ArticleScientific reports2025
HBV reactivation and prognosis after systemic therapy in HCC with undetectable HBV DNA: a multicenter retrospective study.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Comparative efficacy of combination regimens based on interventional therapy and immune checkpoint inhibitors (ICIs) in patients with intermediate- and advanced-stage hepatocellular carcinoma: a systematic review, meta-analysis, and network meta-analysis.Cancer immunology, immunotherapy : CII · 2026Pooled it
- HBV reactivation during immunotherapy for hepatocellular carcinoma: risk factors and clinical management.Frontiers in immunology · 2026Review
- Breaching the immune-cold barrier in pMMR/MSS metastatic colorectal cancer: emerging strategies beyond standard care.Frontiers in immunology · 2026Review
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is a lack of research on hepatitis B virus (HBV) reactivation and prognosis in hepatocellular carcinoma (HCC) patients with undetectable HBV DNA after systemic therapy. This study aims to compare HBV reactivation (HBVr) and prognosis between patients treated with tyrosine kinase inhibitor (TKI) monotherapy and those receiving TKI combined with programmed cell death protein‑1 (PD-1) inhibitors. The retrospective study comprised 877 advanced HCC patients from two medical centers with undetectable HBV DNA, receiving TKI monotherapy (n = 419) or TKI plus PD-1 inhibitors (n = 458). HBVr rates, tumor progression, and overall survival (OS) were analyzed. The HBVr rate markedly higher in the combination cohort compared to the TKI monotherapy cohort (16.6% vs. 12.5%, P = 0.018). Multivariable regression analysis identified the combination therapy (HR 1.295, 95%CI 1.010-1.662, P = 0.042), ALT > 40 U/ml (HR 1.460, 95%CI 1.079-1.978, P = 0.014), Hepatitis B e antigen (HBeAg) positivity (HR 1.570, 95%CI 1.133-2.174, P = 0.007), and tumor size > 5 cm (HR 1.394, 95%CI 1.051-1.848, P = 0.021) as independent predictors of HBVr. Patients receiving antiviral prophylaxis had a lower HBVr rate than those not receiving it (27.4% vs. 33.7%, P = 0.013). Patients with HBVr had shorter progression-free survival (PFS) (P < 0.001) and OS (P < 0.001) compared to those without HBVr. TKI plus PD-1 inhibitors increases the risk of HBVr compared to TKI monotherapy, leading to higher tumor progression and shorter OS. Continuous antiviral therapy can help prevent HBVr after systemic treatment in HCC patients.
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