Clinical Implications of HBV PreS/S Mutations and the Effects of PreS2 Deletion on Mitochondria, Liver Fibrosis, and Cancer Development.
Yuh-Jin LiangWei TengChih-Li ChenCheng-Pu SunRui-Dung TengYen-Hua HuangKung-Hao LiangYi-Wen ChenChung-Chih LinChien-Wei SuMi-Hua TaoJaw-Ching WuPublished in: Hepatology (Baltimore, Md.) (2021)
PreS mutations were significantly associated with HCC development in patients with CHB, including those with low HBV DNA or ALT levels. Antiviral therapy reduced HCC occurrence in patients with CHB, including those with preS mutations. Intracellular accumulation of mutated HBsAg induced or promoted ER stress, calcium overload, mitochondrial dysfunction, impaired energy metabolism, liver fibrosis, and HCC.
Keyphrases
- liver fibrosis
- hepatitis b virus
- liver failure
- risk assessment
- reactive oxygen species
- papillary thyroid
- high glucose
- cell death
- circulating tumor
- stem cells
- squamous cell carcinoma
- oxidative stress
- cell free
- mesenchymal stem cells
- drug induced
- bone marrow
- endothelial cells
- replacement therapy
- lymph node metastasis
- wild type