Mechanisms of cell immortalization mediated by EB viral activation of telomerase in nasopharyngeal c

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Nasopharyngeal carcinoma (NPC) is a common cancer in Southern China and Southeast Asia.The disease is a poorlydifferentiated carcinoma without effective cure,and the mechanism underlying its development remains largely unknown.Of several factors identified in NPC aetiology in recent years,Epstein-Barr virus (EBV) infection has emerged to bemost important.In almost all NPC cells,EBV uses several intracellular mechanisms to cause oncogenic evolution of theinfected cells.One such mechanism by which EBV infection induces cellular immortalization is believed to be throughthe activation of telomerase,an enzyme that is normally repressed but becomes activated during cancer development.Studies show that greater than 85% of primary NPC display high telomerase activity by mechanisms involving EBVinfection,consistent with the notion that EBV is commonly involved in inducing cell immortalization.More recently,different EBV proteins have been shown to activate or inhibit the human telomerase reverse transcriptase gene,bymodulating intracellular signalling pathways.These findings suggest a new model with a number of challenges towardsour understanding,molecular targeting and therapeutic intervention in NPC. Nasopharyngeal carcinoma (NPC) is a common cancer in Southern China and Southeast Asia. The disease is a poorly differentiated carcinoma without effective cure, and the mechanism underlying its development remains crude unknown. Of several factors identified in NPC aetiology in recent years, Epstein-Barr virus (EBV) infection has emerged to bemost important. In almost all NPC cells, EBV uses several intracellular mechanisms to cause oncogenic evolution of theinfected cells. One mechanism of such EBV infection induces cellular immortalization is beaten the activation of telomerase, an enzymes that is normally repressed but becomes activated during cancer development. Projects show that greater than 85% of primary NPC display high telomerase activity by mechanisms involving EBV infection, consistent with the not that that EBV is commonly involved in inducing cell immortalization. More recently, different EBV proteins have been shown to activate or inhibit the human telomerase revers e transcriptase gene, bymodulating intracellular signaling pathways. These findings suggest a new model with a number of challenges towardsour understanding, molecular targeting and therapeutic intervention in NPC.
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