independent high-risk factors for HCC recurrence. A Cox proportional hazards analysis also showed that the combined evaluations of the AJCC stage and serum pre-S2 mutant level provided a reliable predictive marker for HCC recurrence after primary surgery. We developed a Cox prediction model, which indicated the recurrence-free survival rates along with the time after surgery. This model was validated in an independent HCC cohort. Receiver operating characteristic curve analysis revealed that the model showed close sensitivities in the main and validation cohorts (AUC values: 0.741 and 0.704, respectively). Conclusions: The relative level of pre-S2 mutant in serum is, independently of tumor stage, an important predictive high-risk marker for HCC recurrence after a primary hepatic resection. The combined evaluations of the AJCC tumor stage and serum pre-S2 mutant level potentially serve as a convenient high-risk predictive marker for HCC prognosis. Citation Format: Wen-Ya Huang. Hepatitis B virus gene pre-S2 mutant as a high risk serum marker for hepatoma recurrence after a hepatic resection [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3820. doi:10.1158/1538-7445.AM2017-3820