| pubmed-article:10022853 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10022853 | lifeskim:mentions | umls-concept:C0006413 | lld:lifeskim |
| pubmed-article:10022853 | lifeskim:mentions | umls-concept:C0014644 | lld:lifeskim |
| pubmed-article:10022853 | lifeskim:mentions | umls-concept:C0086661 | lld:lifeskim |
| pubmed-article:10022853 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:10022853 | lifeskim:mentions | umls-concept:C1519697 | lld:lifeskim |
| pubmed-article:10022853 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:10022853 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:10022853 | pubmed:dateCreated | 1999-3-25 | lld:pubmed |
| pubmed-article:10022853 | pubmed:abstractText | Loss of the Epstein-Barr virus (EBV) genome from Akata Burkitt lymphoma (BL) cells is coincident with a loss of malignant phenotype, despite the fact that Akata and other EBV-positive BL cells express a restricted set of EBV gene products (type I latency) that are not known to overtly affect cell growth. Here we demonstrate that reestablishment of type I latency in EBV-negative Akata cells restores tumorigenicity and that tumorigenic potential correlates with an increased resistance to apoptosis under growth-limiting conditions. The antiapoptotic effect of EBV was associated with a higher level of Bcl-2 expression and an EBV-dependent decrease in steady-state levels of c-MYC protein. Although the EBV EBNA-1 protein is expressed in all EBV-associated tumors and is reported to have oncogenic potential, enforced expression of EBNA-1 alone in EBV-negative Akata cells failed to restore tumorigenicity or EBV-dependent down-regulation of c-MYC. These data provide direct evidence that EBV contributes to the tumorigenic potential of Burkitt lymphoma and suggest a novel model whereby a restricted latency program of EBV promotes B-cell survival, and thus virus persistence within an immune host, by selectively targeting the expression of c-MYC. | lld:pubmed |
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| pubmed-article:10022853 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10022853 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10022853 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10022853 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10022853 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10022853 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10022853 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:10022853 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:10022853 | pubmed:author | pubmed-author:YangHH | lld:pubmed |
| pubmed-article:10022853 | pubmed:author | pubmed-author:ClevelandJ... | lld:pubmed |
| pubmed-article:10022853 | pubmed:author | pubmed-author:SampleJ TJT | lld:pubmed |
| pubmed-article:10022853 | pubmed:author | pubmed-author:Hutt-Fletcher... | lld:pubmed |
| pubmed-article:10022853 | pubmed:author | pubmed-author:SunH SHS | lld:pubmed |
| pubmed-article:10022853 | pubmed:author | pubmed-author:BorzaC MCM | lld:pubmed |
| pubmed-article:10022853 | pubmed:author | pubmed-author:RhyneP WPW | lld:pubmed |
| pubmed-article:10022853 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10022853 | pubmed:volume | 19 | lld:pubmed |
| pubmed-article:10022853 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10022853 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10022853 | pubmed:pagination | 1651-60 | lld:pubmed |
| pubmed-article:10022853 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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