{"title":"Epstein-Barr virus and Burkitt lymphoma.","authors":"Martin Rowe, Leah Fitzsimmons, Andrew I Bell","doi":"10.5732/cjc.014.10190","DOIUrl":null,"url":null,"abstract":"<p><p>In 1964, a new herpesvirus, Epstein-Barr virus (EBV), was discovered in cultured tumor cells derived from a Burkitt lymphoma (BL) biopsy taken from an African patient. This was a momentous event that reinvigorated research into viruses as a possible cause of human cancers. Subsequent studies demonstrated that EBV was a potent growth-transforming agent for primary B cells, and that all cases of BL carried characteristic chromosomal translocations resulting in constitutive activation of the c-MYC oncogene. These results hinted at simple oncogenic mechanisms that would make Burkitt lymphoma paradigmatic for cancers with viral etiology. In reality, the pathogenesis of this tumor is rather complicated with regard to both the contribution of the virus and the involvement of cellular oncogenes. Here, we review the current understanding of the roles of EBV and c-MYC in the pathogenesis of BL and the implications for new therapeutic strategies to treat this lymphoma. </p>","PeriodicalId":10034,"journal":{"name":"癌症","volume":"33 12","pages":"609-19"},"PeriodicalIF":0.0000,"publicationDate":"2014-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ff/69/cjc-33-12-609.PMC4308657.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"癌症","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.5732/cjc.014.10190","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2014/11/21 0:00:00","PubModel":"Epub","JCR":"Q","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
In 1964, a new herpesvirus, Epstein-Barr virus (EBV), was discovered in cultured tumor cells derived from a Burkitt lymphoma (BL) biopsy taken from an African patient. This was a momentous event that reinvigorated research into viruses as a possible cause of human cancers. Subsequent studies demonstrated that EBV was a potent growth-transforming agent for primary B cells, and that all cases of BL carried characteristic chromosomal translocations resulting in constitutive activation of the c-MYC oncogene. These results hinted at simple oncogenic mechanisms that would make Burkitt lymphoma paradigmatic for cancers with viral etiology. In reality, the pathogenesis of this tumor is rather complicated with regard to both the contribution of the virus and the involvement of cellular oncogenes. Here, we review the current understanding of the roles of EBV and c-MYC in the pathogenesis of BL and the implications for new therapeutic strategies to treat this lymphoma.
期刊介绍：
In July 2008, Landes Bioscience and Sun Yat-sen University Cancer Center began co-publishing the international, English-language version of AI ZHENG or the Chinese Journal of Cancer (CJC). CJC publishes original research, reviews, extra views, perspectives, supplements, and spotlights in all areas of cancer research. The primary criteria for publication in CJC are originality, outstanding scientific merit, and general interest. The Editorial Board is composed of members from around the world, who will strive to maintain the highest standards for excellence in order to generate a valuable resource for an international readership.
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