Hepatitis B Reactivation in a Patient Receiving Chemotherapy for Breast Cancer: A Case Report

Remo, Mylene; Abraham, Ivy; Kankanala, Vineel; Chacra, Wadih; Danciu, Oana Cristina

doi:10.21873/anticanres.11755

Cited by 2 publications

(3 citation statements)

References 10 publications

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“… 23 A case report documented PTX-induced HBV reactivation in a breast cancer patient who eventually died due to severe liver and kidney failure. 11 However, there is no clear consensus on whether HBV reactivation occurs as a result of the underlying disease itself, the PTX treatment, or the interaction between the two factors. 4 In the present study, PTX was found to directly promote HBV replication in vitro in a concentration-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

“…However, clinical trials have reported cases of severe HBV reactivation leading to liver damage in breast cancer patients following PTX treatment. 11 …”

Section: Introductionmentioning

confidence: 99%

“…However, clinical trials have reported cases of severe HBV reactivation leading to liver damage in breast cancer patients following PTX treatment. 11 While previous clinical studies have documented the reactivation of HBV in individuals concurrently diagnosed with HBV infection and tumors following PTX treatment, the direct impact of PTX on HBV itself remains a subject of controversy. Furthermore, there is a paucity of comprehensive investigations elucidating the molecular mechanisms underlying chemotherapeutic drug-induced HBV reactivation.…”

Section: Introductionmentioning

confidence: 99%

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Paclitaxel-induced Immune Dysfunction and Activation of Transcription Factor AP-1 Facilitate Hepatitis B Virus Replication

Chen,

Li,

Luo

et al. 2024

J Clin Transl Hepatol

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Background and Aims Hepatitis B virus (HBV) reactivation is commonly observed in individuals with chronic HBV infection undergoing antineoplastic drug therapy. Paclitaxel (PTX) treatment has been identified as a potential trigger for HBV reactivation. This study aimed to uncover the mechanisms of PTX-induced HBV reactivation in vitro and in vivo , which may inform new strategies for HBV antiviral treatment. Methods The impact of PTX on HBV replication was assessed through various methods including enzyme-linked immunosorbent assay, dual-luciferase reporter assay, quantitative real-time PCR, chromatin immunoprecipitation, and immunohistochemical staining. Transcriptome sequencing and 16S rRNA sequencing were employed to assess alterations in the transcriptome and microbial diversity in PTX-treated HBV transgenic mice. Results PTX enhanced the levels of HBV 3.5-kb mRNA, HBV DNA, HBeAg, and HBsAg both in vitro and in vivo . PTX also promoted the activity of the HBV core promoter and transcription factor AP-1. Inhibition of AP-1 gene expression markedly suppressed PTX-induced HBV reactivation. Transcriptome sequencing revealed that PTX activated the immune-related signaling networks such as IL-17, NF-κB, and MAPK signaling pathways, with the pivotal common key molecule being AP-1. The 16S rRNA sequencing revealed that PTX induced dysbiosis of gut microbiota. Conclusions PTX-induced HBV reactivation was likely a synergistic outcome of immune suppression and direct stimulation of HBV replication through the enhancement of HBV core promoter activity mediated by the transcription factor AP-1. These findings propose a novel molecular mechanism, underscoring the critical role of AP-1 in PTX-induced HBV reactivation.

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Section: Discussionmentioning

confidence: 99%

“…However, clinical trials have reported cases of severe HBV reactivation leading to liver damage in breast cancer patients following PTX treatment. 11 …”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Paclitaxel-induced Immune Dysfunction and Activation of Transcription Factor AP-1 Facilitate Hepatitis B Virus Replication

Chen,

Li,

Luo

et al. 2024

J Clin Transl Hepatol

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Effect of an Electronic Alert System on Hepatitis B Virus Reactivation in Patients Receiving Immunosuppressive Drug Therapy

Asai

Hirai

Yokohama

et al. 2022

JCM

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Hepatitis B virus (HBV) reactivation (HBVr) can occur in patients receiving immunosuppressive drug therapies, causing significant morbidity and mortality. Although the guidelines for HBVr have been proposed by several academic societies, some providers do not follow them, resulting in HBVr and death. As HBV-DNA levels increase before liver enzyme levels do, we previously constructed an electronic alert system that recommends the measurement of HBV-DNA. Here, we investigated whether this alert system improves the HBV-DNA measurement rate and elicits responses according to guidelines. A total of 5329 patients were divided into two groups, before and after the introduction of the alert system, and the HBV-DNA measurement rates in both groups were compared. Because of the introduction of the alert system, the HBV-DNA measurement rate among HBsAg-negative patients with anti-HBs and/or anti-HBc before immunosuppressive drug therapy improved significantly. The HBV-DNA monitoring rate within 3 months also improved significantly (p = 0.0034) in HBV-remission phase patients. HBVr was detected immediately, and the affected patients were treated with nucleotide analogs before severe hepatitis onset. The introduction of the alert system for HBVr improved the HBV-DNA measurement rates in patients receiving immunosuppressive drug therapy, leading to the rapid treatment of patients with HBVr.

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Hepatitis B Reactivation in a Patient Receiving Chemotherapy for Breast Cancer: A Case Report

Cited by 2 publications

References 10 publications

Paclitaxel-induced Immune Dysfunction and Activation of Transcription Factor AP-1 Facilitate Hepatitis B Virus Replication

Paclitaxel-induced Immune Dysfunction and Activation of Transcription Factor AP-1 Facilitate Hepatitis B Virus Replication

Effect of an Electronic Alert System on Hepatitis B Virus Reactivation in Patients Receiving Immunosuppressive Drug Therapy

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