cyclin-d1 and Latent-Infection

Nasopharyngeal carcinoma (NPC) results from the aberrant and uncontrolled growth of the nasopharyngeal epithelium. It is highly associated with the Epstein-Barr virus, especially in regions where it is endemic. In the last decade, significant advances in genetic sequencing techniques have allowed the discovery of many new abnormal molecular processes that undoubtedly contribute to the establishment, growth and spread of this deadly disease. In this review, we consider NPC as EBV induced. We summarise the recent discoveries and how they add to our understanding of the pathophysiology of NPC in the context of genomics first in primary and then in recurrent disease. Overall, we find key early events lead to p16 inactivation and cyclin D1 expression, allowing latent viral infection. Host and viral factors work together to affect a variety of molecular pathways, the most fundamental being activation of NF-κB. Nonetheless, much still yearns to be discovered, especially in recurrent NPC.

Topics: Cyclin D1; Cyclin-Dependent Kinase Inhibitor p16; Epstein-Barr Virus Infections; Genomics; Herpesvirus 4, Human; Host-Pathogen Interactions; Humans; Latent Infection; Nasopharyngeal Carcinoma; Neoplasm Recurrence, Local; NF-kappa B