Epigenetic dysregulation of the host cell genome in Epstein-Barr virus-associated neoplasia.
作者： Hans Helmut Niller , Hans Wolf , Janos Minarovits
DOI: 10.1016/J.SEMCANCER.2009.02.012
关键词: Gene 、 Genetics 、 Gene silencing 、 Epigenetics 、 Transcriptional regulation 、 Cancer research 、 Tumor suppressor gene 、 Methyltransferase 、 DNA methylation 、 Biology 、 Epstein–Barr virus
摘要: Epstein-Barr virus (EBV), a human herpesvirus, is associated with wide variety of malignant tumors. The expression the latent viral RNAs under strict, host-cell dependent transcriptional control. This results in an almost complete silencing EBV genome memory B-cells. In tumor cells, germinal center B-cells and lymphoblastoid distinct latency promoters are active. Epigenetic mechanisms contribute to this strict EBV-infected epigenetic also alter cellular genes, including suppressor genes. Nasopharyngeal Carcinoma, hypermethylation certain attributed upregulation DNA methyltransferases by oncoprotein LMP1 (latent membrane protein 1) via JNK/AP1-signaling. role other products dysregulation remains be established. Analysis alterations EBV-associated neoplasms may result better understanding their pathogenesis facilitate development new therapies.
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