2018/11/01 by Huali Yin, Jiani Qu, Peng Qiu +2 · 4 citations
Medicine · #Eosinophilic Disorders and Syndromes #Lymphoma Diagnosis and Treatment #Viral-associated cancers and disorders
paper · pdf · doi:10.1007/s00430-018-0570-1
openalex publication_date 2018/11/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/31
The early stage of oncogenesis is linked to the disorder of the cell cycle. Abnormal gene expression often leads to cell cycle disorders, resulting in malignant transformation of human cells. Epstein–Barr virus (EBV) is associated with a diverse range of human neoplasms, such as malignant lymphoma, nasopharyngeal carcinoma and gastric cancer. EBV mainly infects human lymphocytes and oropharyngeal epithelial cells. EBV is latent in lymphocytes for a long period of time, is detached from the cytoplasm by circular DNA, and can integrate into the chromosome of cells. EBV expresses a variety of latent genes during latent infection. The interaction between EBV latent genes and oncogenes leads to host cell cycle disturbances, including the promotion of G 1 /S phase transition and inhibition of cell apoptosis, thereby promoting the development of EBV-associated neoplasms. Molecular mechanisms of EBV-driven cell cycle progression and oncogenesis involve diverse genes and signal pathways. Here, we review the molecular mechanisms of EBV-driven cell cycle progression and promoting oncogenesis.