Relevant bibliographies by topics / Endemic Burkitt lymphoma

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

Academic literature on the topic 'Endemic Burkitt lymphoma'

Author: Grafiati
Published: 4 June 2021
Last updated: 18 February 2022

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Journal articles on the topic "Endemic Burkitt lymphoma"

1

Mannucci, Susanna, Anna Luzzi, Alessandro Carugi, Alessandro Gozzetti, Stefano Lazzi, Valeria Malagnino, Monique Simmonds, et al. "EBV Reactivation and Chromosomal Polysomies:Euphorbia tirucallias a Possible Cofactor in Endemic Burkitt Lymphoma." Advances in Hematology 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/149780.

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Burkitt lymphoma is endemic in the Equatorial Belt of Africa, its molecular hallmark is an activated,MYCgene mostly due to a chromosomal translocation. Especially in its endemic clinical variant, Burkitt lymphoma is associated with the oncogenic Epstein-Barr virus (EBV), and holoendemic malaria acts as an amplifier. Environmental factors may also cooperate in Burkitt lymphomagenesis in the endemic regions, such as plants used as traditional herbal remedies.Euphorbia tirucalli, a plant known to possess EBV-activating substances, has a similar geographical distribution to endemic Burkitt’s Lymphoma and is used as a hedge, herbal remedy and toy in the Lymphoma BeltI. In this study we aimed at determining if exposure toEuphorbia tirucallicould contribute to lymphomagenesis, and at which extent. Lymphoblastoid and cord blood-derived cell lines were treated with plant extracts, and the expression of EBV-coded proteins was checked, to assess EBV reactivation. The occurrence of chromosomal translocations was then investigated by FISH. Our preliminary results suggest thatE. tirucalliis able to reactivate EBV and determine chromosomal alterations, which leads to c-MYC altered expression. The existence of genomic alterations might determine the accumulation of further genetic alteration, which could eventually lead to a transformed phenotype.
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Boffano, Paolo, Cesare Gallesio, Rodolfo Benech, and Sid Berrone. "Bilateral Oral Non-Endemic Burkitt Lymphoma." Journal of Craniofacial Surgery 24, no. 3 (May 2013): 1057–58. http://dx.doi.org/10.1097/scs.0b013e31828f268f.

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Blum, Kristie A., Gerard Lozanski, and John C. Byrd. "Adult Burkitt leukemia and lymphoma." Blood 104, no. 10 (November 15, 2004): 3009–20. http://dx.doi.org/10.1182/blood-2004-02-0405.

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Abstract The World Health Organization Classification of Lymphoid Neoplasms identifies Burkitt lymphoma/leukemia as a highly aggressive mature B-cell neoplasm consisting of endemic, sporadic, and immunodeficiency-associated variants. These subtypes share many morphologic and immunophenotypic features, but differences exist in their clinical and geographic presentations. All of these subtypes possess chromosomal rearrangements of the c-myc oncogene, the genetic hallmark of Burkitt lymphoma that contributes to lymphomagenesis through alterations in cell cycle regulation, cellular differentiation, apoptosis, cellular adhesion, and metabolism. Brief-duration, high-intensity chemotherapy regimens containing aggressive central nervous system prophylaxis have had remarkable success in the treatment of this disease, with complete remission rates of 75% to 90% and overall survivals reaching 50% to 70% in adults. Although Burkitt lymphoma cells are extremely chemosensitive, biologically targeted therapies should be developed because current treatment options are suboptimal for patients with poor prognostic features or in the setting of relapsed disease.
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Tang, Weihua, Paula Harmon, Margaret L. Gulley, Charles Mwansambo, Peter N. Kazembe, Francis Martinson, Clifford Wokocha, et al. "Viral Response to Chemotherapy in Endemic Burkitt Lymphoma." Clinical Cancer Research 16, no. 7 (March 16, 2010): 2055–64. http://dx.doi.org/10.1158/1078-0432.ccr-09-2424.

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Velavan, Thirumalaisamy P. "Epstein-Barr virus, malaria and endemic Burkitt lymphoma." EBioMedicine 39 (January 2019): 13–14. http://dx.doi.org/10.1016/j.ebiom.2018.12.041.

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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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Abate, Francesco, Maria Raffaella Ambrosio, Lucia Mundo, Maria Antonella Laginestra, Fabio Fuligni, Maura Rossi, Sakellarios Zairis, et al. "Distinct Viral and Mutational Spectrum of Endemic Burkitt Lymphoma." PLOS Pathogens 11, no. 10 (October 15, 2015): e1005158. http://dx.doi.org/10.1371/journal.ppat.1005158.

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Denburg, Avram. "Cost effectiveness of treating endemic Burkitt lymphoma in Uganda." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e18339-e18339. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e18339.

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e18339 Background: Despite high cure rates achieved in high-income countries, outcomes for children with Burkitt lymphoma (BL) in most low- and middle-income countries (LMICs) remain suboptimal. Perceptions of high cost and resource intensity remain political barriers to the prioritization of BL and other childhood cancer treatment programs in many LMIC health systems. Little to no knowledge exists of the actual cost and cost-effectiveness of treating paediatric cancers in LMICs. To improve outcomes for children with BL, the Uganda Cancer Institute implemented a comprehensive BL treatment program in 2012. Drawing on centralized patient-level data, we undertook an economic evaluation of the program to ascertain the cost-effectiveness of BL therapy in a specific LIC setting. Methods: We compared the treatment of BL (local standard) to usual care (no care), in a cohort of 215 patients treated between 2012 and 2015. Costs included direct, indirect healthcare, and indirect patient costs. Our primary measure of effectivenesswas overall survival (OS). Patient outcomes were determined through electronic chart abstraction. The cost per DALY averted was calculated using WHO-CHOICE methodology and compared to standard definitions of cost-effectiveness. Results: The 2-year OS with treatment was 53% (95% CI, 43% to 62%). Nine percent of patients abandoned therapy. The cost per DALY averted in the treatment group was US$78. Cumulative estimate of national DALYs averted through treatment was 11,046 years, and the total national cost of treatment was US$755,216. The ratio of cost per DALY averted to per capita gross domestic product (GDP) was 0.12, reflecting a very cost-effective intervention. Conclusions: This study demonstrates that treating BL with locally tailored protocols is very cost-effective relative to per capita GDP in Uganda. Studies of this kind will furnish crucial evidence to assist policymakers prioritize the allocation of LMIC health system resources among NCDs, including childhood cancer.
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Gerhard, Daniela S., Bruno Grande, Nicholas Griner, Corey Casper, Sarah E. Gerdts, Abraham Omoding, Jackson Orem, et al. "Burkitt Lymphoma Genome Sequencing Project (BLGSP): Introduction." Blood 128, no. 22 (December 2, 2016): 1760. http://dx.doi.org/10.1182/blood.v128.22.1760.1760.

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Abstract Introduction: Burkitt Lymphoma (BL) is an aggressive B-cell lymphoma with a translocation involving MYC and immunoglobulin(Ig) loci. It is most common in children, but also affects adults, and occurs in sporadic, endemic and HIV-associated forms. The Epstein-Barr virus (EBV)-associated endemic subtype is the most common pediatric cancer in equatorial Africa, but also occurs in other parts of the world, for example in the rain forest of Brazil. Intensive chemotherapy is effective, but the associated toxicity requires supportive care that is not readily available in resource-poor regions. Previously published molecular characterization of small numbers of tumors indicated that the mutation profiles of endemic and sporadic cases are similar, but not identical. One goal of the BLGSP is to conduct comprehensive molecular characterization of BL by sequencing DNA and RNA from a large BL cohort - including endemic, sporadic, pediatric and adult cases - in order to define the genetic and phenotypic features that drive these cancers. These data will be analyzed with an intent toward developing new therapeutic strategies that can be deployed worldwide. Methods: The goal is to collect 160 BL cases, of which 50% will be endemic, 38% sporadic (pediatric and adult) and 12% from HIV+ patients. For the discovery phase, each tumor requires case-matching normal DNA as well as treatment, outcome and other clinical information. The optimal source of tumor DNA and RNA is from frozen tissue with at least 50% tumor nuclei, but FFPE immobilization is also accepted. Accrual locations include Africa, Brazil, Europe and the US. The BLGSP has developed extensive standard operating procedures for tissue collection, pathology review and tissue processing to reduce the variation associated with these parameters in the interpretation of the results (see https://ocg.cancer.gov/programs/cgci/projects/burkitt-lymphoma). The project also established procedures that allow sharing of all clinical and sample information through the National Cancer Institute Genomic Data Commons (https://gdc.cancer.gov). Molecular characterization includes whole genome sequencing of tumor and normal DNA (80X and 40X coverage, respectively), RNA-sequencing (RNA-seq) and micro-RNA sequencing. These data will enable the BLGSP to identify chromosomal rearrangements, chromosomal copy number alternations, somatic mutations (single nucleotide, insertions, deletions), viral insertions, expression signatures, viral expressions and miRNA regulation of transcripts. Results: To date we have accrued 80 cases of BL of which 75% passed diagnostic pathology review. There was an additional 25% attrition at the tissue processing stage, either due to low quality nucleic acids or low percent tumor nuclei. We have completed sequencing for 45 cases, all but one of which have a MYC translocation involving one of the 3 Ig loci; one case has a MYC rearrangement by FISH analysis that is being characterized further. We have identified recurrent mutations in ID3, DDX3X, ARID1A, FOXO1, TP53, SMARCA4 and other genes. Most mutations are supported by the RNA-seq data, which is also useful in defining the pattern of EBV genome transcription. Preliminary unsupervised hierarchical clustering and principal component analysis of gene expression data defined sample clusters that do not correspond to mutation status or EBV infection, warranting further investigation. Some genes accumulated somatic mutations in a BL subtype-specific fashion. Discussion: BLGSP is an ongoing international collaborative project that will provide a comprehensive molecular portrait of BL subtypes when completed, with the potential to suggest new molecular targets for therapy that can eventually lead to effective treatments that are less toxic than the current regimens. Disclosures Casper: Janssen: Consultancy, Research Funding; Roche: Consultancy, Other: Travel, Accommodation, Expenses; TempTime: Consultancy, Other: Travel, Accommodation, Expenses; Up to Date: Patents & Royalties; GSK: Other: Travel, Accommodation, Expenses. Abramson:Kite Pharma: Consultancy; Abbvie: Consultancy; Seattle Genetics: Consultancy; Gilead: Consultancy. Noy:Pharmacyclics, LLC, an AbbVie Company: Other: travel, accommodations, expenses, Research Funding.
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O'Callaghan-Gordo, Cristina, Carlota Dobaño, Cesaltina Lorenzoni, Delphine Casabonne, Quique Bassat, Manolis Kogevinas, Clesio Zaqueu, et al. "Incidence of Endemic Burkitt Lymphoma in Three Regions of Mozambique." American Journal of Tropical Medicine and Hygiene 95, no. 6 (December 7, 2016): 1459–62. http://dx.doi.org/10.4269/ajtmh.16-0424.

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Dissertations / Theses on the topic "Endemic Burkitt lymphoma"

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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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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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Abstract:
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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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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Schlau, Hannah Naomi [Verfasser], and Claudia [Akademischer Betreuer] Rössig. "Eosinophilia in children with endemic Burkitt lymphoma in Malawi as a prognostic factor for survival / Hannah Naomi Schlau ; Betreuer: Claudia Rössig." Münster : Universitäts- und Landesbibliothek Münster, 2014. http://d-nb.info/1138281093/34.

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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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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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Books on the topic "Endemic Burkitt lymphoma"

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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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Book chapters on the topic "Endemic Burkitt lymphoma"

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Rochford, Rosemary, and Amolo S. Asito. "The Many Roles of Malaria in the Etiology of Endemic Burkitt Lymphoma." In Burkitt’s Lymphoma, 241–49. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4313-1_13.

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Molyneux, Elizabeth, Trijn Israels, and Thomas Walwyn. "Endemic Burkitt’s Lymphoma." In Burkitt’s Lymphoma, 95–119. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4313-1_6.

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Otieno, Mwanda Walter. "Non-endemic Burkitt’s Lymphoma." In Burkitt’s Lymphoma, 121–30. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-4313-1_7.

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Servitzoglou, Marina K., Helen Dana, Theodore A. Pipikos, and Georgia Ch Papaioannou. "Burkitt and Burkitt-Like Lymphomas in Children and Adolescents (Sporadic or Endemic B Mature): Introduction." In PET/CT in Lymphomas, 313–25. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-27380-8_20.

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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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Haluska, F. G., G. Russo, M. Andreeff, and C. M. Croce. "Molecular Analysis of an AIDS-Associated Burkitt’s Lymphoma: Near-Identity with Endemic Cases." In Current Topics in Microbiology and Immunology, 75–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74006-0_11.

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Rooney, C. M., M. Rowe, A. B. Rickinson, G. M. Lenoir, D. M. Moss, and M. A. Epstein. "Endemic and Sporadic Cases of Epstein-Barr Virus-Positive Burkitt’s Lymphoma: Immunological Characterization of Derived Cell Lines." In Modern Trends in Human Leukemia VI New Results in Clinical and Biological Research Including Pediatric Oncology, 308–11. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-70385-0_64.

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Lanfrancone, Luisa, Pier-Giuseppe Pelicci, and Riccardo Dalla-Favera. "Structure and Expression of Translocated c-myc Oncogenes: Specific Differences in Endemic, Sporadic and AIDS-Associated Forms of Burkitt Lymphomas." In Current Topics in Microbiology and Immunology, 257–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71562-4_39.

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Conference papers on the topic "Endemic Burkitt lymphoma"

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Forconi, Catherine S., Cliff Oduor, John M. Ong’echa, Jeff Bailey, and Ann M. Moormann. "Abstract A60: Transcriptional profile of CD56negCD16pos Natural Killer cells within endemic Burkitt lymphoma." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-a60.

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Laginestra, Maria Antonella, Francesco Abate, Maryam Etebari, Giulia D. Falco, Fabio Fuligni, Maura Rossi, Sakellarios Zairis, et al. "Abstract 5173: Identification of single-nucleotide variants by high-throughput RNA sequencing in endemic Burkitt Lymphoma." 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.am2014-5173.

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Saikumar-Lakshmi, Priya, Cliff Oduor, Catherine Forconi, Patrick Marsh, John Michael Ong’echa, Jeffrey Bailey, and Ann Moormann. "Abstract A18: Characterization of checkpoint inhibitors in the tumor microenvironment (TME) and peripheral blood in endemic Burkitt Lymphoma." In Abstracts: AACR Special Conference on the Advances in Pediatric Cancer Research; September 17-20, 2019; Montreal, QC, Canada. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.pedca19-a18.

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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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Mbulaiteye, Sam M. "Abstract PL01-03: Molecular patterns of endemic, sporadic, and AIDS-related Burkitt's lymphoma: Clues to distinct biology of subtypes." In Abstracts: AACR International Conference on the Science of Cancer Health Disparities‐‐ Sep 18-Sep 21, 2011; Washington, DC. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1055-9965.disp-11-pl01-03.

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You might also be interested in the extended bibliographies on the topic 'Endemic Burkitt lymphoma' for particular source types:
Journal articles
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