2012
DOI: 10.1073/pnas.1202637109
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Abstract: Undifferentiated nasopharyngeal carcinomas (NPCs) are commonly present with latent EBV infection. However, events regulating EBV infection at early stages of the disease and the role of EBV in disease pathogenesis are largely undefined. Genetic alterations leading to activation of cyclin D1 signaling in premalignant nasopharyngeal epithelial (NPE) cells have been postulated to predispose cells to EBV infection. We previously reported that loss of p16, a negative regulator of cyclin D1 signaling, is a frequent … Show more

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Cited by 136 publications
(147 citation statements)
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“…In contrast, primary epithelial cells entered senescence after EBV infection. This corresponds well with a previous observation that overexpression of cyclin D1 in precancerous tissue is a prerequisite for susceptibility to stable EBV infection (35). We took advantage of an experimental system in which immortalized human keratinocytes undergo vacuolar degeneration and cell death following Ras activation.…”
Section: Discussionmentioning
confidence: 85%
“…In contrast, primary epithelial cells entered senescence after EBV infection. This corresponds well with a previous observation that overexpression of cyclin D1 in precancerous tissue is a prerequisite for susceptibility to stable EBV infection (35). We took advantage of an experimental system in which immortalized human keratinocytes undergo vacuolar degeneration and cell death following Ras activation.…”
Section: Discussionmentioning
confidence: 85%
“…EBV exclusively, lytically infects more differentiated normal epithelial cells (48)(49)(50)(51)(52)(53), and thus, the viral genome remains highly unmethylated (11). However, in the case of NPC, EBV maintains a latent infection and the viral genome becomes highly methylated (54).…”
Section: Tet2 Promotes Ebv Type III Latency Gene Expressionmentioning
confidence: 99%
“…Known as product of protooncogene, cyclin D1 promotes proliferation in malignancy through interaction with oncogenic molecules [30]. It has been reported that over-expressed cyclin D1 facilitates the infection of nasopharyngeal epithelial cells by a lymphotropic human herpesvirus, Epstein-Barr virus (EBV), a ubiquitous human virus that is tightly associated with the occurrence of NPC and Burkitt lymphoma (BL) [31]. It has been proposed that MAPK pathway and cyclin D1 forms a signaling axis to regulate cell proliferation, and amplification of the chromosomal region that harbors CCND1 is a frequent anomaly at cytogenetic level during the occurrence of human tumors [32,33].…”
Section: The Regulation Of Raf-mek-mapk Involving Interactions Betweementioning
confidence: 99%