Relevant bibliographies by topics / EBV cancers

Academic literature on the topic 'EBV cancers'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "EBV cancers"

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Rodriquenz, Maria Grazia, Giandomenico Roviello, Alberto D’Angelo, Daniele Lavacchi, Franco Roviello, and Karol Polom. "MSI and EBV Positive Gastric Cancer’s Subgroups and Their Link with Novel Immunotherapy." Journal of Clinical Medicine 9, no. 5 (May 11, 2020): 1427. http://dx.doi.org/10.3390/jcm9051427.

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Gastric cancers have been historically classified based on histomorphologic features. The Cancer Genome Atlas network reported the comprehensive identification of genetic alterations associated with gastric cancer, identifying four distinct subtypes— Epstein-Barr virus (EBV)-positive, microsatellite-unstable/instability (MSI), genomically stable and chromosomal instability. In particular, EBV-positive and MSI gastric cancers seem responsive to novel immunotherapies drugs. The aim of this review is to describe MSI and EBV positive gastric cancer’s subgroups and their relationship with novel immunotherapy.
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Wong, Yide, Michael T. Meehan, Scott R. Burrows, Denise L. Doolan, and John J. Miles. "Estimating the global burden of Epstein–Barr virus-related cancers." Journal of Cancer Research and Clinical Oncology 148, no. 1 (October 27, 2021): 31–46. http://dx.doi.org/10.1007/s00432-021-03824-y.

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Abstract Background More than 90% of the adult population globally is chronically infected by the Epstein–Barr virus (EBV). It is well established that EBV is associated with a number of malignancies, and advances in knowledge of EBV-related malignancies are being made every year. Several studies have analysed the global epidemiology and geographic distribution of EBV-related cancers. However, most have only described a single cancer type or subtype in isolation or limited their study to the three or four most common EBV-related cancers. This review will present an overview on the spectrum of cancers linked to EBV based on observations of associations and proportions in the published literature while also using these observations to estimate the incidence and mortality burden of some of these cancers. Method We have reviewed the literature on defining features, distribution and outcomes across six cancers with a relatively large EBV-related case burden: Nasopharyngeal carcinoma (NPC), Gastric carcinoma (GC), Hodgkin lymphoma (HL), Burkitt lymphoma (BL), Diffuse large B-cell lymphoma (DLBCL) and Extranodal NK/T-cell lymphoma, Nasal type (ENKTL-NT). We retrieved published region-specific EBV-related case proportions for NPC, GC, HL and BL and performed meta-analyses on pooled region-specific studies of EBV-related case proportions for DLBCL and ENKTL-NT. We match these pooled proportions with their respective regional incidence and mortality numbers retrieved from a publicly available cancer database. Additionally, we also reviewed the literature on several other less common EBV-related cancers to summarize their key characteristics herein. Conclusion We estimated that EBV-related cases from these six cancers accounted for 239,700–357,900 new cases and 137,900–208,700 deaths in 2020. This review highlights the significant global impact of EBV-related cancers and extends the spectrum of disease that could benefit from an EBV-specific therapeutic.
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Oluoch, Peter O., Cliff I. Oduor, Catherine S. Forconi, John M. Ong’echa, Christian Münz, Dirk P. Dittmer, Jeffrey A. Bailey, and Ann M. Moormann. "Kaposi Sarcoma-Associated Herpesvirus Infection and Endemic Burkitt Lymphoma." Journal of Infectious Diseases 222, no. 1 (February 19, 2020): 111–20. http://dx.doi.org/10.1093/infdis/jiaa060.

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Abstract Background Endemic Burkitt lymphoma (eBL) is associated with Epstein-Barr virus (EBV) and Plasmodium falciparum malaria coinfections. However, the role of Kaposi sarcoma-associated herpesvirus (KSHV), also endemic in Africa, has not been evaluated as a cofactor in eBL pathogenesis. Methods Multiplexed seroprofiles for EBV, malaria, and KSHV were generated for 266 eBL patients, 78 non-eBL cancers, and 202 healthy children. KSHV and EBV loads were quantified by PCR. Results KSHV seroprevalence did not differ by study group but was associated with age. Seropositivity, defined by K8.1/LANA or in combination with 5 other KSHV antigens (ORF59, ORF65, ORF61, ORF38, and K5) was associated with antimalarial antibody levels to AMA1 (odds ratio [OR], 2.41, P < .001; OR, 2.07, P < .001) and MSP1 (OR, 2.41, P = .0006; OR, 5.78, P < .001), respectively. KSHV loads did not correlate with antibody levels nor differ across groups but were significantly lower in children with detectable EBV viremia (P = .014). Conclusions Although KSHV-EBV dual infection does not increase eBL risk, EBV appears to suppress reactivation of KSHV while malaria exposure is associated with KSHV infection and/or reactivation. Both EBV and malaria should, therefore, be considered as potential effect modifiers for KSHV-associated cancers in sub-Saharan Africa.
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Sinclair, Alison J., Manal H. Moalwi, and Thomas Amoaten. "Is EBV Associated with Breast Cancer in Specific Geographic Locations?" Cancers 13, no. 4 (February 16, 2021): 819. http://dx.doi.org/10.3390/cancers13040819.

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Epstein–Barr virus (EBV) is a virus that establishes a life-long infection in people, and infection with EBV is nearly ubiquitous by adulthood. EBV was identified from biopsy material from a child with Burkitt’s lymphoma (BL) in sub-Saharan Africa. EBV has a well-characterised role in the development of some cancers, notably, Burkitt’s lymphoma (BL), Hodgkin’s disease (HD), gastric carcinoma (GC), and nasopharyngeal carcinoma (NPC). Links have also been made between EBV and breast cancer (BC), but these have been controversial. For all EBV-associated cancers, the ubiquitous nature of infection with EBV, contrasted with the relatively rare development of cancer, highlights a problem of determining whether EBV is an aetiological agent of cancer. In addition, the geographic distributions of some EBV-associated cancers point to contributions from additional co-factors. Recent meta-analyses of the incidence of EBV within BC biopsies has revealed that the diversity in the conclusions remain, however, they also show more of an association between EBV and BC biopsies in some study locations. Here, we review the evidence linking EBV with BC, and conclude that the evidence for the presence of EBV in BC biopsies is concentrated in specific geographic regions but is currently insufficient to provide a causal link. We pose some questions that could help to resolve the question of whether EBV contributes to BC and probe the contribution EBV might make to the aetiology of BC.
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Farrell, Paul J. "Epstein–Barr Virus and Cancer." Annual Review of Pathology: Mechanisms of Disease 14, no. 1 (January 24, 2019): 29–53. http://dx.doi.org/10.1146/annurev-pathmechdis-012418-013023.

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Epstein–Barr virus (EBV) contributes to about 1.5% of all cases of human cancer worldwide, and viral genes are expressed in the malignant cells. EBV also very efficiently causes the proliferation of infected human B lymphocytes. The functions of the viral proteins and small RNAs that may contribute to EBV-associated cancers are becoming increasingly clear, and a broader understanding of the sequence variation of the virus genome has helped to interpret their roles. The improved understanding of the mechanisms of these cancers means that there are great opportunities for the early diagnosis of treatable stages of EBV-associated cancers and the use of immunotherapy to target EBV-infected cells or overcome immune evasion. There is also scope for preventing disease by immunization and for developing therapeutic agents that target the EBV gene products expressed in the cancers.
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Lo, Angela Kwok-Fung, Christopher W. Dawson, Hong Lok Lung, Ka-Leung Wong, and Lawrence S. Young. "The Therapeutic Potential of Targeting BARF1 in EBV-Associated Malignancies." Cancers 12, no. 7 (July 17, 2020): 1940. http://dx.doi.org/10.3390/cancers12071940.

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Epstein-Barr virus (EBV) is closely linked to the development of a number of human cancers. EBV-associated malignancies are characterized by a restricted pattern of viral latent protein expression which is sufficient for the virus to both initiate and sustain cell growth and to protect virus-infected cells from immune attack. Expression of these EBV proteins in malignant cells provides an attractive target for therapeutic intervention. Among the viral proteins expressed in the EBV-associated epithelial malignancies, the protein encoded by the BamHI-A rightward frame 1 (BARF1) is of particular interest. BARF1 is a viral oncoprotein selectively expressed in latently infected epithelial cancers, nasopharyngeal carcinoma (NPC) and EBV-positive gastric cancer (EBV-GC). Here, we review the roles of BARF1 in oncogenesis and immunomodulation. We also discuss potential strategies for targeting the BARF1 protein as a novel therapy for EBV-driven epithelial cancers.
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Wojtak, Krzysztof, Alfredo Perales-Puchalt, and David B. Weiner. "Novel Synthetic DNA Immunogens Targeting Latent Expressed Antigens of Epstein–Barr Virus Elicit Potent Cellular Responses and Inhibit Tumor Growth." Vaccines 7, no. 2 (May 24, 2019): 44. http://dx.doi.org/10.3390/vaccines7020044.

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Infectious diseases are linked to 15%–20% of cancers worldwide. Among them, Epstein–Barr virus (EBV) is an oncogenic herpesvirus that chronically infects over 90% of the adult population, with over 200,000 cases of cancer and 150,000 cancer-related deaths attributed to it yearly. Acute EBV infection can present as infectious mononucleosis, and lead to the future onset of multiple cancers, including Burkitt lymphoma, Hodgkin lymphoma, nasopharyngeal carcinoma, and gastric carcinoma. Many of these cancers express latent viral genes, including Epstein–Barr virus nuclear antigen 1 (EBNA1) and latent membrane proteins 1 and 2 (LMP1 and LMP2). Previous attempts to create potent immunogens against EBV have been reported but generated mixed success. We designed novel Synthetic Consensus (SynCon) DNA vaccines against EBNA1, LMP1 and LMP2 to improve on the immune potency targeting important antigens expressed in latently infected cells. These EBV tumor antigens are hypothesized to be useful targets for potential immunotherapy of EBV-driven cancers. We optimized the genetic sequences for these three antigens, studied them for expression, and examined their immune profiles in vivo. We observed that these immunogens generated unique profiles based on which antigen was delivered as the vaccine target. EBNA1vax and LMP2Avax generated the most robust T cell immunity. Interestingly, LMP1vax was a very weak immunogen, generating very low levels of CD8 T cell immunity both as a standalone vaccine and as part of a trivalent vaccine cocktail. LMP2Avax was able to drive immunity that impacted EBV-antigen-positive tumor growth. These studies suggest that engineered EBV latent protein vaccines deserve additional study as potential agents for immunotherapy of EBV-driven cancers.
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Stanfield, Brent A., and Micah A. Luftig. "Recent advances in understanding Epstein-Barr virus." F1000Research 6 (March 29, 2017): 386. http://dx.doi.org/10.12688/f1000research.10591.1.

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Epstein-Barr virus (EBV) is a common human herpes virus known to infect the majority of the world population. Infection with EBV is often asymptomatic but can manifest in a range of pathologies from infectious mononucleosis to severe cancers of epithelial and lymphocytic origin. Indeed, in the past decade, EBV has been linked to nearly 10% of all gastric cancers. Furthermore, recent advances in high-throughput next-generation sequencing and the development of humanized mice, which effectively model EBV pathogenesis, have led to a wealth of knowledge pertaining to strain variation and host-pathogen interaction. This review highlights some recent advances in our understanding of EBV biology, focusing on new findings on the early events of infection, the role EBV plays in gastric cancer, new strain variation, and humanized mouse models of EBV infection.
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Sawada, Leila, Antonio Carlos Rosário Vallinoto, and Igor Brasil-Costa. "Regulation of the Immune Checkpoint Indoleamine 2,3-Dioxygenase Expression by Epstein–Barr Virus." Biomolecules 11, no. 12 (November 30, 2021): 1792. http://dx.doi.org/10.3390/biom11121792.

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Epstein–Barr virus (EBV) is an oncovirus ubiquitously distributed and associated with different types of cancer. The reason why only a group of infected people develop cancer is still unknown. EBV-associated cancers represent about 1.8% of all cancer deaths worldwide, with more than 150,000 new cases of cancer being reported annually. Since EBV-associated cancers are described as more aggressive and more resistant to the usual treatment compared to EBV-negative ones, the recent introduction of monoclonal antibodies (mAbs) targeting immune checkpoints (ICs) in the treatment of cancer patients represents a possible therapy for EBV-associated diseases. However, the current mAb therapies available still need improvement, since a group of patients do not respond well to treatment. Therefore, the main objective of this review is to summarize the progress made regarding the contribution of EBV infection to the expression of the IC indoleamine 2,3-dioxygenase (IDO) thus far. This IC has the potential to be used as a target in new immune therapies, such as mAbs. We hope that this work helps the development of future immunotherapies, improving the prognosis of EBV-associated cancer patients.
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Zhang, Baoyi, Kevin Yao, Min Xu, Jia Wu, and Chao Cheng. "Deep Learning Predicts EBV Status in Gastric Cancer Based on Spatial Patterns of Lymphocyte Infiltration." Cancers 13, no. 23 (November 29, 2021): 6002. http://dx.doi.org/10.3390/cancers13236002.

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EBV infection occurs in around 10% of gastric cancer cases and represents a distinct subtype, characterized by a unique mutation profile, hypermethylation, and overexpression of PD-L1. Moreover, EBV positive gastric cancer tends to have higher immune infiltration and a better prognosis. EBV infection status in gastric cancer is most commonly determined using PCR and in situ hybridization, but such a method requires good nucleic acid preservation. Detection of EBV status with histopathology images may complement PCR and in situ hybridization as a first step of EBV infection assessment. Here, we developed a deep learning-based algorithm to directly predict EBV infection in gastric cancer from H&E stained histopathology slides. Our model can not only predict EBV infection in gastric cancers from tumor regions but also from normal regions with potential changes induced by adjacent EBV+ regions within each H&E slide. Furthermore, in cohorts with zero EBV abundances, a significant difference of immune infiltration between high and low EBV score samples was observed, consistent with the immune infiltration difference observed between EBV positive and negative samples. Therefore, we hypothesized that our model’s prediction of EBV infection is partially driven by the spatial information of immune cell composition, which was supported by mostly positive local correlations between the EBV score and immune infiltration in both tumor and normal regions across all H&E slides. Finally, EBV scores calculated from our model were found to be significantly associated with prognosis. This framework can be readily applied to develop interpretable models for prediction of virus infection across cancers.
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Dissertations / Theses on the topic "EBV cancers"

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Swanson, Anna May. "Novel immunotherapies for EBV-associated cancers." Thesis, University of Edinburgh, 2008. http://hdl.handle.net/1842/2683.

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Epstein-Barr virus (EBV) is a gamma herpes virus persistently infecting over 90% of the adult population worldwide. It has been aetiologically linked to a number of human malignancies, including more than 90% of post transplant lymphoproliferative disease (PTLD), 50% of Hodgkin’s lymphoma (HL), virtually all undifferentiated nasopharyngeal carcinoma (NPC), and approximately 10% of gastric carcinoma (GC). As EBV infection in healthy individuals is mainly controlled by virus specific cytotoxic T lymphocytes (CTLs), we hypothesise that engineering T cells with chimeric T cell receptors (cTCRs) specific for EBV latent membrane proteins (LMPs) will confer on these cells the ability to target and kill the malignant cells of cancers associated with Epstein-Barr virus. Thus, the aim of this project was generate these engineered T cells and to set up a severe combined immunodeficient (SCID) mouse model in which to test their effectiveness. Three EBV-infected cell lines derived from HL, NPC and GC gave rise to tumours in 11 of 12 (92%), 12 of 12 (100%) and 10 of 10 (100%) SCID mice respectively, when 1x107 cells were injected subcutaneously. Immunohistochemical analysis showed that the HL SCID tumours were CD4-, CD15-, CD20+, CD30+, consistent with a HL Reed-Sternberg cell phenotype, and NPC and GC SCID tumours expressed the epithelial cell marker cytokeratin. Furthermore, all tumours expressed EBVencoded RNAs (EBERs) and LMP1. This was identical to parent cell line expression patterns, and hence growth in vivo did not affect cell phenotype. T cells were successfully transduced with a retroviral vector encoding a CD19-specific cTCR (CD19- cTCR) with a mean transduction rate of 13%±6%. Transduced cells were cytotoxic for HL-derived L591 cells in vitro, with specific lysis of 24%±11% at an effector to target ratio of 20:1. This was significantly higher than specific lysis seen in mock transduced cells (p>0.05). At a tumour inoculation dose of 5x106, in vivo sc transfer of 5x107 CD19-cTCR transduced cells was able to prevent HL tumour development in 6 of 6 (100%) test mice, whereas 17 of 22 (77%) control mice and 2 of 3 (66%) mice treated with unmodified EBV-specific CTLs developed tumours. Moreover, iv transfer of 5x107 CD19-cTCR transduced cells mediated complete regression of HL SCID tumours in 3 out of 6 (50%) mice. Phage display selection experiments to isolate a single chain antibody fragment (scFv) specific for viral LMPs for incorporation in a cTCR were performed. Linear, biotinylated and cyclised biotinylated peptides derived from the external reverse turn loops of LMP2 were used as target antigens. Despite extensive testing, no reactive clones specific for the peptides were identified. The ability of CD19-cTCR transduced cells to specifically lyse HL cells in vitro, and clear tumour burden in vivo, supports a future role for engineered T cells in the treatment of HL. Despite the lack of success in isolating a scFv for LMP2, the use of viral antigen specific, cTCR redirected T cells remains in principle a valuable therapeutic alternative for EBV-associated malignancies. The SCID models for HL, NPC and GC will provide a useful preclinical tool for investigation of their efficacy in vivo.
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Zha, Shuai. "Lanthanide-based nanomaterials for imaging and inhibition of EBV-related cancers." HKBU Institutional Repository, 2020. https://repository.hkbu.edu.hk/etd_oa/731.

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Nasopharyngeal Carcinoma (NPC) as a typical malignancy that occurs in high-incidence areas, e.g. southern China region, including Hong Kong, and it has aroused wide interests for local researchers to study. The Epstein-Barr virus (EBV) was reported as a vital herpes virus for the growth of NPC. Two significant proteins in EBV, namely Epstein-Barr Nuclear Antigen 1 (EBNA1) and latent infection membrane protein 1 (LMP1) are crucial for virus maintenance and EBV-infected cell development, and essential for cell proliferation and differentiation of EBV latent life cycle, respectively. Thus, inhibition of EBNA1 and LMP1 can be regarded as effective and potent therapy on EBV-associated cancers. In this thesis, the conjugation of core-shell structured upconversion nanoparticles (UCNPs) with distinct EBV-specific peptides including EBNA1 and LMP1 targeting peptides to achieve both impressive inhibition on EBV-positive cancers in vitro/in vivo and visualization on EBV-positive cells with responsive upconversion emission signals were investigated. Taking advantage of lanthanide-based UCNPs, their unique photophysical properties offer deep tissue penetration depth, negligible photobleaching and photocytotoxicity, and therefore provides a solid foundation for convincible theranostic studies. Furthermore, desired inhibitory performance was achieved, it was shown that ~50 mg/mL of nanoprobes can inhibit half of EBV-infected cell viability and only 0.25 mg/tumor of nanoprobes dosage via intravenous injection can prohibit 64.7% of growth inhibition of an EBV-positive tumor
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Jiang, Lijun. "Luminescent bioprobes for imaging and inhibition of EBV associated cancers /Jiang Lijun." HKBU Institutional Repository, 2017. http://repository.hkbu.edu.hk/etd_oa/361.

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The high incidence rate of Nasopharyngeal Carcinoma (NPC) in southern China, including Hong Kong, has attracted worldwide attention. According to the Center for Health Protection in Hong Kong, there were 841 new cases of NPC, with 655 cases of males and 186 cases of females in 2013. The development of NPC is highly associated with the infection of one human herpes virus, the Epstein-Barr virus (EBV). Given that the homodimerization of one of the EBV endogenous protein-Epstein-Barr Nuclear Antigen 1 (EBNA1) is essential for both viral genome maintenance and infected-cell survival, thus the interference of EBNA1 homodimerization would be a novel strategy for the inhibition of EBV-positive tumours. In this thesis we devote to conjugate several kinds of organic fluorophores with various EBV-specific peptides in order to achieve the highly responsive and selective imaging, as well as the effective inhibition of EBV-positive tumours in vitro and in vivo. The first research focused on the conjugation of a styrene pyridine fluorophore with two EBNA1-specific peptides, aiming to develop a dual-probe for the imaging and inhibition of EBV-positive tumour cells. Then we tried to introduce a Nuclear Localization Sequence into the EBNA1-specific peptide, and used an Intra-molecular Charge Transfer characterized fluorophore for the following second research, it showed an impressively responsive signal when the probe binds with EBNA1 both in vitro and in vivo, more importantly, only 4 μg probe can inhibit 92.8% of growth inhibition of an EBV-positive tumour. Along this line, our last research centred on the further improvement of the imaging by taking advantage of lanthanide.
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Movassagh, Mercedeh J. "Comprehensive Computational Assessment And Evaluation of Epstein Barr virus (EBV) Variations, miRNAs, And EBERs in eBL, AML And Across Cancers." eScholarship@UMMS, 2019. https://escholarship.umassmed.edu/gsbs_diss/1022.

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Viruses are known to be associated with 20% of human cancers. Epstein Barr virus (EBV) in particular is the first virus associated with human cancers. Here, we computationally detect EBV and explore the effects of this virus across cancers by taking advantage of the fact that EBV microRNAs (miRNAs) and Epstein Barr virus small RNAs (EBERs) are expressed at all viral latencies. We identify and characterize two sub-populations of EBV positive tumors: those with high levels of EBV miRNA and EBERS expression and those with medium levels of expression. Based on principal component analysis (PCA) and hierarchical clustering of viral miRNAs across all samples we observe a pattern of expression for these EBV miRNAs which is correlated with both the tumor cell type (B cell versus epithelial cell) and with the overall levels of expression of these miRNAs. We further investigated the effect of the levels of EBV miRNAs with the overall survival of patients across cancers. Through Kaplan Meier survival analysis we observe a significant correlation with levels of EBV miRNAs and lower survival in adult AML patients. We also designed a machine learning model for risk assessment of EBV in association with adult AML and other clinical factors. Our next aim was to identify targets of EBV miRNAs, hence, we used a combination of previously known methodologies for miRNA target detection in addition to a multivariable regression approach to identify targets of these viral miRNAs in stomach cancer. Finally, we investigate the variations across EBV subtype specific EBNA3C gene which interacts with the host immune system. Preliminary data suggests potential regional variations plus higher pathogenicity of subtype 1 in comparison to subtype 2 EBV. Overall, these studies further our understanding of how EBV manipulates the tumor microenvironment across cancer subtypes.
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Jones, Richard Julian. "Novel gene therapy for EBV-associated malignancies." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274412.

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Sheng, Wang. "Étude des fonctions oncogènes du virus d'Epstein-Barr (EBV) : détermination des souches du virus impliquées dans les cancers associés à l'EBV en Afrique du Nord : étude de la transformation maligne par l'oncogène viral BARF1 dans les fibroblastes de souris et les lymphocytes B humains." Lyon 1, 2001. http://www.theses.fr/2001LYO1T038.

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Hui, Kwai-fung, and 許貴鋒. "Induction of epstein-barr virus (EBV) lytic cycle and its cellular consequences in EBV-positive epithelial malignancies." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B47849575.

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 In Epstein-Barr virus (EBV)-associated malignancies, the virus is harbored in every tumor cell and persists in a tightly latent form (latency I, II or III) expressing a limited number of viral latent proteins. Induction of EBV lytic cycle, which triggers expression of a much larger number of viral proteins, may lead to therapeutic effects against EBV-associated cancers. We previously found that suberoylanilide hydroxamic acid (SAHA), a FDA-approved histone deacetylase inhibitor, induced EBV lytic cycle and mediated enhanced cell death in EBV-positive gastric carcinoma cells (latency II). In this thesis, we sought to investigate SAHA’s induction of EBV lytic cycle and its cellular consequences in EBV-associated epithelial malignancies, with particular focus on nasopharyngeal carcinoma (NPC) due to its strong association with EBV and high prevalence in southern Chinese populations. SAHA effected strong induction of EBV lytic cycle in EBV-positive epithelial malignancies, including gastric carcinoma and NPC, as evidenced by strong expression of EBV lytic proteins, replication of viral DNA and production of infectious viral particles. Immunofluorescent staining revealed that up to 70% EBV-positive epithelial cancers expressed EBV lytic proteins following treatment with micromolar concentrations of SAHA. However, SAHA could not induce EBV lytic cycle in NK lymphoma cells (both NPC and NK lymphoma express EBV latency II pattern), indicating preferential viral lytic induction in epithelial rather than lymphoid malignancies. EBV lytic cycle induction in NPC by SAHA required activation of protein kinase C-delta (PKC-) and acetylation of non-histone protein but required neither phosphatidylinositol 3’-kinase (PI3K), MAPK/ERK kinase (MEK), c-Jun aminoterminal kinase (JNK) nor p38 stress mitogen-activated protein kinase (MAPK) signaling pathway. Conflicting observations regarding the effect of EBV lytic cycle induction on apoptosis were reported. Thus, we investigated the relationship between EBV lytic cycle induction and apoptosis in NPC following treatment with SAHA. EBV-positive NPC showed a higher percentage of apoptosis and proteolytic cleavage of PARP, caspases-3, -7 and -9 over EBV-negative NPC and greater than 85% of NPC cells co-expressed EBV immediate-early (Zta), early (BMRF1) or late (gp350/220) lytic proteins and cleaved caspase-3. Tracking of expression of these lytic proteins over time demonstrated that NPC proceeded to apoptosis following EBV lytic cycle induction, contrary to the previously reported anti-apoptotic effect of EBV lytic proteins in Burkitt lymphoma. Analyses of cleaved caspase-3 expression upon RNAi knockdown and exogenous expression of Zta further supported that EBV lytic cycle directly led to apoptosis of EBV-positive NPC cells. Interestingly, inhibition of EBV DNA replication and late lytic protein expression by phosphonoformic acid did not impact on SAHA’s induced cell death in NPC, indicating that early rather than late phase of EBV lytic cycle contributed to the apoptotic effect. Finally, in vivo effects of SAHA on EBV lytic cycle induction and tumor growth suppression were observed in NPC tumors established in nude mice. In conclusion, activation of EBV lytic cycle from latent cycle in EBV-positive epithelial malignancies including NPC by SAHA effected apoptosis and tumor growth suppression of the cancer cells and provided experimental evidence for virus-targeted therapy against EBV-positive cancers.
published_or_final_version
Paediatrics and Adolescent Medicine
Doctoral
Doctor of Philosophy
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Ling, Guangsheng, and 寧珖聖. "Development of DNA vaccines encoding Epstein-Barr virus (EBV)-specificantigens potentially for EBV-associated nasopharyngeal carcinoma (NPC)immunotherapy." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36189121.

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Liu, Xuan, and 劉絢. "BARF1 sequence analysis and functional significance in EBV-Related disorders." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B36190445.

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Fitzsimmons, Leah. "Investigating the anti-apoptotic role of EBV in endemic Burkitt lymphona." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5717/.

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Epstein-Barr virus (EBV) has been etiologically associated with Burkitt lymphoma (BL) since its discovery 50 years ago, but despite this long-standing association the precise role of the virus in the pathogenesis of BL remains enigmatic. EBV can be lost spontaneously from EBV-positive BL cell lines, and these EBV-loss clones have been reported to exhibit increased sensitivity to apoptosis. We have confirmed and extended those observations and report that sporadic loss of EBV from BL cells is consistently associated with enhanced sensitivity to apoptosis-inducing agents and conversely, reduced tumorigenicity \(in\) \(vivo\). Importantly, reinfection of EBV-loss clones with EBV can restore apoptosis protection, although surprisingly, individual Latency I genes cannot. We also used inducible pro-apoptotic BH3 ligands to investigate Bcl-2-family dependence in BL clones as well as profiling gene expression changes in response to apoptosis induction in EBV-positive versus EBV-loss clones. We found that EBV-loss was consistently associated with enhanced sensitivity to BH3-ligand-induced death and increased activation of apoptosis signalling pathways, although no individual apoptosis-related gene was responsible. Instead we find that Latency I EBV genes co-operate to co-ordinately repress the BH3-only proteins Bim, Puma and Noxa to inhibit apoptosis in BL.
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Books on the topic "EBV cancers"

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Bulterys, Marc, Julia Brotherton, and Ding-Shinn Chen. Prevention of Infection-Related Cancers. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0066.

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This chapter discusses primary prevention measures that disrupt transmission of oncogenic infections. It begins by discussing vaccination against hepatitis B virus (HBV) and human papillomavirus (HPV), two major causes of cancer for which safe and effective vaccines are currently available. It briefly discusses the importance of treatment and prophylaxis against human immunodeficiency virus type 1 (HIV-1), which potentiates the virulence of other viral infections as well as directly increasing the incidence of non-Hodgkin lymphoma. It does not discuss the treatment of HBV or hepatitis C virus (HCV) infection, since these are considered in Chapters 25 and 33. Also beyond the scope of this chapter are the randomized clinical trials currently underway to assess the efficacy and feasibility of eradication of Helicobacter pylori (Chapters 24, 31), vaccination against Epstein-Barr virus (EBV) (Chapters 24, 26, 39), or the prevention of schistosomiasis and liver flukes (Chapters 24, 33, and 52).
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Epstein-barr Virus Ebv: Transmission, Diagnosis and Role in the Development of Cancers. Nova Science Pub Inc, 2014.

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Chang, Ellen T., and Allan Hildesheim. Nasopharyngeal Cancer. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780190238667.003.0026.

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The main epithelial malignancy arising in the nasopharynx is nasopharyngeal carcinoma (NPC). Although rare throughout most of the world, NPC has a unique geographic distribution, with high-risk endemic areas in southern China and parts of Southeast Asia, intermediate incidence rates elsewhere in Southeast Asia, North Africa, the Arctic, the Middle East, and among Asian and Pacific Islander migrants, and very low risk in other areas. The great majority of NPC cases worldwide are non-keratinizing tumors; these predominate in endemic, high-incidence areas and comprise up to half of tumors in low-incidence populations. The other histologic subtype of NPC, keratinizing squamous cell carcinoma, accounts for 40%–50% of cases in low-incidence areas. Infection with Epstein-Barr virus (EBV) is a necessary but not sufficient cause of non-keratinizing NPC, though it is more weakly associated with keratinizing squamous cell tumors. Tobacco smoking increases the risk of both subtypes.
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Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.

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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.
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Fernandez, Maria E., Patricia Dolan Mullen, Jennifer Leeman, Timothy J. Walker, and Cam Escoffery. Evidence-Based Cancer Practices, Programs, and Interventions. Edited by David A. Chambers, Wynne E. Norton, and Cynthia A. Vinson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190647421.003.0003.

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There are many evidence-based interventions, cancer control practices, programs, treatments, and clinical practice guidelines across cancer control and prevention topic areas that have great potential for decreasing the cancer burden. Nevertheless, challenges in identifying evidence-based interventions (EBIs) that match the needs of community and practice settings, adapting EBIs for new populations and contexts, and implementing EBIs in real-world settings limit the public health impact of cancer control research and its products. This chapter provides an introduction to existing EBIs for cancer control and provides examples of different types of EBIs across the cancer continuum. It highlights issues related to the identification of EBIs, including the evaluation of EBI resources. It also describes processes that can be used to enhance the development, adaptation, and implementation of evidence-based cancer control interventions.
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Current Problems in the Epidemiology of Cancer and Lymphomas: Symposium of the "Gesellschaft zur Bekämpfung der Krebskrankheiten Nordrhein-Westfalen e.V." Düsseldorf, 4th-6th November, 1971. Springer, 2012.

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Book chapters on the topic "EBV cancers"

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Pearson, Gary R. "Immunobiology of EBV-Associated Cancers." In The Herpesviruses, 183–99. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-8021-8_9.

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Castillo, Jorge J. "EBV-Positive Diffuse Large B-Cell Lymphoma of the Elderly." In Hematologic Cancers: From Molecular Pathobiology to Targeted Therapeutics, 83–98. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5028-9_5.

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Kenney, Shannon C., and Joyce D. Fingeroth. "The Molecular Basis of Lytic Induction Therapy in Relation to Gamma herpesvirus (KSHV, EBV)-Associated, AIDS-Related Tumors." In Molecular Basis for Therapy of AIDS-Defining Cancers, 111–35. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1513-9_7.

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Lanier, Anne P., Sarala Krishnamurthy, Susan E. Clift, Kathy T. Kline, Georg W. Bornkamm, Werner Henle, Allen Gown, and David Thorning. "An EBV-Associated Salivary Gland Cancer." In Epstein-Barr Virus and Associated Diseases, 145–50. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2625-0_12.

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Long, Scott M., and Clare E. Sample. "EBV-Associated Diseases in the AIDS Patient." In Cancer Treatment and Research, 163–83. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-46816-7_6.

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Upadhyay, Santosh Kumar, Hem Chandra Jha, Abhik Saha, and Erle S. Robertson. "Lymphocryptoviruses: EBV and Its Role in Human Cancer." In Cancer Associated Viruses, 169–99. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0016-5_8.

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Brumbaugh, Jeffrey, Robert L. Ferris, and Shen Hu. "HPV and EBV in Head and Neck Cancer." In Head and Neck Cancer, 163–79. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27601-4_8.

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Brumbaugh, Jeffrey, Robert L. Ferris, and Shen Hu. "HPV and EBV in Head and Neck Cancer." In Head and Neck Cancer, 121–34. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-9464-6_7.

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Ayodele, Olubukola, and Lillian L. Siu. "New Drugs for Recurrent or Metastatic Nasopharyngeal Cancer." In Critical Issues in Head and Neck Oncology, 337–52. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63234-2_23.

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AbstractChemotherapy has been the backbone for the treatment of recurrent or metastatic nasopharyngeal carcinoma (RMNPC), which remains an incurable disease. Currently the most active area of therapeutic investigations in RMNPC is in immunotherapy, especially after the results of five anti-programmed death-1 (anti-PD-1) antibodies, i.e. pembrolizumab, nivolumab, camrelizumab, toripalimab and tislelizumab, have demonstrated monotherapy objective response rates of 21%–43%. Combinations using anti-PD1/L1 antibodies as backbone to evaluate their additivity or synergy with cytotoxic chemotherapy, molecularly targeted agents, or other immuno-oncology compounds are actively being developed. Besides immune checkpoint blockade, additional ways to modulate the host immune system, such as Epstein-Barr virus (EBV)-directed vaccination against viral antigens (such as EBNA1, LMP1, LMP2) with dendritic cells or peptides, adoptive cell transfer of autologous or HLA-matched allogeneic EBV-specific cytotoxic T lymphocytes, CAR or TCR T-cell therapy, personalized cancer vaccines and oncolytic viruses are being explored. Finally, novel molecularly targeted agents that have entered human testing in RMNPC include apatinib and anlotinib (antiangiogenic agents), MAK683 (an embryonic ectoderm development or EED protein inhibitor), among others. This review provides an update of ongoing clinical trials evaluating these new compounds in RMNPC.
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Bajaj, Bharat G., Masanao Murakami, and Erle S. Robertson. "Molecular Biology of EBV in Relationship to AIDS-Associated Oncogenesis." In Cancer Treatment and Research, 141–62. Boston, MA: Springer US, 2007. http://dx.doi.org/10.1007/978-0-387-46816-7_5.

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Conference papers on the topic "EBV cancers"

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Nagi, Karim, Ishita Gupta, Hamda A. Al-Thawadi, Ayesha Jabeen, Mohammed I. Malk, Semir Vranic, and Ala-Eddin Al-Moustafa. "Comparison of Co-Presence of Epstein-Barr Virus and High-Risk Human Papillomaviruses in Colorectal Cancers in the Middle East Region." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0121.

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Background: Several studies have shown the presence of onco viral DNA in colorectal tumor tissues. Viral infection by onco-viruses such as Human papillomaviruses (HPVs) and Epstein–Barr virus (EBV) are well-known to be involved in the onset and/or progression of numerous human carcinomas. Methods: We explored the co-presence of high-risk HPVs and EBV in a cohort of colorectal cancer samples from Lebanon (94) and Syria (102) by PCR, immunohistochemistry and tissue microarray. Results: The results of the study point out that 54% of colorectal cancer cases in Syria are positive for high-risk HPVs, while 30% of the cases in Lebanon are positive for these viruses; the most frequent high-risk HPV types in these populations are 16, 18, 31, 33 and 35. Analysis of LMP1 showed similar results in both populations; 36% of Syrian and 31% of Lebanese samples. Additionally, we report that EBV and high-risk HPVs are co-present in these samples. In Syrian samples, EBV and HPVs are co-present in 16% of the population, however, in the Lebanese samples, 20% of the cases are positive for both EBV and HPVs; their co-presence is associated with high/intermediate grade invasive carcinomas. Conclusion: These data suggest that EBV and high-risk HPVs are co-present in human colorectal cancers where they can cooperate in the progression of these cancers. Nevertheless, further studies are needed to elucidate the role of those oncoviruses in the development of human colorectal carcinomas.
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McGreal, Analise, Aimee Minko, Melissa A. Visalli, Robert J. Visalli, and Gretchen L. Bentz. "Abstract 3791: Understanding the function of LMP1 CTAR3 in EBV-associated cancers." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-3791.

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McGreal, Analise, Aimee Minko, Melissa A. Visalli, Robert J. Visalli, and Gretchen L. Bentz. "Abstract 3791: Understanding the function of LMP1 CTAR3 in EBV-associated cancers." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-3791.

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Chiang, Alan K. S., Stephanie PT Yiu, Kwai F. Hui, Chung K. Choi, Richard YT Kao, and Dan Yang. "Abstract 1252: Intracellular iron chelation by a novel compound, C7, reactivates Epstein-Barr virus (EBV) lytic cycle via the ERK-autophagy axis in EBV-positive epithelial cancers." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1252.

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Chiang, Alan K. S., Stephanie PT Yiu, Kwai F. Hui, Chung K. Choi, Richard YT Kao, and Dan Yang. "Abstract 1252: Intracellular iron chelation by a novel compound, C7, reactivates Epstein-Barr virus (EBV) lytic cycle via the ERK-autophagy axis in EBV-positive epithelial cancers." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1252.

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Moon, Jae Seung, Jung Ho Kim, and Sang Kyou Lee. "Abstract B049: Immunotherapy of EBV associated gastric cancer using EBV specific T cells." In Abstracts: Second CRI-CIMT-EATI-AACR International Cancer Immunotherapy Conference: Translating Science into Survival; September 25-28, 2016; New York, NY. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/2326-6066.imm2016-b049.

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Lee, Woochan. "Abstract 4377: EBV associated gastric cancer in Korean." In Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4377.

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Camargo, M. Constanza, Angelika Michel, Kyoung-Mee Kim, Keitaro Matsuo, Linda M. Liao, Javier Torres, Jovanny Zabaleta, et al. "Abstract 277: Multiplex Epstein-Barr virus (EBV) serology in EBV-positive and -negative gastric cancer." In Proceedings: AACR Annual Meeting 2014; April 5-9, 2014; San Diego, CA. American Association for Cancer Research, 2014. http://dx.doi.org/10.1158/1538-7445.am2014-277.

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Kim, Hyemi, Hyun Gyu Lee, Jeon Han Park, and Jae Myun Lee. "Abstract 2760: Gemcitabine induced lytic EBV replication and confers ganciclovir susceptibility to EBV-positive gastric cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-2760.

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Li, C., L. Pusztai, EN Cohen, F. Symmans, B. Wang, B. Lee, GN Hortobagyi, M. Cristofanilli, and JM Reuben. "Epstein-Barr virus (EBV) in fine needle aspirates containing inflammatory breast cancer cells." In CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-3084.

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Reports on the topic "EBV cancers"

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Ghosh, Sajal K. Do EBV Encoded Small RNAs Interfere with Tumor Suppressor APC in EBV Associated Breast Cancers. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada462843.

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Dahm, Philipp, Michelle Brasure, Elizabeth Ester, Eric J. Linskens, Roderick MacDonald, Victoria A. Nelson, Charles Ryan, et al. Therapies for Clinically Localized Prostate Cancer. Agency for Healthcare Research and Quality (AHRQ), September 2020. http://dx.doi.org/10.23970/ahrqepccer230.

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Objective. To update findings from previous Agency for Healthcare Research and Quality (AHRQ)- and American Urological Association (AUA) funded reviews evaluating therapies for clinically localized prostate cancer (CLPC). Sources. Bibliographic databases (2013–January 2020); ClinicalTrials.gov; systematic reviews Methods. Controlled studies of CLPC treatments with duration ≥5 years for mortality and metastases and ≥1 year for quality of life and harms. One investigator rated risk of bias (RoB), extracted data, and assessed certainty of evidence; a second checked accuracy. We analyzed English-language studies with low or medium RoB. We incorporated findings from randomized controlled trials (RCTs) identified in the prior reviews if new RCTs provided information on the same intervention comparison. Results. We identified 67 eligible references; 17 were unique RCTs. Among clinically rather than prostate specific antigen (PSA) detected CLPC, Watchful Waiting (WW) may increase mortality and metastases versus Radical Prostatectomy (RP) at 20+ years. Urinary and erectile dysfunction were lower with WW versus RP. WW’s effect on mortality may vary by tumor risk and age but not by race, health status, comorbidities, or PSA. Active Monitoring (AM) probably results in little to no difference in mortality in PSA detected CLPC versus RP or external beam radiation (EBR) plus Androgen Deprivation (AD) regardless of tumor risk. Metastases were slightly higher with AM. Harms were greater with RP than AM and mixed between EBR plus AD versus AM. 3D-conformal EBR and AD plus low-dose-rate brachytherapy (BT) provided a small reduction in all-cause mortality versus three dimensional conformal EBR and AD but little to no difference on metastases. EBR plus AD versus EBR alone may result in a small reduction in mortality and metastases in higher risk disease but may increase sexual harms. EBR plus neoadjuvant AD versus EBR plus concurrent AD may result in little to no difference in mortality and genitourinary toxicity. Conventionally fractionated EBR versus ultrahypofractionated EBR may result in little to no difference in mortality and metastases and urinary and bowel toxicity. Active Surveillance may result in fewer harms than photodynamic therapy and laparoscopic RP may result in more harms than robotic-assisted RP. Little information exists on other treatments. No studies assessed provider or hospital factors of RP comparative effectiveness. Conclusions. RP reduces mortality versus WW in clinically detected CLPC but causes more harms. Effectiveness may be limited to younger men or to those with intermediate risk disease and requires many years to occur. AM results in little to no mortality difference versus RP or EBR plus AD. EBR plus AD reduces mortality versus EBR alone in higher risk CLPC but may worsen sexual function. Adding low-dose-rate BT to 3D-conformal EBR and AD may reduce mortality in higher risk CLPC. RCTs in PSA-detected and MRI staged CLPC are needed.
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Flemington, Erik K. Development of an EBV-Mammary Epithelial Cell Model for Addressing the Role of EBV in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada409341.

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Flemington, Erik K. Development of an EBV-Mammay Epithelial Cell Model for Addressing the Role of EBV in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2003. http://dx.doi.org/10.21236/ada420086.

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Sealy, Linda J. C/EBP(Beta) Isoforms - An Innovative Transcription Factor Therapy for Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, May 2002. http://dx.doi.org/10.21236/ada406154.

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Zahnow, Cynthia A. A Novel Role for C/EBP in Mammary Development and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 1997. http://dx.doi.org/10.21236/ada340339.

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Zahnow, Cynthia A. A Novel Role for C/EBP in Mammary Development and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1998. http://dx.doi.org/10.21236/ada359168.

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Zahnow, Cynthia A. A Novel Role for C/EBP In Mammary Development and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 1999. http://dx.doi.org/10.21236/ada381707.

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Cheng, Genhong. Determining if EBV Infection Contributes to Breast Carcinogenesis: Does LMP-1-Mediated Upregulation of EGFR and Bcl-x Affect Breast Cancer Pathogenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada408770.

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Grimm, Sandra L., and Jeffrey M. Rosen. Gene Targets of C/EBP/Beta Involved in Mammary Gland Development and Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396636.

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