Relevant bibliographies by topics / Epstein-Barr Virus Burkitt's Lymphoma

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  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Epstein-Barr Virus Burkitt's Lymphoma'

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Published: 14 March 2023

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Journal articles on the topic "Epstein-Barr Virus Burkitt's Lymphoma"

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Farzanehpour, Mahdieh, Amir M. M. Fard, and Hadi E. G. Ghaleh. "A brief overview of the Epstein Barr virus and its association with Burkitt's lymphoma." Romanian Journal of Military Medicine 125, no. 3 (August 1, 2022): 373–81. http://dx.doi.org/10.55453/rjmm.2022.125.3.4.

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Epstein Barr virus (EBV) is known as an oncovirus and associates with several human malignancies such as Burkitt's lymphoma, other non-Hodgkin lymphomas, nasopharyngeal carcinoma, Hodgkin's disease, gastric adenocarcinoma, etc. in Burkitt's lymphoma, and the key event is the translocation of MYC gene, that increase of cell survival and aberrant expression of MYC gene. The biology of EBV and its function in the development of Burkitt's lymphoma are discussed in this review
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Shah, K. M., and L. S. Young. "Epstein–Barr virus and carcinogenesis: beyond Burkitt's lymphoma." Clinical Microbiology and Infection 15, no. 11 (November 2009): 982–88. http://dx.doi.org/10.1111/j.1469-0691.2009.03033.x.

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Okano, M., G. M. Thiele, J. R. Davis, H. L. Grierson, and D. T. Purtilo. "Epstein-Barr virus and human diseases: recent advances in diagnosis." Clinical Microbiology Reviews 1, no. 3 (July 1988): 300–312. http://dx.doi.org/10.1128/cmr.1.3.300.

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Since the discovery of Epstein-Barr virus (EBV) from a cultured Burkitt's lymphoma cell line in 1964, the virus has been associated with Burkitt's lymphoma, nasopharyngeal carcinoma, and infectious mononucleosis. During the recent decade, EBV has been etiologically implicated in a broad spectrum of human diseases. The precise role of this virus in these diseases is not well understood, but clearly, defective immunosurveillance against the virus may permit an uncontrolled proliferation of EBV-infected cells. As a result, a growing number of cases of EBV-associated B-cell proliferative diseases or lymphoma have been noted in patients with primary and acquired immunodeficiencies. These lymphoproliferative diseases and others, such as chronic mononucleosis syndrome, are leading to new areas of investigation which are providing information regarding the pathogenetic mechanisms of EBV-induced diseases. The early accurate diagnosis of EBV infection can be achieved by performing EBV-specific serology, detecting for EBV-determined nuclear antigen in tissues, establishing spontaneous lymphoid cell lines, and using molecular hybridization techniques for demonstrating the presence of viral genome in affected lesions.
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Tosato, G., C. Sgadari, K. Taga, KD Jones, SE Pike, A. Rosenberg, JM Sechler, IT Magrath, LA Love, and K. Bhatia. "Regression of experimental Burkitt's lymphoma induced by Epstein-Barr virus-immortalized human B cells." Blood 83, no. 3 (February 1, 1994): 776–84. http://dx.doi.org/10.1182/blood.v83.3.776.776.

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Abstract Epstein-Barr virus (EBV)-immortalized human B cells survive only transiently when injected subcutaneously into athymic mice, whereas Burkitt's lymphoma cells give rise to progressively growing subcutaneous tumors. In this study, we tested whether these Burkitt's tumors could be induced to regress via a bystander effect induced by EBV-immortalized B cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in the same subcutaneous site resulted in tumors that regressed with necrosis and scarring. Similarly, simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in separate subcutaneous sites resulted in regression of a proportion of the Burkitt's tumors. Furthermore, most of the established human Burkitt's tumors regressed with necrosis and scarring after intratumor inoculations with EBV-immortalized B cells. The EBV-immortalized B cells continued to exert this antitumor effect even when killed with irradiation. The experimental approach to Burkitt's lymphoma treatment described here exploits the ability of athymic mice to reject EBV-immortalized B cells to target an effective antitumor response to malignant cells normally incapable of eliciting it.
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Tosato, G., C. Sgadari, K. Taga, KD Jones, SE Pike, A. Rosenberg, JM Sechler, IT Magrath, LA Love, and K. Bhatia. "Regression of experimental Burkitt's lymphoma induced by Epstein-Barr virus-immortalized human B cells." Blood 83, no. 3 (February 1, 1994): 776–84. http://dx.doi.org/10.1182/blood.v83.3.776.bloodjournal833776.

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Epstein-Barr virus (EBV)-immortalized human B cells survive only transiently when injected subcutaneously into athymic mice, whereas Burkitt's lymphoma cells give rise to progressively growing subcutaneous tumors. In this study, we tested whether these Burkitt's tumors could be induced to regress via a bystander effect induced by EBV-immortalized B cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in the same subcutaneous site resulted in tumors that regressed with necrosis and scarring. Similarly, simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in separate subcutaneous sites resulted in regression of a proportion of the Burkitt's tumors. Furthermore, most of the established human Burkitt's tumors regressed with necrosis and scarring after intratumor inoculations with EBV-immortalized B cells. The EBV-immortalized B cells continued to exert this antitumor effect even when killed with irradiation. The experimental approach to Burkitt's lymphoma treatment described here exploits the ability of athymic mice to reject EBV-immortalized B cells to target an effective antitumor response to malignant cells normally incapable of eliciting it.
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Stebbing, Justin, and Mark Bower. "Epstein-Barr virus in Burkitt's lymphoma: the missing link." Lancet Oncology 10, no. 4 (April 2009): 430. http://dx.doi.org/10.1016/s1470-2045(09)70045-2.

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Kamranvar, S. A., B. Gruhne, A. Szeles, and M. G. Masucci. "Epstein–Barr virus promotes genomic instability in Burkitt's lymphoma." Oncogene 26, no. 35 (February 26, 2007): 5115–23. http://dx.doi.org/10.1038/sj.onc.1210324.

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Goldstein, J. A., and R. L. Bernstein. "Burkitt's Lymphoma and the Role of Epstein-Barr Virus." Journal of Tropical Pediatrics 36, no. 3 (June 1, 1990): 114–20. http://dx.doi.org/10.1093/tropej/36.3.114.

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Joob, Beuy, and Viroj Wiwanitkit. "Malaria, Epstein-Barr virus, vitamin A and Burkitt's lymphoma." International Journal of Cancer 142, no. 4 (October 31, 2017): 863. http://dx.doi.org/10.1002/ijc.31118.

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Sánchez-Giler, Sunny, Alan Herrera-Vásquez, Claudia Castillo-Zambrano, Luis Solórzano-Alava, Dolores Zambrano-Castro, Cristina Kuon-Yeng, Alba Silva-Orellana, Juan Murillo-Zambrano, and Genaro Cucalón-González. "Detección del Virus de Epstein-Barr en linfoma mediante qPCR //Detection of Epstein-Barr Virus (EBV) in lymphoma through qPCR." Ciencia Unemi 11, no. 26 (June 5, 2018): 126. http://dx.doi.org/10.29076/issn.2528-7737vol11iss26.2018pp126-133p.

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Virus Epstein Barr (VEB) ha sido relacionado con una serie de tumores malignos de origen epitelial y linfoide. Existe una clara correlación entre este virus y enfermedades linfoproliferativas como Linfoma de Burkitt (LB), Linfoma Hodgkin (LH), Linfoma no Hodgkin (LNH) y carcinoma gástrico. Se han desarrollado diversas técnicas para la detección de VEB en células tumorales: hibridación in situ (RISH) que detecta RNAs (ácido ribonucleico) pequeños codificados para VEB (EBERs) en las células con infección latente, considerado el estándar de oro para la identificación del virus; la reacción en cadena de la polimerasa (PCR) que permite la detección de la cepa viral y representa un ensayo importarte en el diagnóstico del virus. Se realizó un estudio retrospectivo a partir de muestras de tejidos en parafina de pacientes con linfoma y se buscó al virus mediante PCR y RISH. La prevalencia del virus fue de 58,82%, el género más afectado fue el masculino y el grupo más afectado fue el de 31/40 años. La presencia del virus fue similar en ambos tipos de linfoma: Hodking y No Hodking. La técnica de RISH se mostró más eficiente para detectar la presencia del virus. AbstractEpstein Barr Virus (EBV) is linked to a number of malignant tumors of epithelial and lymphoid origin. There is a strong correlation between this virus and lymphoproliferative diseases such as Burkitt's lymphoma (BL), Hodgkin lymphoma (HL), non-Hodgkin lymphoma (NHL) and gastric carcinoma. There are various techniques developed to detect EBV in tumor cells: in situ hybridization (ISH) detects small coded RNAs (ribonucleic acid) to VEB (EBERs) in latently infected cells. This is considered the gold standard for virus identification. The polymerase chain reaction (PCR) allows the detection of the viral strain and represents an important fact in the virus diagnose. We conducted a retrospective study in paraffin from tissue samples of patients with lymphoma and we sought the virus through PCR and RISH. The virus prevalence was 58.82%, the most affected gender was male and the most affected group was 31/40 years. The virus was similar in both types of lymphoma: Hodgkin and non-Hodgkin. RISH technique seemed to be more efficient to detect the virus.
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Dissertations / Theses on the topic "Epstein-Barr Virus Burkitt's Lymphoma"

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MUNDO, LUCIA. "Infectious agents and cancer: A look into EBV pathways involved in the transition from infection to lymphomagenesis." Doctoral thesis, Università di Siena, 2017. http://hdl.handle.net/11365/1012697.

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Epidemiological and biological studies have conclusively proved that infectious agents are among the main causes of cancer worldwide. Approximately 18% of all human cancer have been linked to persistent infections from RNA or DNA viruses that include Epstein-Barr virus (EBV), human papilloma virus and Human T-lymphotropic virus type 1. Although each virus has its own specific mechanism for promoting carcinogenesis, the most common outcome for virus-induced reprogramming is genomic instability, including accumulation of mutations, aberrations and DNA damage. The progression to cancer as result of infection is usually a rare event and when it occurs it requires years to decades from the initial infection to tumour development. EBV, classified as class I carcinogen by WHO for its ability of transforming B-cell and functioning as oncogenic factor, is one of the many factors that can be linked to human malignancies. It is estimated that it accounts for more than 200,000 cases of cancer each year and that 1.8% of all cancer deaths are due to EBV. Here, we described several molecular mechanisms underlying the virus-induced carcinogenesis, expecially in Burkitt’s and Plasmablastic lymphoma. We performed RNA-Seq on 20 eBL cases from Uganda and we showed that the mutational and viral landscape of eBL is more complex than previously reported. First, we found the presence of other herpesviridae family members in 8 cases (40%), in particular human herpesvirus 5 and human herpesvirus 8 and confirmed their presence by immunohistochemistry in the adjacent non-neoplastic tissue. Second, we identified a distinct latency program in EBV involving lytic genes in association with TCF3 activity. Third, by comparing the eBL mutational landscape with published data on sporadic Burkitt lymphoma (sBL), we detected lower frequencies of mutations in MYC, ID3, TCF3 and TP53, and a higher frequency of mutation in ARID1A in eBL samples. Recurrent mutations in two genes not previously associated with eBL were identified in 20% of tumors: RHOA and cyclin F (CCNF). We also observed that polyviral samples showed lower numbers of somatic mutations in common altered genes in comparison to sBL specimens, suggesting dual mechanisms of transformation, mutation versus virus driven in sBL and eBL respectively. We also identified a subset of cellular and viral microRNAs differentially expressed between Epstein-Barr-positive and Epstein-Barr-negative Burkitt lymphoma cases. Of these, we characterized the effects of viral BART6-3p on regulation of cellular genes. In particular, we analyzed the IL-6 receptor genes (IL-6Rα and IL-6ST), PTEN and WT1 expression for their possible relevance to Burkitt lymphoma. By means of immunohistochemistry, we observed a down-regulation of the IL-6 receptor and PTEN specifically in Epstein-Barr-positive Burkitt lymphoma cases, which may result in the impairment of key cellular pathways and may contribute to malignant transformation. On the contrary, no differences were observed between Epstein-Barr-positive and Epstein-Barr-negative Burkitt lymphoma cases for WT1 expression. The oncogenic role of EBV was also investigated in Plasmablastic lymphoma. Our analysis revealed a non-canonical latency program with the partial expression of some proteins characterizing latency II and the activation of an abortive lytic cycle. We also performed microRNAs expression profiling through next generation sequencing to investigate the cellular and viral pattern of Plasmastic lymphoma. We identify a subset of viral miRNAs differentially expressed and showed an important role of EBV-miRNAs-Bart-19 in affecting many cellular pathways including lipid metabolism and cell proliferation. Finally, we considered the fact EBV might have contributed to lymphomagenesis in more samples than those remaining EBV positive by exploting a “hit and run” mechanism. We investigated a total of 10 cases and we found that all the samples (n=6) diagnosed as EBV negative by immunohistochemistry and EBER-ISH demonstrated the presence of EBV-microRNAs and EBV genome. This points at the possibility that EBV might have contributed to lymphomagenesis in all our patients, and propose microRNAs detection as the most specific and sensitive tool to recognize EBV vestiges. Collectively, our preliminary results point at an active role for the Epstein-Barr virus in lymphomagenesis and suggest new possible mechanisms used by the virus in determining dysregulation of the host cell physiology. Moreover, our data would have considerable implications for EBV-related diseases control and development of novel EBV-detection strategies.
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Donati, Daria. "Malaria, B lymphocytes and Epstein-Barr virus : emerging concepts on Burkitt's lymphoma pathogenesis /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-403-1/.

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Kaymaz, Yasin. "Genomic and Transcriptomic Investigation of Endemic Burkitt Lymphoma and Epstein Barr Virus." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/914.

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Endemic Burkitt lymphoma (eBL) is the most common pediatric cancer in malaria-endemic equatorial Africa and nearly always contains Epstein-Barr virus (EBV), unlike sporadic Burkitt Lymphoma (sBL) that occurs with a lower incidence in developed countries. Despite this increased burden the study of eBL has lagged. Additionally, while EBV was isolated from an African Burkitt lymphoma tumor 50 years ago, however, the impact of viral variation in oncogenesis is just beginning to be fully explored. In my thesis research, I focused on investigating molecular genetics of the endemic form of this lymphoma with a particular emphasis on the role of the virus and its variation in pathogenesis using novel sequencing and bioinformatic strategies. First, we sought to understand pathogenesis by investigating transcriptomes using RNA sequencing (RNAseq) from 30 primary eBL tumors and compared to sBL tumors. BL tumor samples were prospectively obtained from 2009 until 2012 in Kenya. Within eBL tumors, minimal expression differences were found based on anatomical presentation site, in-hospital survival rates, and EBV genome type; suggesting that eBL tumors are homogeneous without marked subtypes. The outstanding difference detected using surrogate variable analysis was the significantly decreased expression of key genes in the immunoproteasome complex in eBL tumors carrying type 2 EBV compared to type 1 EBV. Secondly, in comparison to previously published pediatric sBL specimens, the majority of the expression and pathway differences were related to the PTEN/PI3K/mTOR signaling pathway and was correlated most strongly with EBV status rather than the geographic designation. Moreover, the common mutations were observed significantly less frequently in eBL tumors harboring EBV type 1, with mutation frequencies similar between tumors with EBV type 2 and without EBV. In addition to the previously reported genes, we identified a set of new genes mutated in BL. Overall, these suggested that EBV, particularly EBV type 1, supports BL oncogenesis alleviating the need for particular driver mutations in the human genome. Second, we sought to comprehensively define sequence variations of EBV across the viral genome in eBL tumor cells and normal infections, and correlate variations with clinical phenotypes and disease risk. We investigated the whole genome sequence of EBV from primary tumors (N=41) and plasma from eBL patients (N=21) as well as EBV in the blood of healthy children (N=29) within the same malaria endemic region. We conducted a genome wide association analysis study with viral genomes of healthy kids and BL kids. Furthermore, we found that the frequencies of EBV types among healthy kids were at equal levels while they were skewed in favor of type 1 (70%) among eBL kids. To pinpoint the fundamental divergence between viral genome subtypes, type 1 and type 2, we constructed phylogenetic trees comparing to all public EBV genomes. The pattern of variation defined the substructures correlated with the subtypes. This investigation not only deciphers the puzzling pathogenic differences between subtypes but also helps to understand how these two EBV types persist in the population at the same time. Overall, this research provides insight into the molecular underpinning of eBL and the role of EBV. It further provides the groundwork and means to unravel the complexity of EBV population structure and provide insight into the viral variation that may influence oncogenesis and outcomes in eBL and other EBV-associated diseases. In addition, genomic and mutational analyses of Burkitt lymphoma tumors identify key differences based on viral content and clinical outcomes suggesting new avenues for the development of prognostic molecular biomarkers and therapeutic interventions.
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Kaymaz, Yasin. "Genomic and Transcriptomic Investigation of Endemic Burkitt Lymphoma and Epstein Barr Virus." eScholarship@UMMS, 2007. http://escholarship.umassmed.edu/gsbs_diss/914.

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Endemic Burkitt lymphoma (eBL) is the most common pediatric cancer in malaria-endemic equatorial Africa and nearly always contains Epstein-Barr virus (EBV), unlike sporadic Burkitt Lymphoma (sBL) that occurs with a lower incidence in developed countries. Despite this increased burden the study of eBL has lagged. Additionally, while EBV was isolated from an African Burkitt lymphoma tumor 50 years ago, however, the impact of viral variation in oncogenesis is just beginning to be fully explored. In my thesis research, I focused on investigating molecular genetics of the endemic form of this lymphoma with a particular emphasis on the role of the virus and its variation in pathogenesis using novel sequencing and bioinformatic strategies. First, we sought to understand pathogenesis by investigating transcriptomes using RNA sequencing (RNAseq) from 30 primary eBL tumors and compared to sBL tumors. BL tumor samples were prospectively obtained from 2009 until 2012 in Kenya. Within eBL tumors, minimal expression differences were found based on anatomical presentation site, in-hospital survival rates, and EBV genome type; suggesting that eBL tumors are homogeneous without marked subtypes. The outstanding difference detected using surrogate variable analysis was the significantly decreased expression of key genes in the immunoproteasome complex in eBL tumors carrying type 2 EBV compared to type 1 EBV. Secondly, in comparison to previously published pediatric sBL specimens, the majority of the expression and pathway differences were related to the PTEN/PI3K/mTOR signaling pathway and was correlated most strongly with EBV status rather than the geographic designation. Moreover, the common mutations were observed significantly less frequently in eBL tumors harboring EBV type 1, with mutation frequencies similar between tumors with EBV type 2 and without EBV. In addition to the previously reported genes, we identified a set of new genes mutated in BL. Overall, these suggested that EBV, particularly EBV type 1, supports BL oncogenesis alleviating the need for particular driver mutations in the human genome. Second, we sought to comprehensively define sequence variations of EBV across the viral genome in eBL tumor cells and normal infections, and correlate variations with clinical phenotypes and disease risk. We investigated the whole genome sequence of EBV from primary tumors (N=41) and plasma from eBL patients (N=21) as well as EBV in the blood of healthy children (N=29) within the same malaria endemic region. We conducted a genome wide association analysis study with viral genomes of healthy kids and BL kids. Furthermore, we found that the frequencies of EBV types among healthy kids were at equal levels while they were skewed in favor of type 1 (70%) among eBL kids. To pinpoint the fundamental divergence between viral genome subtypes, type 1 and type 2, we constructed phylogenetic trees comparing to all public EBV genomes. The pattern of variation defined the substructures correlated with the subtypes. This investigation not only deciphers the puzzling pathogenic differences between subtypes but also helps to understand how these two EBV types persist in the population at the same time. Overall, this research provides insight into the molecular underpinning of eBL and the role of EBV. It further provides the groundwork and means to unravel the complexity of EBV population structure and provide insight into the viral variation that may influence oncogenesis and outcomes in eBL and other EBV-associated diseases. In addition, genomic and mutational analyses of Burkitt lymphoma tumors identify key differences based on viral content and clinical outcomes suggesting new avenues for the development of prognostic molecular biomarkers and therapeutic interventions.
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Amoroso, Richard Benjamin Couture. "Studies on the expression and function of Epstein-Barr virus encoded microRNAs in Burkitt lymphoma." Thesis, University of Birmingham, 2013. http://etheses.bham.ac.uk//id/eprint/3694/.

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Epstein-Barr virus (EBV) encodes at least 40 microRNAs (miRNAs), an important class of negative regulators that control gene expression through posttranscriptional mechanisms. However the contribution of these EBV-encoded miRNAs to the pathogenesis of virus-associated lymphomas remains poorly understood. Using newly-developed PCR assays, we first quantified the levels of viral BHRF1 and BART miRNAs in a range of EBV-positive cell lines. We show for the first time that all three BHRF1 miRNAs are abundantly expressed in Wp-restricted Burkitt lymphoma (BL) cells, but not Latency I BL cells lacking detectable Cp- or Wp-initiated EBNA transcripts. In contrast to some earlier reports, we also detected robust expression of BART miRNAs in B cell lines, although there was wide variation between individual miRNAs in a given cell. Analysis of BHRF1 and BART transcription, both in latent and lytic infection, suggested that maturation may be a key step in regulating steady-state miRNA levels. We also successfully generated lentiviral systems to express the BHRF1 miRNAs and developed reporter constructs to measure BHRF1 miRNA-dependent repression \(in\) \(vivo\). While attempts to identify BHRF1 miRNA-induced changes on the BL transcriptome were inconclusive, our data suggest that the BHRF1 miRNAs are insufficient to affect BL cell growth and cell survival.
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Boyce, Andrew John. "Epstein-Barr virus genome loss from endemic Burkitt lymphoma and its effect on cell phenotype." Thesis, University of Birmingham, 2009. http://etheses.bham.ac.uk//id/eprint/4731/.

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Epstein-Barr virus (EBV), a B cell growth-transforming human herpesvirus, is linked to several human malignancies, in particular endemic Burkitt lymphoma (eBL). Though always present in this tumour, EBV‟s role remains unclear since, in most cases, viral gene expression is restricted to the viral genome maintenance protein, EBNA1 and the non-coding EBERs, BARTs and BART-derived microRNAs (Latency I infection). This study first asked whether EBV was required for continued BL growth in vitro by screening a panel of Latency I BL cell lines for EBV-loss clones. Such clones were isolated from 5/12 BL lines tested. In each case these cells proved to be more sensitive to apoptosis than their EBV-positive counterparts, an effect which could be reversed by reinfection with a recombinant EBV. Cellular gene expression profiling of EBV-positive and EBV-loss clones on four BL backgrounds revealed transcriptional differences but none that were common to all four tumours. To examine the responsible viral function, a doxycycline-regulated vector was used to express EBNA1 and EBERs at physiologic and supra-physiologic levels in EBV-loss cells on two BL backgrounds. Contrary to previous reports, neither EBNA1 nor EBERs conferred apoptosis resistance, a result which implicates the BARTs or BART-derived microRNAs as novel anti-apoptotic effectors.
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Leung, Yuen-ying, and 梁婉瑩. "Effects of histone deacetylase and proteasome inhibitors on Epstein-barr virus-positive Burkitt lymphoma and lymphoblastoid cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/207474.

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Burkitt lymphoma (BL) was the first tumor found to be strongly associated with Epstein-Barr virus (EBV). Almost 100% of the lymphoma cells are cycling, necessitating dose- and time-intense multi-agent chemotherapy regimens to achieve a cure of the disease. Whilst standard risk BL can be cured with this approach, high risk BL with leukaemic and CNS disease has significantly inferior survival. The intensive chemotherapy regimen causes considerable toxicity to the patients and relapse of BL is largely incurable. Thus, novel therapeutic approaches for high risk and relapsed BL are needed. Histone deacetylase inhibitors (HDACis) represent a novel class of drugs with potent anti-cancer effect in a wide range of malignancies. In the first part of this study, we tested HDACis of different classes for their ability to inhibit cell proliferation and activate the lytic cycle of EBV in a panel of EBV-positive BL cells of different latent viral gene expression patterns (type I, Wp-restricted and type III latency with highly restrictive, partial and full spectrum of EBV latent gene expression, respectively). Different HDACis could inhibit proliferation of EBV-positive BL cells in a time- and dose-dependent manner but only weakly activate the viral lytic cycle indicating that the drugs’ cytotoxic effect is independent of the EBV lytic cycle. Of note, BL cells of Wp-restricted or type III latency were more resistant to killing by HDACis than those of latency I, suggesting a possible link between relative resistance to the drug and expression of the latent viral genes. Bortezomib, a proteasome inhibitor, may have synergistic action with HDACis on lymphoid malignancies. We hypothesized that Bortezomib could potentiate the killing of EBV-positive BL cells by HDACis. In the second part, we tested the effect of combination of a FDA-approved HDACi, suberoylanilide hydroxamic acid (SAHA) and Bortezomib in the same panel of BL cells and also EBV-transformed lymphoblastoid cell lines (LCLs) which represent an in-vitro model of EBV-associated post-transplant lymphoproliferative disorder (PTLD). Interestingly, combination of SAHA and Bortezomib significantly enhanced the killing of BL cells of Wp-restricted or type III latency. Furthermore, the resistance to either SAHA or Bortezomib alone in contrast to synergistic killing by the combination of the two drugs could be observed in LCLs which also have the type III latency pattern. Compared with either drug alone, combination of SAHA and Bortezomib induced enhanced apoptosis in Wp-restricetd BL cells and LCLs as shown by the increase in the percentage of annexin V-positive cell, sub-G1 population and the proteolytic cleavage of apoptotic markers including PARP, caspase-3 and -9. The drug combination hyper-acetylated histone and induced cell cycle arrest. Combination of SAHA and Bortezomib was further shown to suppress the growth of BL xenograft in nude mice. In conclusion, our data indicated that expression of partial or full spectrum of viral latent genes in EBV-positive BL cells of Wp-restricted or type III latency confers resistance of the tumor cells to cytotoxic effect of HDACis. Bortezomib could potentiate SAHA-induced apoptosis of both BL cells and LCLs and might overcome mechanism of drug resistance.
published_or_final_version
Paediatrics and Adolescent Medicine
Master
Master of Philosophy
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Rao, Sieta Padmaja. "Zebularine reactivates silenced E-cadherin but unlike 5-Azacytidine does not induce switching from latent to lytic Epstein-Barr virus infection in Burkitt's lymphoma Akata cells /." [S.l.] : [s.n.], 2008. http://opac.nebis.ch/cgi-bin/showAbstract.pl?sys=000253262.

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Imreh, Marta P. "Modulation of cellular and viral functions in Epstein-Barr virus infected cells /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-171-3.

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Cherdoud-Chelouah, Sonia. "Rôle fonctionnel de la protéine de latence EBNA-LP exprimée dans les cellules de lymphome de Burkitt infectées par la souche P3HR1 du virus d’Epstein-Barr." Thesis, Paris 11, 2012. http://www.theses.fr/2012PA11T023.

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Notre équipe à montré que les cellules de lymphome de Burkitt (LB) infectées par le variant P3HR1 du virus d’Epstein Barr (EBV) sont plus résistantes à l’apoptose que les cellules de LB EBV(-) ou infectées par la souche sauvage. Le variant P3HR1 porte une délétion de son génome à l’origine de l’expression d’une forme tronquée d’EBNA-LP (EBNA-LPt). Nous avons étudié le rôle fonctionnel d’EBNA-LPt dans les cellules de LB infectées par le variant P3HR1. Nous avons, dans un premier temps, identifié par une étude protéomique ses partenaires cellulaires et viraux. Nous avons ainsi confirmé l’interaction entre EBNA-LPt et la PP2A, déjà établie par notre équipe, et montré qu’elle forme également des complexes avec d’autres protéines impliquées dans de nombreux processus cellulaires, notamment dans l’apoptose et dans la régulation transcriptionnelle. Nous avons ensuite, par une étude du transcriptome, montré le rôle de régulateur transcriptionnel des deux formes d’EBNA-LP exprimées de façon stable dans les cellules de LB EBV(-). En effet, nous avons montré que les deux formes d’EBNA-LP sont capables de réguler l’expression des gènes cellulaires indépendamment du contexte viral. Certains de ces gènes sont communs aux deux formes d’EBNA-LP, d’autres sont spécifiques de chaque forme. Nous avons constaté que le domaine Y1Y2 est indispensable à la surexpression, par EBNA-LP, du gène cellulaire codant pour la protéine ID1 qui est impliquée dans la stabilisation de la LMP1 et dans l’immortalisation cellulaire. Nous avons également remarqué que certains gènes sont régulés de la même façon en présence d’EBNA-LP seule ou dans un contexte viral complet. Enfin et pour mieux comprendre les mécanismes de résistance à l’apoptose dans les cellules de LB infectées par la souche P3HR1, nous avons élargi notre étude du transcriptome à des cellules traitées ou non par un inducteur de l’apoptose, la cycloheximide. Nos résultats préliminaires montrent que les voies de signalisation des récepteurs au TNF (TNFR1 et 2) sont rapidement et fortement induites dans les cellules sensibles alors qu’elles sont faiblement et tardivement induites dans les cellules résistantes. Cette étude montre également que la voie de signalisation JNK est probablement activée de façon très précoce dans les cellules sensibles contrairement aux cellules résistantes
Our group has previously shown that Burkitt’s lymphoma (BL) cells infected by the P3HR1 variant of Epstein-Barr virus (EBV) are more resistant to apoptotsis than EBV (-) BL cells or cells infected by wild-type EBV. The genome of the P3HR1 variant carries a deletion responsible for the expression of a truncated form of EBNA-LP (tEBNA-LP). We studied the functional role of tEBNA-LP in BL cells infected by the P3HR1 variant. A proteomic study allow us to identify cellular and viral partners of tEBNA-LP. These results confirmed the interaction between tEBNA-LP and PP2A, already established by our group, and showed that tEBNA-LP can form complexes with other proteins involved in many cellular processes including apoptosis and regulation of transcription. We have then demonstrated by a transcriptomic study, the transcriptional regulatory role of both forms of EBNA-LP stably expressed in EBV(-) BL cell lines. Indeed, we showed that both forms of EBNA-LP can regulate the expression of cellular genes independently of viral context. Some of these genes are common to both forms of EBNA-LP, others are specific to each form. We found that Y1Y2 domaine of EBNA-LP is essential to overexpression of the cellular gene encoding ID1 protein which is involved in LMP1 stabilization and cellular mmortalization. We also noted that some genes are similarly regulated in the presence of EBNA-LP alone or in the presence of viral genome. Finally, to better undertand the mecanisms of resistance to apoptosis in BL cell lines infected by the P3HR1 variant we extended our transcriptomic analysis to cell lines treated or not with an apoptosis inducer, cycloheximide. Our preliminary results show that TNF receptors signaling pathways (TNFR1 and 2) are rapidly and strongly induced in sensitive cell lines while being weakly and belatedly induced in the resistant cell lines. This study also shows that the JNK signaling pathway is probably activated very early in the sensitive cells in contrast to resistant cell lines
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Books on the topic "Epstein-Barr Virus Burkitt's Lymphoma"

1

ed, Epstein M. A., and Achong, B. G., 1928- ed., eds. The Epstein-Barr virus: Recent advances. New York: Wiley, 1986.

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A, Epstein M., and Achong B. G. 1928-, eds. The Epstein-Barr virus: Recent advances. New York: J. Wiley, 1986.

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Lindholm, Carita. Contribution of Epstein-Barr virus genes to Burkitt's lymphoma phenotype. Birmingham: University of Birmingham, 1989.

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Bianca, Leonardo, ed. A holistic protocol for the immune system: HIV/ARC/AIDS, candidiasis, Epstein-Barr, herpes, and other opportunistic infections. Palm Springs, CA: Tree of Life Publications, 1989.

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M. A. Epstein (Other Contributor) and B. G. Achong (Other Contributor), eds. The Epstein-Barr virus: Recent advances (A Wiley medical publication). J. Wiley, 1986.

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Keane, Maccon M. Epstein-Barr virus and lymphocyte morphology in lymphoma. 1995.

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MacMahon, Eithne Mary Edana. Epstein-Barr virus and AIDS-related primary CNS lymphoma. 1996.

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Gregory, Scott J. A Holistic Protocol for the Immune System: HIV/ARC/AIDS/Candidiasis/Epstein-Barr/Herpes and other opportunistic infections. 6th ed. Progressive Press, 1995.

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Scott, Gregory J., and Scott Gregory. A Holistic Protocol for the Immune System: HIV/ARC/AIDS, Candidiasis, Epstein-Barr, Herpes, and Other Opportunistic Infections. Progressive Press, 1991.

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(Contributor), WHO, ed. Epstein-Barr Virus and Kaposi's Sarcoma Herpes Virus/Human Herpesvirus 8 (IARC Monographs on Eval of Carcinogenic Risk to Humans). World Health Organisation, 1997.

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Book chapters on the topic "Epstein-Barr Virus Burkitt's Lymphoma"

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Banerjee, Shuvomoy, Hem Chandra Jha, Qiliang Cai, and Erle S. Robertson. "Epstein–Barr Virus and Burkitt’s Lymphoma." In Burkitt’s Lymphoma, 175–209. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4313-1_10.

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de Thé, Guy. "Epstein-Barr Virus and Burkitt’s Lymphoma." In Infectious Causes of Cancer, 77–92. Totowa, NJ: Humana Press, 2000. http://dx.doi.org/10.1007/978-1-59259-024-7_5.

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Wiels, J., E. H. Holmes, N. Cochran, S. I. Hakomori, and T. Tursz. "Mechanisms of Expression of a Burkitt Lymphoma-Associated Antigen (Globotriaosylceramide) in Burkitt Lymphoma and Lymphoblastoid Cell Lines." In Epstein-Barr Virus and Associated Diseases, 588–99. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2625-0_55.

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Takada, K. "Role of Epstein-Barr Virus in Burkitt’s Lymphoma." In Current Topics in Microbiology and Immunology, 141–51. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-642-56515-1_9.

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Itakura, Hideyo, and Kan Toriyama. "Geopathological Coincidence of Burkitt’s Lymphoma and Endemic Kaposi’s Sarcoma in Western Kenya." In Epstein-Barr Virus and Human Disease, 453–54. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4590-2_97.

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Magrath, Ian T. "Clinical and Pathobiological Features of Burkitt’s Lymphoma and their Relevance to Treatment." In Epstein-Barr Virus and Associated Diseases, 631–43. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2625-0_58.

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Nkrumah, F. K., G. Pizza, D. Viza, J. Neequaye, C. De Vinci, and P. H. Levine. "EBV-Specific Transfer Factor in the Treatment Of African Burkitt’s Lymphoma: A Pilot Study." In Epstein-Barr Virus and Associated Diseases, 666–72. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2625-0_61.

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Rooney, Cliona M., M. Brimmell, G. Allan, P. Farrell, and M. Buschle. "EBNA-2 Influences Promoter Function in Burkitt Lymphoma Cells." In Epstein-Barr Virus and Human Disease • 1990, 65–67. Totowa, NJ: Humana Press, 1991. http://dx.doi.org/10.1007/978-1-4612-0405-3_9.

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Neequaye, J., G. Pizza, D. Viza, C. de Vinci, P. H. Levine, and F. K. Nkrumah. "Ebv-Specific Transfer Factor in the Treatment of Abdominal Burkitt’s Lymphoma in Ghana, West Africa." In Epstein-Barr Virus and Human Disease, 503–7. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4590-2_107.

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Crawford, D. H., and M. G. Doyle. "Stimulation of EB Virus-Specific Helper T Cells by Burkitt’s Lymphoma and Lymphblastoid Cell Lines." In Epstein-Barr Virus and Human Disease, 393–94. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4590-2_83.

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Conference papers on the topic "Epstein-Barr Virus Burkitt's Lymphoma"

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El-Mallawany, Nader Kim, Janet Ayello, Nancy Day, Carmella Van de Ven, Matthew Benson, Kevin Conlon, Damian Fermin, et al. "Abstract 1199: Global proteomic evaluation of the relationship between Epstein-Barr virus (EBV) and c-myc deregulation in endemic versus sporadic Burkitt lymphoma (BL)." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1199.

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Rasim, K., S. Suttner, M. Vogelhuber, W. Herr, A. Gessner, B. Seelbach-Goebel, and E. Reuschel. "Epstein-Barr-Virus (EBV)-assoziiertes Burkitt-Lymphom in der Schwangerschaft." In Kongressabstracts zur Tagung 2020 der Deutschen Gesellschaft für Gynäkologie und Geburtshilfe (DGGG). © 2020. Thieme. All rights reserved., 2020. http://dx.doi.org/10.1055/s-0040-1718347.

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Rouce, Rayne H., Serena K. Perna, Gayatri Vyas, Sandhya Sharma, Natalia Lapteva, Ann Leen, Cliona M. Rooney, and Helen E. Heslop. "Abstract B17: Banked Epstein-Barr virus specific T-cells for treatment of EBV+ lymphoma." In Abstracts: AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/2326-6074.tumimm14-b17.

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Pereira, V., S. Boudjemaa, C. Besson, P. Simon, T. Leblanc, and J. Landman-Parker. "Epstein Barr Virus in children and adolescents with classical Hodgkin Lymphoma: analysis of a cohort of 299 patients." In ISCAYAHL 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1701828.

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Jain, Nitesh K., Hasnain S. Bawaadam, Aman Sethi, Ashok Fulambarker, Peter Morawiecki, and Rashid Nadeem. "Epstein-Barr Virus Associated Diffuse Large B-Cell Lymphoma Presenting As A Lung Mass In An Immunocompetent Patient." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4393.

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Bolanos, Rachel, Amie Hwang, Jose Aparicio, Chun Chao, Naba Qurashi, Christopher Flowers, Sheeja Pullarkat, et al. "Abstract B092: Epstein-Barr virus prevalence in classical Hodgkin lymphoma tumors by race/ethnicity in a multiethnic U.S. population." In Abstracts: Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; September 20-23, 2019; San Francisco, CA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7755.disp19-b092.

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Chao, Chun R., Donald Abrams, Michael J. Silverberg, Reina Haque, Hongbin D. Zha, Otoniel Martinez-Maza, Michelle McGuire, et al. "Abstract 4643: Epstein-Barr virus infection (EBV) and expression of B-cell oncogenic markers in HIV+ diffuse large B-cell lymphoma (DLBCL)." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-4643.

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Vilimas, Tomas, Gloryvee Rivera, Brandie Fullmer, Wiem Lassoued, Lindsay Dutko, William Walsh, Amanda Peach, et al. "Abstract 1038: Xenograft-associated B cell lymphoproliferative disease as a surrogate model to study Epstein-Barr virus (EBV) driven lymphoma of the elderly." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-1038.

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Bolanos, Rachel, Amie Hwang, Chun Chao, Christopher Flowers, Sheeja Pullarkat, Jose Aparicio, Sophia Wang, et al. "Abstract 5053: Epstein-Barr virus prevalence in classical Hodgkin lymphoma tumors is explained by histologic subtype, not race/ethnicity in a multiethnic US population." 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.sabcs18-5053.

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Bolanos, Rachel, Amie Hwang, Chun Chao, Christopher Flowers, Sheeja Pullarkat, Jose Aparicio, Sophia Wang, et al. "Abstract 5053: Epstein-Barr virus prevalence in classical Hodgkin lymphoma tumors is explained by histologic subtype, not race/ethnicity in a multiethnic US population." 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.am2019-5053.

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