Hepatitis B Virus (HBV) DNA integrations into the human genome are considered major causative factors to HBV-associated hepatocellular carcinoma development. In the present study, we investigated whether HBV preferentially integrates parts of its genome in specific genes and evaluated the contribution of the integrations in HCC development per gene. We applied dedicated in-house developed pipelines on all of the available HBV DNA integration data and performed a statistical analysis to identify genes that could be characterized as hotspots of integrations, along with the evaluation of their association with HBV-HCC. Our results suggest that 15 genes are recurrently affected by HBV integrations and they are significantly associated with HBV-HCC. Further studies that focus on HBV integrations disrupting these genes are mandatory in order to understand the role of HBV integrations in clonal advantage gain and oncogenesis promotion, as well as to determine whether inhibition of the HBV-disrupted genes can provide a therapy strategy for HBV-HCC.
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http://dx.doi.org/10.3390/microorganisms10020253 | DOI Listing |
Front Immunol
January 2025
National Key Laboratory of Draggability Evaluation and Systematic Translational Medicine, Tianjin's Clinical Research Center for Cancer, Department of Bone and Soft Tissue Tumors, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, China.
Background: Hepatocellular carcinoma (HCC) is one of the most prevalent causes of cancer-related morbidity and mortality worldwide. Late-stage detection and the complex molecular mechanisms driving tumor progression contribute significantly to its poor prognosis. Dysregulated R-loops, three-stranded nucleic acid structures associated with genome instability, play a key role in the malignant characteristics of various tumors.
View Article and Find Full Text PDFAnal Methods
January 2025
Department of Public Health Laboratory Sciences, College of Public Health, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Hepatitis B virus (HBV) is a major pathogen posing significant challenges to global public health, making early diagnosis critical for preventing severe liver diseases. We previously developed a fluorescent biosensor named PAM-dependent dsDNA Target-activated Cas12f1 Trans Reporter (PDTCTR). However, its reliance on specialized fluorescence equipment and lack of visual readout limited its application in resource-limited settings.
View Article and Find Full Text PDFCureus
December 2024
Internal Medicine, California Institute of Behavioral Neurosciences & Psychology, Fairfield, USA.
Viral hepatitis B is infamous for being contracted in young adulthood and adolescence, as high-risk behaviors like unprotected sexual intercourse and intravenous drug abuse are common. Most infections caused by the hepatitis B virus (HBV) are cleared without any long-term sequelae, but some may persist and cause chronic hepatitis B (CHB). This chronicity may produce a state of prolonged inflammation and significantly increase the risk of developing colorectal adenomas (CRA) and colorectal carcinomas (CRC).
View Article and Find Full Text PDFClin Res Hepatol Gastroenterol
January 2025
Department of Molecular and Cellular Medicine, Institute of Liver and Biliary Sciences, New Delhi, India. Electronic address:
Background: Covalently closed circular DNA (cccDNA) is a stable, episomal form of HBV DNA. cccDNA is a true marker for the intrahepatic events in controlled CHB infection. Quantifying cccDNA is critical for monitoring disease progression, and efficacy of anti-viral therapies.
View Article and Find Full Text PDFToxicology
January 2025
Department of Pharmacology, Shantou University Medical College, Shantou 515041, China. Electronic address:
Aflatoxin B1 (AFB1) has been reported to synergize with hepatitis B virus (HBV) to induce development of hepatocellular carcinoma (HCC). Precise daily exposure to AFB1 and its contribution to liver injury have not been quantified and have even been disregarded due to lack of convenient detection, and the strong species specificity of HBV infection has restricted research on their synergistic harm. Hence, our objective was to investigate the molecular mechanisms by which AFB1 exacerbates HBV-related injury.
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