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Copyright: ©Author(s) 2026. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial (CC BY-NC 4.0) license. No commercial re-use. See permissions. Published by Baishideng Publishing Group Inc.
World J Hepatol. Sep 27, 2026; 18(9): 123791
Published online Sep 27, 2026. doi: 10.4254/wjh.123791
Molecular characteristics and carcinogenic mechanisms of aflatoxin B1-associated hepatocellular carcinoma: Recent advances
Fei Li, Qin-Qin Long, Feng-Qin Tian, Mei-Jin Huang, Xi-Dai Long
Fei Li, Qin-Qin Long, Feng-Qin Tian, Clinicopathological Diagnosis and Research Center, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Fei Li, Qin-Qin Long, Feng-Qin Tian, Xi-Dai Long, Department of Basic Research, Key Laboratory of Tumor Molecular Pathology (Youjiang Medical University for Nationalities), Education Department of Guangxi Zhuang Autonomous Region, Baise 533000, Guangxi Zhuang Autonomous Region, China
Fei Li, Qin-Qin Long, Feng-Qin Tian, Xi-Dai Long, Department of Basic Research, Key Laboratory of Tumor Molecular Pathology of Baise, Baise 533000, Guangxi Zhuang Autonomous Region, China
Mei-Jin Huang, Department of Infection, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Xi-Dai Long, Department of Pathology, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi Zhuang Autonomous Region, China
Co-first authors: Fei Li and Qin-Qin Long.
Author contributions: Li F, Long QQ, Tian FQ, and Huang MJ completed the collection, reading, analysis, and summary of relevant literature, and drafted the manuscript; Long XD conducted the conceptualization, methodology, supervision, and critical review of manuscript, and received grant support; Li F and Long QQ made crucial and indispensable contributions towards the completion of the project; All authors contributed to the data acquisition and interpretation and reviewed and approved the final version. Li F, Long QQ, Tian FQ, and Huang MJ contributed equally to this work and are considered co-first authors.
AI contribution statement: All scientific analyses, discussions, and writing of this review were independently completed by the authors. Literature sorting and linguistic polishing were assisted by the artificial intelligence tool Doubao AI, which is hereby clarified.
Supported by Baise Talent Highland, No. Bairencaiban-2020-3-2; Building Projects of Guangxi Bagui Scholars, No. Guirencaiban-2024-39; Building Projects of Key Laboratory of Tumor Molecular Pathology (Youjiang Medical University for Nationalities), Education Department of Guangxi Zhuang Autonomous Region, No. Guijiaokeyan-2022-10; Building Projects of the Key Laboratory of Molecular Pathology in Tumor of Baise, No. Baikezi-2022-38; Building Projects from the Key Laboratory of Molecular Pathology (Hepatobiliary Diseases) of Guangxi, No. Guiweikejiaofa-2020-17; and Clinical Key Specialty Building Project (For Pathology) of Guangxi, No. Guiweiyifa-2022-21.
Conflict-of-interest statement: The authors have no conflicts of interest to declare.
Corresponding author: Xi‐Dai Long, MD, PhD, Professor, Department of Pathology, the Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Youjiang, Zhongshan 2nd Road, Baise 533000, Guangxi Zhuang Autonomous Region, China. sjtulongxd@263.net
Received: May 29, 2026
Revised: July 16, 2026
Accepted: July 30, 2026
Published online: September 27, 2026
Processing time: 112 Days and 1.7 Hours
Core Tip

Core Tip: Aflatoxin B1 (AFB1) is a potent carcinogen characterized by hepatotropism, genotoxicity and carcinogenicity. AFB1-associated hepatocellular carcinoma (AAHCC) possesses distinct molecular profiles (including tumor protein p53 R249S mutation, C > A transversion, GCN motif preference, strand bias, and abnormal epigenetic modifications) and pathogenic mechanisms (including the formation of AFB1-exo-8,9-epoxide and AFB1-DNA adducts, abnormal DNA damage repair, and the accumulation of somatic mutation), exhibiting substantial heterogeneity from non-AAHCC.

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