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10.1016/j.semcancer.2014.01.002 http://scihub22266oqcxt.onion/10.1016/j.semcancer.2014.01.002 C4048781!4048781!24457012     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24457012&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Semin+Cancer+Biol 2014 ; ä (ä): 60-8 Nephropedia Template TP {{tp|p=24457012|t=2014. Regulation of the latent-lytic switch in Epstein?Barr virus |pdf=|usr=}}{{24457012}} gab.com Text Regulation of the latent-lytic switch in Epstein Barr virus JO: Semin Cancer Biol http://www.kidney.de/pget.php?&tw=1&pmid=24457012 #FOAvip Epstein?Barr virus (EBV) infection contributes to the development of several different types of human malignancy, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, EBV can establish latent or lytic infection in cells. EBV-positive tumors are composed almost exclusively of cells with latent EBV infection. Strategies for inducing the lytic form of EBV infection in tumor cells are being investigated as a potential therapy for EBV-positive tumors. In this article, we review how cellular and viral proteins regulate the latent-lytic EBV switch in infected B cells and epithelial cells, and discuss how harnessing lytic viral reactivation might be used therapeutically. Twit Text FOAVip Regulation of the latent-lytic switch in Epstein Barr virus ????Semin Cancer Biol http://www.kidney.de/pget.php?&tw=1&pmid=24457012 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24457012 #FOAvip English Wikipedia <ref>{{Cite pmid|24457012}}</ref> Regulation of the latent-lytic switch in Epstein?Barr virus #MMPMID24457012 Kenney SC; Mertz JE Semin Cancer Biol 2014[Jun]; ä (ä): 60-8 PMID24457012show ga Epstein?Barr virus (EBV) infection contributes to the development of several different types of human malignancy, including Burkitt lymphoma, Hodgkin lymphoma, and nasopharyngeal carcinoma. As a herpesvirus, EBV can establish latent or lytic infection in cells. EBV-positive tumors are composed almost exclusively of cells with latent EBV infection. Strategies for inducing the lytic form of EBV infection in tumor cells are being investigated as a potential therapy for EBV-positive tumors. In this article, we review how cellular and viral proteins regulate the latent-lytic EBV switch in infected B cells and epithelial cells, and discuss how harnessing lytic viral reactivation might be used therapeutically. äRegulation of the latent-lytic switch in Epstein?Barr virus (epmc).pdf DeepDyve Pubget Overpricing