Infection of HHV-8+ primary effusion lymphoma cells with a recombinant Epstein-Barr virus leads to restricted EBV latency, altered phenotype, and increased tumorigenicity without affecting TCL1 expression.
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Distinct subsets of primary effusion lymphoma can be identified based on their cellular gene expression profile and viral associationThe viral etiology of AIDS-associated malignanciesCo-infections and Pathogenesis of KSHV-Associated MalignanciesEpstein-Barr Virus-associated lymphoproliferative disorders: experimental and clinical developmentsCo-infection of Epstein-Barr virus and human papillomavirus in human tumorigenesisMutual inhibition between Kaposi's sarcoma-associated herpesvirus and Epstein-Barr virus lytic replication initiators in dually-infected primary effusion lymphomaDual expression of Epstein-Barr virus, latent membrane protein-1 and human papillomavirus-16 E6 transform primary mouse embryonic fibroblasts through NF-κB signalingConvergence of Kaposi's sarcoma-associated herpesvirus reactivation with Epstein-Barr virus latency and cellular growth mediated by the notch signaling pathway in coinfected cellsKaposi's sarcoma-associated herpesvirus transactivator Rta induces cell cycle arrest in G0/G1 phase by stabilizing and promoting nuclear localization of p27kip.Epstein-barr virus-positive diffuse large B-cell lymphoma of the elderly: what we know so far.Epigenetic regulation of EBV and KSHV latencyCD20-negative diffuse large B cell lymphoma: a comprehensive analysis of 695 cases.Porcine CD74 is involved in the inflammatory response activated by nuclear factor kappa B during porcine circovirus type 2 (PCV-2) infection.X-box binding protein 1 induces the expression of the lytic cycle transactivator of Kaposi's sarcoma-associated herpesvirus but not Epstein-Barr virus in co-infected primary effusion lymphoma.EBV is necessary for proliferation of dually infected primary effusion lymphoma cells.Epstein-Barr virus inhibits Kaposi's sarcoma-associated herpesvirus lytic replication in primary effusion lymphomas.BFRF1 of Epstein-Barr virus is essential for efficient primary viral envelopment and egress.Epigenetic mechanisms do not control viral latency III in primary effusion lymphoma cells infected with a recombinant Epstein-Barr virus.KSHV oral shedding and plasma viremia result in significant changes in the extracellular tumorigenic miRNA expression profile in individuals infected with the malaria parasite.Gene essentiality landscape and druggable oncogenic dependencies in herpesviral primary effusion lymphoma
P2860
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P2860
Infection of HHV-8+ primary effusion lymphoma cells with a recombinant Epstein-Barr virus leads to restricted EBV latency, altered phenotype, and increased tumorigenicity without affecting TCL1 expression.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年論文
@yue
2003年論文
@zh-hant
2003年論文
@zh-hk
2003年論文
@zh-mo
2003年論文
@zh-tw
2003年论文
@wuu
2003年论文
@zh
2003年论文
@zh-cn
name
Infection of HHV-8+ primary ef ...... out affecting TCL1 expression.
@en
type
label
Infection of HHV-8+ primary ef ...... out affecting TCL1 expression.
@en
prefLabel
Infection of HHV-8+ primary ef ...... out affecting TCL1 expression.
@en
P2093
P1433
P1476
Infection of HHV-8+ primary ef ...... hout affecting TCL1 expression
@en
P2093
Alberto Faggioni
Claudia Zompetta
Elena Anastasiadou
Kenzo Takada
Kumi Takazawa
Laura Cuomo
Luigi Frati
Pankaj Trivedi
Stefania Uccini
P304
P356
10.1182/BLOOD-2003-05-1710
P407
P577
2003-09-11T00:00:00Z