This dissertation, "Sequence Analysis of Epstein-barr Virus Genomes in Nasopharyngeal Carcinoma" by Hin, Kwok, 郭軒, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: ... ZRL5P4 can also specifically elevate Dicer1 and PML expression, molecular events that have been reported to occur after the depletion of EBNA1 expression in EBV-infected cells (44, 76). Furthermore, ZRL5P4 can disrupt transactivation and induce EBV reactivation more potently than L2P4, suggesting that EBNA1 oligomers are more important than the dimer in some of EBNA1's functions (75). Pharmacologic activation of lytic Epstein-Barr virus gene expression without virion production. Nat Commun. 65. Int J Cancer. Introduction. The results from these studies suggested that small molecule-based pharmacological blockade of AT-hook activity may effectively perturb the viral latency in EBV-infected cancer cells. doi: 10.1128/JVI.01602-10, 106. Autophagy-dependent reactivation of Epstein-Barr virus lytic cycle and combinatorial effects of autophagy-dependent and independent lytic inducers in nasopharyngeal carcinoma. J Virol. Wang L, Shan L, Lo KW, Yin J, Zhang Y, Sun R, et al. doi: 10.1021/acschembio.9b00191, 70. Nasopharyngeal cancer is a disease in which malignant (cancer) cells form in the tissues of the nasopharynx. Notably, the strongest association with NPC risk has been consistently found in several variants of major histocompatibility complex (MHC) class I genes (4). Sun LQ, Cairns MJ, Saravolac EG, Baker A, Gerlach WL. Please enable it to take advantage of the complete set of features! Nasopharyngeal carcinoma is more common in Southeast Asia and is frequently, but not always, caused by Epstein-Barr virus (EBV). Background. Lytic replication in EBV-positive NPC cells will result in cell disruption, for the release of infectious viral particles. The editor and reviewers' affiliations are the latest provided on their Loop research profiles and may not reflect their situation at the time of review. In this cancer model, we identified the . Furthermore, our earlier genomic and functional studies have indicated that several specific genetic alterations (such as inactivation of CDNK2A/p16 and tumor suppressors at chromosome 3p) in the premalignant nasopharyngeal epithelium support a cellular switch to state that maintains persistent latent EBV infection and predisposes individuals to NPC transformation (21–23). Here, we review the approaches that have been examined for the disruption of EBNA1 functions and the feasibility of targeting EBNA1 for treatment EBV-associated diseases (Figure 2, Table 1). 2001;1:75–82. Males are more commonly affected, with a male to female ratio of 3:1. 2021 Aug 6;13(16):3981. doi: 10.3390/cancers13163981. Virus Genes. Thus, targeting LMP1 is hypothesized to be a potential therapeutic intervention for NPC, even in tumors exhibiting weak LMP1 expression. -, Young LS, Rickinson AB. We thank Core Utilities of Cancer Genome and Pathobiology of the Faculty of Medicine, The Chinese University of Hong Kong for providing support for our studies. 2021 Aug 13;14(1):310. doi: 10.1186/s13104-021-05727-0. Background Nasopharyngeal carcinoma is often associated with neck lymph node (LN) metastases, which in many cases is the only manifestation of this disease. Virology. Nasopharyngeal carcinoma (also known as NPC) is a rare tumor of the head and neck which originates in the nasopharynx. Epstein-Barr virus and carcinogenesis: beyond Burkitt's lymphoma. J Virol. Di Renzo L, Avila-Carino J, KleinE. Introduction. Definition of the sequence requirements for binding of the EBNA-1 protein to its palindromic target sites in Epstein-barr virus DNA. Tsai MH, Lin X, Shumilov A, Bernhardt K, Feederle R, Poirey R, Kopp-Schneider A, Pereira B, Almeida R, Delecluse HJ. Although these antiviral agents have no effect on latently infected cells, phosphorylation of these prodrugs by EBV PK and TK during lytic reactivation induces premature termination of the nascent DNA and thus induces apoptosis, facilitating the cytotoxicity and bystander effect in the lytic and adjacent tumor cells (Figure 3) (92). The detection of the Epstein-Barr virus (EBV) nuclear antigen and viral DNA in nasopharyngeal carcinoma has revealed that EBV can infect epithelial cells and is associated with their malignant transformation. Tsao SW, Tsang CM, Lo KW. Cell cycle and apoptosis were analyzed by flow cytometry analysis. doi: 10.1128/JVI.00487-19, 71. (2011) 6:e19407. One of the inhibitors, VK-2019, is now in Phase I/IIa clinical trial (NCT03682055) in patients with EBV-positive NPC. Table 2. Although mc-oriP-miR-31 inhibits cell proliferation and migration of C666-1 in vitro by EBV-specific induction of miR-31, in vivo studies on systemic delivery of this vector in NPC xenografts are needed to prove its therapeutic efficacy (83). Nat Rev Cancer. Furthermore, different efficiencies of HDACis or PKC activators in activating EBV lytic genes were observed in EBV-positive NPC cell lines (e.g., C666-1, NPC43, and C17) (25, 102–104). Fragment-based protein-protein interaction antagonists of a viral dimeric protease. Scientists have found risk factors that make a person more likely to develop nasopharyngeal cancer (NPC). EBV-induced hypermethylation may be a host defence response or the direct action of viral genes, such as, EBV infection and progressive genomic changes drive clonal evolution of nasopharyngeal carcinoma. NPC. 2017;1018:75-90. doi: 10.1007/978-981-10-5765-6_6. doi: 10.1128/JVI.02659-10, 122. The fluorophore L2 was coupled with P4 to form the second-generation EBNA1 bioprobe L2P4, which generates a responsive fluorescent signal when it binds with EBNA1 via induction of intermolecular charge transfer (ICT) in the L2 fluorophore molecule. doi: 10.3390/diseases7040057, 120. doi: 10.1016/0165-2478(93)90008-P, 126. Theranostics. A BARF1 protein encoded by the Bam H1-A fragment is a homolog of human colony-stimulating factor 1 (CSF1) receptor, and this secreted viral protein is believed to enhance NPC tumorigenicity through activation of the CSF-1 signaling axis, suppression of apoptosis by activation of BCL-2, and upregulation of expression of NF-κB, RelA, and cyclin D1 (35). Nasopharyngeal carcinoma (NPC) is consistently associated with Epstein-Barr virus (EBV) infection in regions in which it is endemic, including Southern China and Southeast Asia. These findings show that clinical benefit of CLVA treatment needs further evaluation in large-scale clinical studies that include a patient group receiving gemcitabine treatment only. Tsao SW, Yip YL, Tsang CM, Pang PS, Lau VM, Zhang G, et al. Essential role of PKCdelta in histone deacetylase inhibitor-induced Epstein-Barr virus reactivation in nasopharyngeal carcinoma cells. Cell. The EBV lytic reactivation ability of these chemotherapeutic agents may contribute to the chemosensitivity of EBV-associated NPC. Nevertheless, >60% of newly diagnosed patients have a poor clinical outcome, as they usually present with advanced-stage disease. Epstein-Barr virus microRNA miR-BART20-5p suppresses lytic induction by inhibiting BAD-mediated caspase-3-dependent apoptosis. doi: 10.1016/j.oraloncology.2014.02.006, 6. This EBNA1-driven BRLF1 viral vector was observed to cause lytic EBV DNA replication and cell death in infected tumor cells. Like other types of head and neck cancer, nasopharyngeal cancer is frequently associated with a viral infection. EBV infection could drive NPC pathogenesis…, EBV infection and progressive genomic changes drive clonal evolution of nasopharyngeal carcinoma. Carcinoma-risk variant of EBNA1 deregulates Epstein-Barr Virus episomal latency. The World Health Organization (WHO) has classified nasopharyngeal carcinoma into the three subtypes based on histology. Cancer Res. Adv Exp Med Biol. A novel signaling mechanism in which ROS induces EBV reactivation was proposed by Huang and colleagues, based on the fact that ROS activates multiple signaling pathways, such as ATM, p38 MAPK, and JNKs, to induce p53-dependent EBV reactivation (111). Found insideUnder the motto “Healthcare Technology for Developing Countries” this book publishes many topics which are crucial for the health care systems in upcoming countries. Found insideThis book offers a state-of-the-art report on recent discoveries concerning viral, bacterial, and parasite infectious cancers. doi: 10.1038/mt.2013.257, 88. Yip KW, Li A, Li JH, Shi W, Chia MC, Rashid SA, et al. Therapeutic evaluation of Epstein-Barr virus-encoded latent membrane protein-1 targeted DNAzyme for treating of nasopharyngeal carcinomas. The association of nasopharyngeal carcinoma (NPC) with the Epstein-Barr virus (EBV) was firmly established as early as 1973. In early studies using a high-throughput virtual screen of 90,000 low molecular weight compounds, Li and coworkers demonstrated that a series of four compounds (SC7, SC11, SC19, and SC27) with an IC50 of ~20 μM could physically inhibit EBNA1-DNA binding and reduce the number of EBV episomes in latently infected cells (65). , The body fights the virus, but the infection is ignored. The NLS sequence in P4 can form salt bridges with the adjacent dimerization interface, including several residues in the aspartate-rich tail of EBNA1 (D602, D601, D605), which further enhances the interaction between P4and the EBNA1 monomer. Infection with the Epstein-Barr virus. When latent EBV are induced into the lytic cycle, the IE proteins BZLF1 and BRLF1 must be expressed, as these further activate the transcription of early and late proteins to progress continue the lytic infection cycle (92). Rev Med Virol. NF-κB Signaling Regulates Expression of Epstein-Barr Virus BART MicroRNAs and Long Noncoding RNAs in Nasopharyngeal Carcinoma. Through inducing the IE genes BZLF1 and BRLF1, the chemical inducers switch on EBV lytic cycle. doi: 10.1002/rmv.441. (2010) 137:13–22. LMP2A is another integral membrane protein that promotes stem-like properties and various oncogenic phenotypes by regulating multiple signaling pathways, such as PI3K/AKT, ERK, and RhoA (36, 38, 39). Subsequently, cellular kinases catalyze the formation of the cytotoxic diphosphate and triphosphate forms of the drugs. (2012) 22:144–53. doi: 10.1007/s12011-009-8555-y, 124. Ambinder RF, Shah WA, Rawlins DR, Hayward GS, Hayward SD. Ambinder RF, Mullen MA, Chang YN, Hayward GS, Hayward SD. Li YY, Chung GT, Lui VW, To KF, Ma BB, Chow C, et al. Thus, iron chelators appear to activate hypoxic signaling and autophagy to trigger lytic reactivation in EBV-positive epithelial cancer cells (110). Serum and Tissue Level of TLR9 in EBV-Associated Oropharyngeal Cancer. Found insideThis open access book discusses the most current issues in head and neck cancer with a focus on current trends such as biomarkers, precision medicine and immunotherapy. It is a rare cancer among whites in Europe and North America. EBV infection promotes a hypermethylation phenotype in the host and induces the inactivation of tumour suppressor genes. A late event in a very few carriers of this virus is the emergence of Burkitt's lymphoma and nasopharyngeal carcinoma, two rare cancers. Epstein-Barr virus: 40 years on. (2018) 10:109. doi: 10.3390/cancers10040109, 42. de Leo A, Calderon A, Lieberman PM. Mol Ther. Lee V, Kwong D, Leung TW, Lam KO, Tong CC, Lee A. Palliative systemic therapy for recurrent or metastatic nasopharyngeal carcinoma - how far have we achieved? Moreover, the underlying mechanisms of the induction of IE genes by these treatments have generally not been investigated and therefore remain elusive. The viral-encoded latent proteins EBNA1, LMP1, and LMP2 are expected to be potential therapeutic targets in NPC cells. Cell cycle and apoptosis were analyzed by flow cytometry analysis. Identification of novel small organic compounds with diverse structures for the induction of Epstein-Barr virus (EBV) lytic cycle in EBV-positive epithelial malignancies. The nasopharynx is located at the very back of the nose near the Eustachian tubes (Figure). Wilson JB, Manet E, Gruffat H, Busson P, Blondel M, Fahraeus R. EBNA1: oncogenic activity, immune evasion and biochemical functions provide targets for novel therapeutic strategies against Epstein-Barr virus-associated cancers. This volume explores data from the applications of molecular biological methods and the applications of recent immunological and cytogenetic methods in Epstein-Barr Virus (EBV) that will offer readers possible new solutions to the ... In contrast, BRLF1 indirectly binds to the BZLF1 promoter (Zp) via interaction with other cellular factors, forming a positive loop to drive their transcription. Extensive studies have also revealed that multiple cellular events, such as aberrant protein kinase C (PKC), TGF-β and other signaling pathways, cell differentiation, hypoxia, DNA damage, and reactive oxygen species (ROS) induction play key roles in EBV lytic reactivation in B cells and epithelial cells, by activating the promoters of BZLF1 and BRLF1 (92). 12 More than 97% of NPC are EBV-positive, 13 and the tight link between NPC and EBV is observed worldwide. Diet. This study was aimed to investigate the association between p63 and NPC. It has previously been demonstrated that EBNA1 recruits the cellular origin recognition complex (ORC) to origin of replication (oriP) for episome maintenance or replication initiation (52). J Cancer Res Clin Oncol. doi: 10.1128/JVI.79.19.12280-12285.2005, 28. The above studies have identified the clinically available iron chelators as a novel class of lytic inducer for potential cytolytic therapy. Kenney SC, Mertz JE. Aside from EBNA1 and LMP1, only a few other latent EBV gene products have been targeted in NPC. The role of the EBV-encoded latent membrane proteins LMP1 and LMP2 in the pathogenesis of nasopharyngeal carcinoma (NPC). Signs of nasopharyngeal cancer include trouble breathing, speaking, or hearing. Structural and functional basis for an EBNA1 hexameric ring in Epstein-Barr virus episome maintenance. Circulating cancer-derived EBV-DNA in plasma is an established tumor marker for nasopharyngeal cancer, with a sensitivity of 96% and a specificity of 93%. It is now clear that EBNA1 interacts with certain host cell components to establish viral latency and mediate oncogenic transformation of the host cells (26, 41). Nat Rev Cancer. In regions where NPC is endemic, undifferentiated subtypes constitute most cases and are invariably associated with Epstein-Barr virus (EBV) infection, whereas the differentiated subtype is more common in other parts of the world. Tsao SW, Tsang CM, To KF, Lo KW. Among these latent gene products, EBNA1 is the only protein that is expressed in all of the EBV-associated cancers: it is essential for governing the replication and mitotic segregation of the EBV episomes, thereby maintaining EBV genomes in latently infected cells. Curr Top Microbiol Immunol. (2016) 16:789–802. Additional genetic and epigenetic changes occur after EBV infection. Treatment results for nasopharyngeal carcinoma in the modern era: the Hon g Kong experience. (2013) 3:299. doi: 10.3389/fonc.2013.00299, 5. EBV can cause genetic changes in cells that make them more likely . Using a yeast-based genetic screening assay, Lista and coworkers found that nucleolin can directly interact with G-quadruplexes formed in GAr-encoding EBNA1 mRNA. Genome sequencing analysis identifies Epstein-Barr virus subtypes associated with high risk of nasopharyngeal carcinoma. Bookshelf Disclaimer, National Library of Medicine Virology. (Upper) Domains of EBNA1. In addition, recent advances in chemical bioengineering are driving the development of therapeutic agents targeting the critical functional regions of EBNA1. 2017. Once cells have become infected, EBV latent genes provide growth and survival benefits, resulting in the development of NPC. 2014 Nov;33(11):549-55. doi: 10.5732/cjc.014.10169. The exosomal EBV-encoded BHRF1 miRNA cluster are not expressed in NPC, but the exosomal EBV-miR-BARTs are present in the serum of mice transplanted with human nasopharyngeal carcinoma and in the serum of nasopharyngeal cancer patients . (2000) 60:5365–70. Lanthanide-mediated upconversion is a well-known photophysical phenomenon characterized by the generation of high-energy photon/emission from low-energy photon/excitations. Nasopharyngeal carcinoma (NPC) is a rare malignancy worldwide, but it is endemic in a few areas including Southern China, Southeast Asia, North Africa and the Arctic. Addition of an imaging moiety to the molecularly targeted agent would greatly facilitate the monitoring of the drug inside the cells or animal models. This bystander effect then further promotes tumor shrinkage. (2018) 10:15632–40. Using the recombinant EBV-infected epithelial cancer cell lines AGS-BX1 and NA, Choi and colleagues performed a high-throughput phenotypic screening of 50,240 novel small organic compounds for chemical inducers of the EBV lytic cycle (108). Two compounds, PyDH2 and PhenDH2, were found to enhance the expression of EBNA1 in H1299 cells in a GAr-dependent manner (61). Bethesda, MD 20894, Help The important roles of the DNA damage response and ROS induction in EBV reactivation imply that the status of TP53 mutations in NPC cells may determine their response to lytic-inducer treatment. (2017) 28:415–27. Hammerschmidt W, Sugden B. EBV is spread through body fluids, including saliva. Cell Death Dis. Daigle D, Gradoville L, Tuck D, Schulz V, Wang'ondu R, Ye J, et al. doi: 10.1128/JVI.66.8.5030-5039.1992, 99. Teh JL, Abdul Rahman SF, Domnic G, Satiyasilan L, Chear NJY, Singh D, Mohana-Kumaran N. BMC Res Notes. Early symptoms of NPC are unspecific, so most NPC patients are diagnosed at a late stage. DNAzymes are synthetic, single-stranded catalytic DNA molecules with excellent stability and activity in downregulating gene expression. Oncogene. Cancers. RNA-dependent recruitment of the origin recognition complex. (20), both EBV latent gene products (e.g., EBERs and LMP1) and homogeneous lengths of TR repeats were detected in NPC and precancerous lesions, suggesting that the clonal latent EBV infection is a crucial event in the initiation of this virus-associated cancer (20). (2019) 394:64–80. 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Expression and viral replication the urgent need and will prove essential reading for the imaging and inhibition of cancers...

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