Log in

Relevant bibliographies by topics / Endemic Burkitt lymphoma / Journal articles

To see the other types of publications on this topic, follow the link: Endemic Burkitt lymphoma.

Journal articles on the topic 'Endemic Burkitt lymphoma'

Author: Grafiati

Published: 4 June 2021

Last updated: 18 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Endemic Burkitt lymphoma.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

4

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

7

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

10

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Mbulaiteye, Sam. "G-102 Endemic Burkitt lymphoma and infectious agents in cancer." JAIDS Journal of Acquired Immune Deficiency Syndromes 77 (April 2018): 44. http://dx.doi.org/10.1097/01.qai.0000532615.95518.91.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Marjerrison, S., C. V. Fernandez, V. E. Price, E. Njume, and P. Hesseling. "The use of ultrasound in endemic Burkitt lymphoma in Cameroon." Pediatric Blood & Cancer 58, no. 3 (March 2, 2011): 352–55. http://dx.doi.org/10.1002/pbc.23050.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

&NA;. "The Use of Ultrasound in Endemic Burkitt Lymphoma in Cameroon." Ultrasound Quarterly 28, no. 3 (September 2012): 172–73. http://dx.doi.org/10.1097/01.ruq.0000419396.93907.3b.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Campidelli, Cristina, Anna Gazzola, Francesca Vitone, Stefano A. Pileri, and Lynnette Tumwine. "HIV infection and c-MYC status in endemic Burkitt lymphoma." Human Pathology 39, no. 9 (September 2008): 1408–9. http://dx.doi.org/10.1016/j.humpath.2008.06.002.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Jacobson, Caron, and Ann LaCasce. "How I treat Burkitt lymphoma in adults." Blood 124, no. 19 (November 6, 2014): 2913–20. http://dx.doi.org/10.1182/blood-2014-06-538504.

Full text

Abstract:

Abstract Burkitt lymphoma (BL) is an aggressive B-cell non-Hodgkin lymphoma that is almost uniformly associated with translocations involving the gene for MYC on chromosome 8. The 3 subtypes of BL, endemic, sporadic, and immunodeficiency-associated, differ from epidemiologic and clinical perspectives but may be genetically similar. Prompt administration of multiagent immunochemotherapy regimens is associated with favorable outcomes for the majority of patients. Survival is inferior in older patients, likely reflecting increased therapy-related toxicity, possibly resulting in decreased treatment intensity. Central nervous system prophylaxis, tumor lysis prevention and treatment, and management of infectious complications from myelosuppressive regimens are critical. Prognosis of refractory or relapsed disease is poor and patients are best treated on clinical trials when available.

APA, Harvard, Vancouver, ISO, and other styles

16

Piccaluga, Pier Paolo, Giulia De Falco, Manjunath Kustagi, Anna Gazzola, Claudio Agostinelli, Claudio Tripodo, Eleonora Leucci, et al. "Gene expression analysis uncovers similarity and differences among Burkitt lymphoma subtypes." Blood 117, no. 13 (March 31, 2011): 3596–608. http://dx.doi.org/10.1182/blood-2010-08-301556.

Full text

Abstract:

Abstract Burkitt lymphoma (BL) is classified into 3 clinical subsets: endemic, sporadic, and immunodeficiency-associated BL. So far, possible differences in their gene expression profiles (GEPs) have not been investigated. We studied GEPs of BL subtypes, other B-cell lymphomas, and B lymphocytes; first, we found that BL is a unique molecular entity, distinct from other B-cell malignancies. Indeed, by unsupervised analysis all BLs clearly clustered apart of other lymphomas. Second, we found that BL subtypes presented slight differences in GEPs. Particularly, they differed for genes involved in cell cycle control, B-cell receptor signaling, and tumor necrosis factor/nuclear factor κB pathways. Notably, by reverse engineering, we found that endemic and sporadic BLs diverged for genes dependent on RBL2 activity. Furthermore, we found that all BLs were intimately related to germinal center cells, differing from them for molecules involved in cell proliferation, immune response, and signal transduction. Finally, to validate GEP, we applied immunohistochemistry to a large panel of cases and showed that RBL2 can cooperate with MYC in inducing a neoplastic phenotype in vitro and in vivo. In conclusion, our study provided substantial insights on the pathobiology of BLs, by offering novel evidences that may be relevant for its classification and possibly future treatment.

APA, Harvard, Vancouver, ISO, and other styles

17

Molyneux, Elizabeth, Ed Schwalbe, George Chagaluka, Kondwani Banda, Trijn Israels, Sarita Depani, Kirstin Mittermayer-Vassallo, et al. "The use of anthracyclines in the treatment of endemic Burkitt lymphoma." British Journal of Haematology 177, no. 6 (November 28, 2016): 984–90. http://dx.doi.org/10.1111/bjh.14440.

Full text

APA, Harvard, Vancouver, ISO, and other styles

18

Coffey, David G., Katharine A. Lombardo, Andrea M. H. Towlerton, Sarah E. Gerdts, Corey Casper, Jackson Orem, and Edus H. Warren. "Comparative Analysis of Endemic and Sporadic Burkitt Lymphoma By RNA Sequencing." Blood 126, no. 23 (December 3, 2015): 3896. http://dx.doi.org/10.1182/blood.v126.23.3896.3896.

Full text

Abstract:

Abstract Introduction: Burkitt lymphoma (BL) is an aggressive B-lineage non-Hodgkin lymphoma that has traditionally been classified into 3 subtypes: "endemic", "sporadic", and HIV-associated. The highest incidence of BL - prompting the "endemic" classification - is observed in children in sub-Saharan Africa, where the distribution of the disease is closely associated with that of P. falciparum malaria. The tumor cells in most cases of BL from sub-Saharan Africa are infected with Epstein Barr virus (EBV). In contrast, a minority of BL tumors from Europe and North America - which are commonly described as "sporadic" - are EBV positive. Although excellent outcomes have been observed for patients with BL treated with multi-agent chemotherapy in Europe and North America, the outcomes of BL patients in sub-Saharan Africa are suboptimal. We hypothesized that improved understanding of the molecular heterogeneity that exists within BL, particularly the molecular features that distinguish cases from sub-Saharan Africa from those from Europe/North America, will enable more effective treatment strategies that can readily be implemented in low-resources settings. Methods: Tumor biopsies were collected from 19 pediatric patients who presented to the Uganda Cancer Institute with maxillofacial tumors histologically confirmed to be BL. Total RNA was extracted and polyA-selected sequencing libraries were prepared. Paired-end, 50-base pair sequencing was performed on the Illumina HiSeq 2500 platform at a depth of 100 million reads per sample. A publicly available RNA sequencing dataset from 28 BL cases from Europe and North America that were previously analyzed by both microarray (NEJM 2006; 354[23]: 2431-2442) and RNA sequencing (Nature 2012; 490[7418]: 116-120) was analyzed in parallel for comparison. RNA sequencing on the 28 sporadic BL tumors was performed on polyA-selected sequencing libraries with paired-end, 108-base pair sequence reads generated on the Illumina HiSeq 2000 platform. The reads from all 47 BL tumors were aligned to the human and EBV (GenBank ID KC207813.1) genomes using the STAR aligner. Tumors were deemed EBV positive if the ratio of mapped viral reads to human reads exceeded 0.001%, since the EBV genome is 0.005% the size of the human genome. Normalization and differential expression analysis were performed on aligned reads using the DESeq2 R package. Somatic variants were identified by the Genome Analysis Tool Kit. Analysis of alterative splicing was performed with the SGSeq R package. Results: All of the Uganda BL cases but only 70% of the previously published European/North American cases were obtained from children less than 18 years; 61% and 87% were from male patients, respectively. One half of patients in both groups presented with Ann Arbor stage I or II disease, while the remainder presented with higher stage disease. The median survival in the 19 Ugandan patients was less than one year. Sequence reads from 15 (79%) of the Ugandan tumors and 4 (15%) of the European/North American tumors aligned to the EBV genome. Although BL is reported to express only latency type I EBV genes, expression of latency type I, II, and III genes was detected. Among the 4 tumors from Uganda that did not contain EBV-derived reads, 1 was from a child who was HIV-seropositive, while the others were from HIV-seronegative patients. Unsupervised hierarchical clustering and principal component analysis of all annotated genes failed to separate EBV positive and EBV negative tumors. Cluster analysis of the Ugandan tumors revealed no association with clinical variables. Ongoing analyses are being performed to identify associations between differentially expressed genes and somatic mutations and alternative splicing that may distinguish the tumor subtypes. Conclusions: While the terms "endemic" and "sporadic" have traditionally been used to classify BL, this nomenclature is archaic and does not accurately capture the underlying biology of the tumor subtypes. We performed a comparative whole transcriptome analysis of BL tumors from patients in Uganda to a dataset of BL tumors from patients in Europe/North America to identify features that distinguish the two cohorts. While cluster analysis failed to clearly separate tumors by their EBV or clinical status, ongoing analyses are being performed to identify alterations that may contribute to their distinct gene expression profiles. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

19

Lombardo, Katharine, Andrea M. H. Towlerton, Alicia Morales, Sarah Gerdts, Innocent Mutyaba, Abrahams Omoding, Jackson Orem, Erica Sessle, Corey Casper, and Edus Warren. "Next Generation Sequencing of B Cell Antigen Receptors Expressed in African Endemic Burkitt Lymphoma." Blood 124, no. 21 (December 6, 2014): 1687. http://dx.doi.org/10.1182/blood.v124.21.1687.1687.

Full text

Abstract:

Abstract The endemic form of Burkitt lymphoma (eBL), the most common pediatric cancer in sub-Saharan Africa, is the prototypic infection-related malignancy. Virtually 100% of eBL tumor cells carry Epstein-Barr virus (EBV) DNA, and eBL is closely ecologically associated with holoendemic P. falciparum malaria. The cell that undergoes transformation in eBL is an antigen-experienced B lymphocyte that has reached the germinal center and initiated the process of somatic hypermutation (SHM). The tumor cells in eBL express functional B-cell antigen receptors (BCRs), most commonly of the IgM isotype. The rearranged immunoglobulin heavy (IGH) and light (IGκ/λ) chain genes that encode Burkitt BCRs show evidence of SHM, demonstrating that eBL cells have uncoupled the processes of class switch recombination and SHM. Several lines of evidence suggest that BCR signaling pathways are active in eBL cells and that BCR signaling may contribute to the pathogenesis and maintenance of the disease. The uniquely rearranged BCR genes in eBL also represent a tumor-specific molecular signature that can be used to detect and quantitate eBL tumor cells in different tissue compartments. Therefore, Burkitt-associated BCRs have potential as both a disease biomarker and a therapeutic target. We utilized next-generation sequencing (NGS) to identify BCR gene rearrangements in eBL tumor cells obtained at the time of diagnosis from 22 patients, ages 4 to 12 (median: 7 years), with histologically confirmed Burkitt lymphoma who presented to the Uganda Cancer Institute in Kampala, Uganda. Thirteen of the patients were male and 9 were female; 3 patients were HIV-positive. Genomic DNA was isolated from cryopreserved tumor biopsies, and NGS of the IGH and IGκ/λ loci was performed to identify dominant BCR rearrangements in the eBL tumor cells. Sequence reads spanned a 130-nucleotide interval from the middle of framework region 3 (FR3) in the V gene segment to the 5’ region of the J gene segment. The reads captured the entirety of the CDR3 region. A single dominant IGH V-D-J rearrangement comprising >35% of all sequence reads was identified in 16 of the 22 samples. A single dominant IGκ or IGλ rearrangement was likewise seen in most cases with a single dominant IGH rearrangement. Two dominant but independent light chain rearrangements were seen in three eBL cases with a single dominant IGH rearrangement; whether both productive light chains are expressed at the RNA level is under active investigation. The utilization of IGH V- and J-gene segments in Burkitt-associated BCRs from this cohort of 22 patients was highly non-uniform, with utilization of IGHJ04-01 observed in 10 of the 16 cases with a single dominant IGH rearrangement. Analysis of BCR SHM patterns has revealed enrichment in CDRs as compared to FRs, suggesting antigen selection in eBL tumor cells, as well as a higher than expected rate of somatic mutations that create potential N-linked glycosylation sites. Deep sequencing of DNA extracted from peripheral blood mononuclear cells (PBMC) obtained at the time of diagnosis from 13 of the 22 patients identified sequences that were identical to the dominant IGH sequences observed in each patient’s tumor in 9 cases (69%). 5 of the 9 patients had early stage (Ziegler A) disease, demonstrating that Burkitt lymphoma cells commonly circulate in the blood. Current studies include sequencing of rearranged IGH genes present in PBMC after completion of primary therapy to determine if response is correlated with disappearance of the putative tumor-associated BCR sequences. Each eBL tumor sample is undergoing RNA analysis to confirm expression of the established dominant IGH and IGκ/λ rearrangements, as well as to determine the dominant BCR isotype. The complete light and heavy chain variable region sequences of the tumor-associated BCRs are being cloned by PCR with V gene leader peptide- and CDR3-specific primers to enable comprehensive assessment of SHM and BCR stereotypy. Identification of complete variable region sequences will also lay the foundation for synthesis of recombinant full-length membrane-associated and soluble forms of Burkitt BCRs. Reconstitution of Burkitt BCRs in vitro will allow evaluation of their antigenic specificity and signaling properties. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

20

Palmos, Denice Mae, Rikhia Chakraborty, Harshal Abhyankar, Joy C. Jayaseelan, Maria F. Cardenas, Joyce Kambugu, Jeff Otiti, et al. "Whole Exome Analysis Reveals Key Genomic Differences between Sporadic and Endemic Pediatric Burkitt Lymphoma." Blood 132, Supplement 1 (November 29, 2018): 4117. http://dx.doi.org/10.1182/blood-2018-99-110762.

Full text

Abstract:

Abstract Introduction Burkitt Lymphoma (BL) is a highly aggressive hematological malignancy that originates from germinal center B-cells, is characterized by IG/MYC translocation, and affects both children and adults. Clinical and biological differences have been noted between endemic BL, which occurs in equatorial Africa and is virtually always associated with Epstein-Barr virus (EBV) infection, and sporadic BL that is infrequently associated with EBV. BL is highly curable using an aggressive chemotherapy regimen, but the intensive supportive care required to manage the toxicities of this treatment precludes its use for most patients with endemic BL, resulting in poorer survival for those patients. Although previous genetic studies have identified recurrent mutations in BL (including alterations in ID3 and its downstream targets TCF3 and CCND3), endemic BL has not been as well characterized and the extent of differences between sporadic and endemic BL (and their potential relation to pathogenesis and response to therapy) is not yet clear. Therefore, more extensive genomic characterization of both sporadic and endemic BL is needed to provide insight into tumor biology and to identify novel therapeutic targets that can be utilized to provide less toxic treatments. Methods We interrogated frozen tumor and matched normal blood samples from a cohort of 30 pediatric BL cases, 12 of which were collected from Uganda and 18 from Texas Children's Cancer Center (Houston, TX). Whole exome sequencing (WES) and copy number analysis were performed on the Illumina platform using the OmniExpress array and VCrome 2.1 WES capture reagent and analyzed utilizing the Baylor College of Medicine Human Genome Sequencing Center bioinformatic pipeline. A median of 135x average coverage and >97% of targeted bases with at least 20x coverage was observed for WES. Results WES revealed a median of 46 nonsilent somatic mutations per case for endemic BL (range 19-207), and 32 per case for sporadic BL (range 13-119). Evidence of the EBV genome was detected in all endemic BL samples and 3/18 (17%) of sporadic BL cases. Mutations were found in genes known to be frequently mutated in BL, including MYC in 7/12 (58%) of endemic cases and 12/18 (67%) of sporadic cases and TP53 in 5/12 (42%) and 9/18 (50%), respectively. Of note, mutations in DDX3X (7/12 [58%] endemic, 9/18 [50%] sporadic) and FOXO1 (5/12 [42%] endemic, 7/18 [39%] sporadic) were identified frequently in our cohort. As previously described, the ID3 pathway was more frequently targeted by mutations in sporadic BL: ID3 in 8/18 (44%) sporadic cases vs 3/12 (25%) endemic, TCF3 in 3/18 (17%) vs. 1/12 (8%), and CCND3 in 7/18 (39%) vs 2/12 (17%), respectively. Mutations in the SWI/SNF chromatin-remodeling genes ARID1A and SMARCA4 have been reported to occur in BL in a mutually exclusive fashion. In our cohort, mutations in SMARCA4 were exclusive to sporadic cases (9/18, 50%) and not found in endemic tumors (P = 0.01). Conversely, ARID1A mutations were much more frequent in endemic cases (7/12, 58%) as compared to sporadic ones (3/18, 17%) (P < 0.05). Only one sporadic case was found to have both genes mutated. Copy number analysis did not reveal recurrent focal copy number deletions. Amplification of 13q31.2 - q32.2 was detected in sporadic cases (4/18, 22%) but not in endemic cases, while focal amplification of 7p14.1 (3/10, 30%) and 14q11.2 (4/10, 40%) were exclusive to endemic tumors. Conclusions These findings provide novel insight into the landscapes of genomic alterations in pediatric endemic and sporadic BL. Our data confirm the recurrence of mutated genes previously associated with BL and highlight differences between endemic and sporadic BL, most notably, the exclusivity of SMARCA4 mutations in sporadic BL cases in this cohort. The recurrence of mutations in ARID1A and SMARCA4 emphasizes the critical role of these SWI/SNF proteins in BL. More extensive molecular studies (whole genome and transcriptome sequencing) of this cohort are ongoing and may reveal additional differences between endemic and sporadic BL. Additional studies will be required to more precisely assess the frequency of these alterations in BL and their link to clinical features of the disease, as well as the biological relevance of the BL genes identified through these genomic analyses. Figure. Figure. Disclosures No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

21

Murray, Paul G., and Lawrence S. Young. "An etiological role for the Epstein-Barr virus in the pathogenesis of classical Hodgkin lymphoma." Blood 134, no. 7 (August 15, 2019): 591–96. http://dx.doi.org/10.1182/blood.2019000568.

Full text

Abstract:

Abstract Although a pathogenic role for the Epstein-Barr virus (EBV) is largely undisputed for tumors that are consistently EBV genome positive (eg, nasopharyngeal carcinoma, endemic Burkitt lymphoma), this is not the case for classical Hodgkin lymphoma (cHL), a tumor with only a variable EBV association. In light of recent developments in immunotherapeutics and small molecules targeting EBV, we believe it is now timely to reevaluate the role of EBV in cHL pathogenesis.

APA, Harvard, Vancouver, ISO, and other styles

22

Haluska, F. G., G. Russo, J. Kant, M. Andreef, and C. M. Croce. "Molecular resemblance of an AIDS-associated lymphoma and endemic Burkitt lymphomas: implications for their pathogenesis." Proceedings of the National Academy of Sciences 86, no. 22 (November 1, 1989): 8907–11. http://dx.doi.org/10.1073/pnas.86.22.8907.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Zhou, Peixun, Alex E. Blain, Alexander M. Newman, Masood Zaka, George Chagaluka, Filbert R. Adlar, Ugonna T. Offor, et al. "Sporadic and endemic Burkitt lymphoma have frequent FOXO1 mutations but distinct hotspots in the AKT recognition motif." Blood Advances 3, no. 14 (July 12, 2019): 2118–27. http://dx.doi.org/10.1182/bloodadvances.2018029546.

Full text

Abstract:

Abstract FOXO1 has an oncogenic role in adult germinal center–derived lymphomas, in which mutations, predominately within the AKT recognition motif, cause nuclear retention of FOXO1, resulting in increased cell proliferation. To determine the prevalence and distribution of FOXO1 mutations in pediatric Burkitt lymphoma (BL), we sequenced a large number of sporadic and endemic BL patient samples. We report a high frequency of FOXO1 mutations in both sporadic and endemic BL at diagnosis, occurring in 23/78 (29%) and 48/89 (54%) samples, respectively, as well as 8/16 (50%) cases at relapse. Mutations of T24 were the most common in sporadic BL but were rare in endemic cases, in which mutations of residue S22, also within the AKT recognition motif, were the most frequent. FOXO1 mutations were almost always present in the major tumor cell clone but were not associated with outcome. Analysis of other recurrent mutations reported in BL revealed that FOXO1 mutations were associated with mutations of DDX3X and ARID1A, but not MYC, TCF3/ID3, or members of the phosphatidylinositol 3-kinase signaling pathway. We further show common nuclear retention of the FOXO1 protein, irrespective of mutation status, suggesting alternative unknown mechanisms for maintaining FOXO1 transcriptional activity in BL. CRISPR/Cas9 knockout of FOXO1 in an endemic cell line produced a significant decrease in cell proliferation, supporting an oncogenic role for FOXO1 in endemic BL. Thus, FOXO1 is frequently mutated in both sporadic and endemic BL and may offer a potential therapeutic target for pediatric BL patients worldwide.

APA, Harvard, Vancouver, ISO, and other styles

24

Ogwang, Martin D., Kishor Bhatia, Robert J. Biggar, and Sam M. Mbulaiteye. "Incidence and geographic distribution of endemic Burkitt lymphoma in northern Uganda revisited." International Journal of Cancer 123, no. 11 (December 1, 2008): 2658–63. http://dx.doi.org/10.1002/ijc.23800.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Aka, Peter, Benjamin Emmanuel, Maria Candida Vila, Amar Jariwala, Francis Nkrumah, Maria V. Periago, Janet Neequaye, et al. "Elevated serum levels of interleukin-6 in endemic Burkitt lymphoma in Ghana." Hematological Oncology 32, no. 4 (January 6, 2014): 218–20. http://dx.doi.org/10.1002/hon.2121.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Mutyaba, I., S. McGoldrick, E. Krantz, M. Ulrickson, S. Gerdts, A. Omoding, F. Geriga, J. B. Kambugu, J. Orem, and C. Casper. "Outcomes of endemic Burkitt lymphoma patients treated using a patient-oriented approach." Annals of Global Health 82, no. 3 (August 20, 2016): 591. http://dx.doi.org/10.1016/j.aogh.2016.04.554.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Staudt, Louis M. "Chronic Active B-Cell Receptor Signaling in Lymphoma." Blood 120, no. 21 (November 16, 2012): SCI—26—SCI—26. http://dx.doi.org/10.1182/blood.v120.21.sci-26.sci-26.

Full text

Abstract:

Abstract Abstract SCI-26 We have developed loss-of-function, RNA interference-based screens to reveal genes essential for cancer cell proliferation and survival. In parallel, we are using high-throughput RNA resequencing (RNA-seq) to identify somatic mutations and other structural abnormalities in cancer. The intersection of these two data sets has helped us to discover novel pathogenetic pathways in lymphoma that are amenable to therapeutic attack. The activated B-cell-like (ABC) subtype of diffuse large B-cell lymphoma (DLBCL) has constitutive activation of the NF-κB pathway, which we traced to the signaling adapter CARD11. In some ABC DLBCL biopsies (∼10%), somatic mutations produce CARD11 isoforms that spontaneously activate NF-κB signaling. In ABC DLBCL tumors with wild-type CARD11, we defined a “chronic active” form of B-cell receptor (BCR) signaling that activates NF-κB. Such ABC DLBCLs are killed by knockdown of BCR signaling components, such as Bruton's tyrosine kinase (BTK), or components of the BCR itself. Over one-fifth of ABC DLBCLs have mutations in the CD79B or CD79A subunits of the BCR. In 18 percent of cases, mutations occur in a single tyrosine residue in the critical “ITAM” signaling motif, generating BCRs that avoid negative autoregulation by the LYN tyrosine kinase. Based on these findings, we are conducting clinical trials of ibrutinib in relapsed/refractory DLBCL. Ibrutinib is an irreversible and highly selective small-molecule inhibitor of BTK. Thus far, ibrutinib monotherapy has induced many complete and partial responses in patients with ABC DLBCL, including those with “primary refractory” tumors that had never responded to any prior therapy. One patient has been in a sustained complete response for over 19 months, taking ibrutinib daily with no discernible side effects. Of note, ABC DLBCL tumors with and without CD79B mutations have responded, suggesting that BCR pathway addiction may be a prevalent feature in this lymphoma subtype. More recently, we have uncovered a “tonic” form of BCR signaling in Burkitt lymphoma that engages the prosurvival PI(3) kinase pathway. Two-thirds of Burkitt lymphoma cell lines die upon knockdown of BCR subunits or the proximal kinase SYK, due to loss of PI(3) kinase signaling. Moreover, a gene expression signature of PI(3) kinase activity is more highly expressed in Burkitt lymphoma biopsies than in biopsies of other aggressive lymphomas. Tonic BCR signaling in Burkitt lymphoma is mechanistically distinct from chronic active BCR signaling in ABC DLBCL, since it does not engage BTK, CARD11, or NF-κB. RNA-seq revealed that 70 percent of sporadic Burkitt lymphoma cases harbor somatic mutations that potentiate the action of the transcription factor TCF3 by preventing its inhibitory heterodimerization with the DNA-binding inhibitor ID3. TCF3 promotes tonic BCR signaling and PI(3) kinase activity in Burkitt lymphoma by transactivating the immunoglobulin heavy- and light-chain genes, thereby increasing surface BCR expression, and by repressing the phosphatase SHP-1, a potent negative regulator of BCR signaling. Hence, inhibitors of proximal BCR signaling and the PI(3) kinase pathway should be evaluated in Burkitt lymphoma, especially in patients for whom high-dose chemotherapy is infeasible, such as older individuals and those with the endemic form of this lymphoma. Disclosures: Off Label Use: I will be discussing clinical trials of ibrutinib (PCI-32765) in lymphoma. Ibrutinib is an investigational drug that has not yet received FDA approval for any indication.

APA, Harvard, Vancouver, ISO, and other styles

28

Chabay, Paola, Daniela Lens, Rocio Hassan, Socorro María Rodríguez Pinilla, Fabiola Valvert Gamboa, Iris Rivera, Fuad Huamán Garaicoa, et al. "Lymphotropic Viruses EBV, KSHV and HTLV in Latin America: Epidemiology and Associated Malignancies. A Literature-Based Study by the RIAL-CYTED." Cancers 12, no. 8 (August 4, 2020): 2166. http://dx.doi.org/10.3390/cancers12082166.

Full text

Abstract:

The Epstein–Barr virus (EBV), Kaposi sarcoma herpesvirus (KSHV) and human T-lymphotropic virus (HTLV-1) are lymphomagenic viruses with region-specific induced morbidity. The RIAL-CYTED aims to increase the knowledge of lymphoma in Latin America (LA), and, as such, we systematically analyzed the literature to better understand our risk for virus-induced lymphoma. We observed that high endemicity regions for certain lymphomas, e.g., Mexico and Peru, have a high incidence of EBV-positive lymphomas of T/NK cell origin. Peru also carries the highest frequency of EBV-positive classical Hodgkin lymphoma (HL) and EBV-positive diffuse large B cell lymphoma, not otherwise specified (NOS), than any other LA country. Adult T cell lymphoma is endemic to the North of Brazil and Chile. While only few cases of KSHV-positive lymphomas were found, in spite of the close correlation of Kaposi sarcoma and the prevalence of pathogenic types of KSHV. Both EBV-associated HL and Burkitt lymphoma mainly affect young children, unlike in developed countries, in which adolescents and young adults are the most affected, correlating with an early EBV seroconversion for LA population despite of lack of infectious mononucleosis symptoms. High endemicity of KSHV and HTLV infection was observed among Amerindian populations, with differences between Amazonian and Andean populations.

APA, Harvard, Vancouver, ISO, and other styles

29

Zhu, Delin, Chen Feng Qi, Herbert C. Morse, Siegfried Janz, and Freda K. Stevenson. "Deregulated expression of the Myc cellular oncogene drives development of mouse “Burkitt-like” lymphomas from naive B cells." Blood 105, no. 5 (March 1, 2005): 2135–37. http://dx.doi.org/10.1182/blood-2004-07-2573.

Full text

Abstract:

Abstract Chromosomal translocations juxtaposing immunoglobulin (Ig) and MYC genes are the hallmarks of human Burkitt lymphoma (BL), with deregulated MYC expression being a critical factor in pathogenesis. By inserting an intact mouse Myc gene into the mouse genome, proximal to the Ig enhancer Eμ, the effect of a precise mimic of the major t(8;14) translocation of human endemic BL (eBL) could be investigated. Knock-in mice developed IgM-positive B-cell tumors, with most being typical of eBL by histology and immunophenotype, including expression of the germinal center (GC)–associated protein, BCL6. Unlike eBL, however, analysis of Ig VH sequences revealed no significant level of somatic mutation. Thus, constitutive expression of Myc in the knock-in mice is apparently able to induce “Burkitt-like” lymphomas before antigen stimulation and formation of a GC. In contrast, human eBL development occurs in a GC or post-GC site with a likely contribution to pathogenesis from Epstein-Barr virus (EBV) and other epigenetic factors.

APA, Harvard, Vancouver, ISO, and other styles

30

Fujita, Shuichi, Nathan Buziba, Atsushi Kumatori, Masachika Senba, Akira Yamaguchi, and Kan Toriyama. "Early Stage of Epstein-Barr Virus Lytic Infection Leading to the “Starry Sky” Pattern Formation in Endemic Burkitt Lymphoma." Archives of Pathology & Laboratory Medicine 128, no. 5 (May 1, 2004): 549–52. http://dx.doi.org/10.5858/2004-128-549-esoevl.

Full text

Abstract:

Abstract Context.—Burkitt lymphoma (BL) is histologically characterized by a “starry sky” appearance, representing scattered macrophages that have phagocytosed cell debris among proliferating lymphoma cells. As is well known, almost all the neoplastic cells of endemic BL are infected with Epstein-Barr virus (EBV). Previous studies have indicated that most of the EBV in B cells is latent, and few virus particles enter the lytic cycle. Objective.—To examine the histologic relationship between EBV infection stages and the formation of the starry sky pattern in African endemic BL tissues. Design.—Tissue samples from 44 patients with African endemic BL were examined with immunohistochemistry and in situ hybridization. We used EBV-encoded small RNA (EBER) as a marker of latent infection, and BamHI H left frame 1 (BHLF1) and BamHI Z EBV replication activator (ZEBRA) as lytic cycle markers. Results.—In all cases, signals for EBER were found in most neoplastic lymphocytes, and in 73% of cases, signals for BHLF1 and/or ZEBRA were recognized in the lymphoma cells within and around the lacunae in starry sky figures. The mean number of lacunae per unit area in cases positive for lytic cycle markers was significantly higher than that in negative cases (P < .001). Conclusions.—Our findings suggest that EBV-infected lymphoma cells in the lytic cycle, which eventually lapse into cell death, are phagocytosed prior to their rupture by macrophages that have migrated into the parenchyma. We emphasize that transition of EBV-infected lymphoma cells to the lytic cycle is one of the histomorphogenetic factors influencing the formation of starry sky pattern in endemic BL.

APA, Harvard, Vancouver, ISO, and other styles

31

Hesseling, P., E. Molyneux, S. Kamiza, T. Israels, and R. Broadhead. "Endemic Burkitt lymphoma: a 28-day treatment schedule with cyclophosphamide and intrathecal methotrexate." Annals of Tropical Paediatrics 29, no. 1 (March 2009): 29–34. http://dx.doi.org/10.1179/146532809x402006.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Kelly, Gemma L., and Alan B. Rickinson. "Burkitt Lymphoma: Revisiting the Pathogenesis of a Virus-Associated Malignancy." Hematology 2007, no. 1 (January 1, 2007): 277–84. http://dx.doi.org/10.1182/asheducation-2007.1.277.

Full text

Abstract:

AbstractBurkitt lymphoma (BL), a tumor occurring in endemic, sporadic and AIDS-associated forms, is the classic example of a human malignancy whose pathogenesis involves a specific cellular genetic change, namely, a chromosomal translocation deregulating expression of the c-myc oncogene, complemented in many cases by the action of an oncogenic virus, the Epstein-Barr virus (EBV). Here we review recent work in two complementary areas of research: (1) on cellular genetic changes that occur in addition to the c-myc translocation in BL, in particular the capacity of p53/ ARF pathway breakage or of c-myc mutation to decouple the pro-proliferative effects of c-myc deregulation from its pro-apoptotic effects; and (2) on a postulated role for EBV in BL pathogenesis, through adopting restricted forms of virus latent gene expression that remain compatible with the c-myc–driven growth program but offer the tumor additional protection from apoptosis. We stress the many fundamental questions that remain to be resolved and, in that regard, highlight the general lessons that might be learned through understanding how two other infectious agents, malaria and HIV, dramatically enhance BL incidence.

APA, Harvard, Vancouver, ISO, and other styles

33

Persing, David H., and Franklyn G. Prendergast. "Infection, Immunity, and Cancer." Archives of Pathology & Laboratory Medicine 123, no. 11 (November 1, 1999): 1015–22. http://dx.doi.org/10.5858/1999-123-1015-iiac.

Full text

Abstract:

Abstract A significant percentage of human cancers worldwide are associated with infections due to known viruses, including human papillomaviruses (cervical cancer and other skin cancers), human T-lymphotropic viruses (adult T-cell leukemias and lymphomas in endemic areas), hepatitis B virus (liver cancer), and Epstein-Barr virus (Burkitt lymphoma and nasopharyngeal carcinoma). The fraction of human cancers attributable to infection may now need to be revised in light of the fact that new viral associations have been discovered and other nonviral associations have been identified. This article addresses the increasingly recognized role of infectious agents as precipitants of human neoplasia and the possibility that novel diagnostic, therapeutic, and chemopreventive strategies may emanate directly from research directed at identifying and understanding these agents.

APA, Harvard, Vancouver, ISO, and other styles

34

Oduor, Cliff I., Kiprotich Chelimo, David H. Mulama, Collins Ouma, Joslyn Foley, John Vulule, Ann M. Moormann, and Jeffrey A. Bailey. "Interleukin-6 and Interleukin-10 Gene Promoter Polymorphisms and Risk of Endemic Burkitt Lymphoma." American Journal of Tropical Medicine and Hygiene 91, no. 3 (September 3, 2014): 649–54. http://dx.doi.org/10.4269/ajtmh.13-0616.

Full text

APA, Harvard, Vancouver, ISO, and other styles

35

McGoldrick, Suzanne M., Abrahams Omoding, Sarah E. Gerdts, Innocent Mutyaba, Elizabeth Krantz, Jackson Orem, and Corey Casper. "Impact of a Quality Improvement Project on Pediatric Endemic Burkitt Lymphoma Outcomes in Uganda." Blood 128, no. 22 (December 2, 2016): 156. http://dx.doi.org/10.1182/blood.v128.22.156.156.

Full text

Abstract:

Abstract Background: Endemic Burkitt Lymphoma (eBL) is the most common childhood cancer in many countries of sub-Saharan Africa (SSA). Reported overall survival (OS) rates in SSA are low at 30-50%, especially compared to survival of children with sporadic Burkitt Lymphoma treated in high-resource settings (OS 85-95%)(Patte, Auperin et al. 2007, Buckle, Maranda et al. 2016, Stanley, Westmoreland et al. 2016). The Burkitt Lymphoma (BL) project in Uganda was initiated as a collaboration between the Fred Hutchinson Cancer Research Center and Uganda Cancer Institute (UCI) in July 2012. The project provided resources for timely pathologic diagnosis, chemotherapy during stock-outs, case management to improve adherence, transportation, and standardized recording of care and clinical outcomes. We sought to determine OS and response to treatment in this patient population with eBL who received enhanced care through this demonstration project. Methods:Every child presenting to the UCI with suspected BL and enrolled in the BL project between July 2012 and December 2014 underwent diagnostic evaluation with a core needle biopsy of the tumor, abdominal ultrasound, and chest radiography. Patients with confirmed BL at enrollment, as determined by pathology review and physician assessment, were staged based on physical exam according to Ziegler. Most received first-line therapy consisting of cyclophosphamide, vincristine and methotrexate (COM) every two weeks for six planned cycles. Treatment response was evaluated ≤ 3 months from starting the 6th cycle of COM. Following completion of therapy, patients were followed monthly for three months, then every three months for up to a year. Follow-up data through March 26, 2015 was included. Kaplan-Meier methodology was used to estimate 1-year OS. Results:A total of 202 patients with suspected BL were followed by the BL project during this time period. Of these, 142 (70%) were confirmed to have BL. The remainder had other cancers or benign diseases (24%) or had inadequate diagnostic data (6%). The median age of patients with BL was 7 years and the majority were male (63%). Approximately half of patients had late-stage disease (49% Ziegler stages C, D or AR) and had a high LDH at presentation (54%). Of the 142 with BL, 78% initiated COM, 6% other chemotherapy, and 16% were not treated with chemotherapy (18 died in the first 40 days and 5 were exited). Among 110 patients who initiated COM, the treatment response after 6 cycles was complete response (CR) for 46%, partial response (PR) for 7%, stable (SD) or progressive disease (PD) for 2%, relapsed disease (RD) for 1%, but there was no response assessment within 3 months of the 6th cycle for 10%. The remaining patients who did not complete 6 cycles either switched to second line therapy (7%), abandoned treatment (9%), died (9%), exited the program (3%), or were censored (6%) within 6 months of starting treatment. Among the subset of 73 patients who completed six cycles of treatment, the responses after 6 cycles were as follows: CR 70%, PR 11%, SD or PD 3%, RD 1%, unknown 15%. At 1 year, OS for the entire cohort with confirmed eBL was 53% (95% CI 43%, 62%; Figure 1). Among the patients who initiated COM, survival at 1 year post treatment initiation was 60% (95% CI 49%, 70%; Figure 2). These data represent preliminary results of our ongoing analysis. An updated analysis, along with associations of baseline factors, including CNS status, anemia, thrombocytopenia, B symptoms, tumor lysis syndrome and HIV status, as well as other infections (malaria, Hepatitis B), with clinical outcomes will be presented. Conclusion:Survival ofpatients with eBL treated in a low-resource setting remains inferior compared to children treated for sporadic BL in higher resource settings. The BL project was able to provide pathologic diagnoses, assure access to chemotherapy, enhance supportive care, and reduce abandonment to less than 10%, but still only slightly more than half of patients with a confirmed diagnosis survived one year. Ongoing obstacles to improving outcomes are inaccurate diagnosis and lacking supportive care to allow more intensive therapies. Improved diagnostic capacity as well as the ability to provide more potent and potentially less toxic treatment modalities may help to address the poor survival of children with a disease that is so successfully treated in higher resource settings. Disclosures Casper: Up to Date: Patents & Royalties; TempTime: Consultancy, Other: Travel, Accommodation, Expenses; Janssen: Consultancy, Research Funding; GSK: Other: Travel, Accommodation, Expenses; Roche: Consultancy, Other: Travel, Accommodation, Expenses.

APA, Harvard, Vancouver, ISO, and other styles

36

Coghill, Anna E., Carla Proietti, Zhiwei Liu, Lutz Krause, Jeff Bethony, Ludmila Prokunina-Olsson, Adeola Obajemu, et al. "The Association between the Comprehensive Epstein–Barr Virus Serologic Profile and Endemic Burkitt Lymphoma." Cancer Epidemiology Biomarkers & Prevention 29, no. 1 (October 16, 2019): 57–62. http://dx.doi.org/10.1158/1055-9965.epi-19-0551.

Full text

APA, Harvard, Vancouver, ISO, and other styles

37

Kaymaz, Yasin, Cliff I. Oduor, Hongbo Yu, Juliana A. Otieno, John Michael Ong'echa, Ann M. Moormann, and Jeffrey A. Bailey. "Comprehensive Transcriptome and Mutational Profiling of Endemic Burkitt Lymphoma Reveals EBV Type–Specific Differences." Molecular Cancer Research 15, no. 5 (January 30, 2017): 563–76. http://dx.doi.org/10.1158/1541-7786.mcr-16-0305.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Kaymaz, Yasin, Cliff I. Oduor, Hongbo Yu, Juliana A. Otieno, John Michael Ong'echa, Ann M. Moormann, and Jeffrey A. Bailey. "Comprehensive Transcriptome and Mutational Profiling of Endemic Burkitt Lymphoma Reveals EBV Type–Specific Differences." Molecular Cancer Research 15, no. 5 (May 2017): 563–76. http://dx.doi.org/10.1158/1541-7786.mcr-16-0305-t.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

Rainey, Jeanette J., Peter O. Sumba, Ann M. Moormann, Mark L. Wilson, Dickens Kowuor, and Rosemary Rochford. "Family Environment Is Associated with Endemic Burkitt Lymphoma: A Population-based Case-control Study." American Journal of Tropical Medicine and Hygiene 78, no. 2 (February 1, 2008): 338–43. http://dx.doi.org/10.4269/ajtmh.2008.78.338.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Kotepui, Kwuntida Uthaisar, and Manas Kotepui. "Malaria Infection and Risk for Endemic Burkitt Lymphoma: A Systematic Review and Meta-Analysis." International Journal of Environmental Research and Public Health 18, no. 11 (May 30, 2021): 5886. http://dx.doi.org/10.3390/ijerph18115886.

Full text

Abstract:

Background: Malaria infection is reportedly linked to endemic Burkitt lymphoma (eBL) in malaria-endemic areas. This study aimed to pool the overall risk (or odds) of eBL among children with previous or concurrent malaria infection. Methods: We searched PubMed, Web of Science, Scopus, and reference lists of publications for potentially relevant studies on malaria infection and eBL. The quality of the included studies was assessed using the Joanna Briggs Institute for case-control studies. Random-effects meta-analysis was used to summarize whether the odds of eBL can be increased by (1) malaria infection or (2) elevated titer of IgGs to malaria antigen. The level of heterogeneity was evaluated using Cochran’s Q statistic and I2. The individual study data, pooled odds, and confidence interval (CI) were illustrated using the forest plot. Publication bias was assessed using funnel plots and Egger’s test. Results: Ten studies were included, reporting the number of malaria cases in eBL and non-eBL (5 studied malaria infection and the odds of eBL; five studied the burden of IgGs to malarial antigens and the odds of eBL). According to the meta-analysis results, the odds of eBL was not increased by malaria infection (p = 0.562, OR: 0.87, 95% CI: 0.54–1.39, I2: 93.5%, malaria in eBL: 604/1506 cases, malaria in non-eBL: 2117/4549 cases) and the elevated titer of IgGs to malaria antigen (p = 0.051, OR: 1.50, 95% CI: 1.00–2.25, I2: 89%, increased IgG titer in eBL: 1059/1736 cases, increased IgG titer in non-eBL: 847/1722 cases). In meta-regression analysis, sex was not a confounding factor for the effect size of malaria infection and eBL (p = 0.10) and that of increased IgGs and eBL (p = 0.80). Conclusions: Malaria infection and IgG titer elevation did not increase the risk for eBL among children. However, the included studies, which are only few, do not generally agree on this point. Therefore, the risk for eBL in children diagnosed with malaria should be investigated further by longitudinal studies to confirm our evidence-based approach.

APA, Harvard, Vancouver, ISO, and other styles

41

Amato, Teresa, Francesco Abate, Pierpaolo Piccaluga, Michele Iacono, Chiara Fallerini, Alessandra Renieri, Giulia De Falco, et al. "Clonality Analysis of Immunoglobulin Gene Rearrangement by Next-Generation Sequencing in Endemic Burkitt Lymphoma Suggests Antigen Drive Activation of BCR as Opposed to Sporadic Burkitt Lymphoma." American Journal of Clinical Pathology 145, no. 1 (December 28, 2015): 116–27. http://dx.doi.org/10.1093/ajcp/aqv011.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

El-Mallawany, Nader Kim, Mercy Mutai, Idah Mtete, Satish Gopal, Christopher C. Stanley, Peter Wasswa, Mary Mtunda, et al. "Beyond Endemic Burkitt Lymphoma: Navigating Challenges of Differentiating Childhood Lymphoma Diagnoses Amid Limitations in Pathology Resources in Lilongwe, Malawi." Global Pediatric Health 4 (January 2017): 2333794X1771583. http://dx.doi.org/10.1177/2333794x17715831.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

El-Mallawany, Nader, Janet Ayello, Nancy Day, Carmella van de Ven, Kevin P. Conlon, Damian Fermin, Venkatesha Basrur, Kojo S. J. Elenitoba-Johnson, Megan S. Lim, and Mitchell S. Cairo. "Global Proteomic Profiling of Endemic Versus Sporadic Epstein-Barr Virus (EBV) Positive Burkitt Lymphoma (BL)." Blood 114, no. 22 (November 20, 2009): 4779. http://dx.doi.org/10.1182/blood.v114.22.4779.4779.

Full text

Abstract:

Abstract Abstract 4779 Background EBV infection of normal B-cells is commonly associated with the pathogenesis of BL (Brady et al, Clin Path, 2007). Endemic BL (eBL) is characteristically positive (100%) for EBV, contrasting with sporadic BL (sBL), where approximately 30% of cases are positive for EBV. eBL vs. sBL have significantly different breakpoint regions within c-myc (Shiramizu/Magrath et al, Blood, 1991). Overexpression of c-myc is the sine quae non of BL. C-myc interactions with other genes/proteins is multilayered and complex (Basso/Della-Favera, Nat Gen, 2005). Apoptotic pathway disruption is propelled by EBV and is critically important in c-myc deregulation and subsequent lymphomagenesis that occurs in EBV+ eBL vs. sBL (Ruf et al, J Vir, 2000). Global analysis of proteins expressed in EBV+ eBL vs. sBL may provide insights into biologic, pathogenetic, and molecular differences between the two subtypes of lymphoma, and potentially identify targets for the development of therapeutic agents. Objectives To compare the proteomic expression profile and signal transduction pathways of EBV+ eBL vs. sBL. Methods Whole cell lysates obtained from the EBV+ eBL cell line Raji and the EBV+ sBL cell line NC37 were digested and labeled with iTRAQ” labeling reagents, following manufacturer's protocol. The peptides were resolved by 2D-LC technique (off-line Strong cation exchange followed by on-line reverse-phase liquid chromatography). Data-dependant High energy C-trap Dissociation MS/MS spectra were acquired using an Orbitrap XL Tandem Mass Spectrometer (ThermoFisher). The MS/MS data was searched using X!Tandem/TPP software suite against human IPI database (v3.50) appended with decoy (reverse) sequences. iTRAQ” ratios of proteins (ProteinProphet probability of >0.9) were normalized and differentially expressed proteins were determined through Mixture Modeling. Protein interactions were further analyzed using the GoMiner and Ingenuity pathway analysis tools. Results Over 400 proteins were identified as being differentially expressed by a ≥ 1.25 fold change between the two cell lines. We identified differentially expressed proteins in both cell lines that are involved in a wide array of cellular processes as exhibited in Figure 1. Cellular processes uniquely involved by proteins over-expressed in eBL included immune response, hematopoiesis, cell proliferation, heat shock, and B-cell activation, while those uniquely identified in sBL included cell division, response to virus, and NF-kB cascade proteins. Specific cell-regulatory pathways implicated by the differential protein profile expressions (with associated proteins in parentheses) included the p53 apoptosis pathway (PCNA, MSH6, C1QBP, MAP4, and BAX), the caspase network of apoptosis (HCLS1, ACIN1, and AIFM1), the tumor suppressor protein RB network (MCM7, PA2G4, and API5), general apoptotic pathways (HSP90 and PDCD4), B-cell differentiation and proliferation pathways (TPD52 and IKBKG), and the ubiquitin-proteasome pathway (UBE2J1, UBE2C, and UBE2S). Seven of these proteins are c-myc target genes. Ingenuity protein network analysis revealed nine proteins identified in the experiment with interactions connected through the p53, caspase, and tumor necrosis factor apoptosis pathways. Conclusion Proteomic profile analysis of EBV+ eBL and sBL revealed over and under-expression of multiple proteins that may be implicated in the multi-factorial nature of disease pathogenesis. This is the first MS-based direct proteomic comparison of eBL and sBL. Our results suggest that there are potentially different mechanisms driving cell proliferation and resistance to apoptosis in eBL versus sBL and that EBV infection may be involved in the processes that drive lymphomagenesis. Ultimately, identification of proteins unique to the distinct disease subtypes will serve to establish tumor markers that may enable development of new diagnostic, prognostic, and therapeutic strategies. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

44

Hesseling, P. B., G. Mbah, F. Kouya, C. Kimbi, P. Nfor, J. Kaah, R. Kuruvilla, A. Best, and P. Wharin. "Endemic Burkitt Lymphoma: Long-term Outcome in 87 Patients Who Presented With Paraplegia in Cameroon." Pediatric Hematology and Oncology 32, no. 8 (November 17, 2015): 525–28. http://dx.doi.org/10.3109/08880018.2015.1085936.

Full text

APA, Harvard, Vancouver, ISO, and other styles

45

Moormann, Ann M., Kevin N. Heller, Kiprotich Chelimo, Paula Embury, Robert Ploutz-Snyder, Juliana A. Otieno, Margaret Oduor, Christian Münz, and Rosemary Rochford. "Children with endemic Burkitt lymphoma are deficient in EBNA1-specific IFN-γ T cell responses." International Journal of Cancer 124, no. 7 (April 1, 2009): 1721–26. http://dx.doi.org/10.1002/ijc.24014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

El-Mallawany, Nader Kim, Nancy Day, Janet Ayello, Carmella Van de Ven, Kevin Conlon, Damian Fermin, Venkatesha Basrur, Kojo Elenitoba-Johnson, Megan Lim, and Mitchell S. Cairo. "Differential proteomic analysis of endemic and sporadic Epstein–Barr virus-positive and negative Burkitt lymphoma." European Journal of Cancer 51, no. 1 (January 2015): 92–100. http://dx.doi.org/10.1016/j.ejca.2014.10.017.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Ogwang, Martin D., Weiqiang Zhao, Leona W. Ayers, and Sam M. Mbulaiteye. "Accuracy of Burkitt Lymphoma Diagnosis in Constrained Pathology Settings: Importance to Epidemiology." Archives of Pathology & Laboratory Medicine 135, no. 4 (April 1, 2011): 445–50. http://dx.doi.org/10.5858/2009-0443-ep.1.

Full text

Abstract:

Abstract Context.—Burkitt lymphoma (BL) is endemic in Uganda and because of the high incidence, diagnosis is often presumed during clinical care and epidemiologic studies. Objectives.—To assess the accuracy of the clinical and the local pathology diagnosis of BL as assessed by an outside pathology review diagnosis and to understand the limitations on histopathology practice in a resource-constrained setting at 1 hospital in Uganda. Design.—Clinically presumed pediatric (<15 years) BL cases with biopsies and pathology reports, from 1993 to 2007, were identified at St Mary's Hospital, Lacor (Gulu, Uganda). Local histopathology procedures, hematoxylin-eosin–stained tissue sections, and formalin-fixed paraffin-embedded blocks were reviewed onsite by an outside pathologist, followed by outside study that included tissue microarray immunohistochemistry and in situ hybridization. Results.—Local pathology laboratory procedures were inconsistent and suboptimal, especially for tissue fixation. There were 88 clinically presumed BL cases. Sixty-three could be reviewed by outside pathology (25 cases of lost blocks or no remaining tumor) and showed a clinical diagnostic accuracy of 75% (47 confirmed of 63), with a possible range of 62% to 85%, depending on the actual diagnosis of the 25 nonevaluable cases. There were 64 BL cases diagnosed by local pathology. Forty-five could be reviewed by outside pathology (19 cases of lost blocks or no remaining tumor) and showed a local pathology diagnostic accuracy of 82% (37 confirmed of 45), with a possible range of 58% to 88%, depending on the actual diagnosis of the 19 nonevaluable cases. Non-BL diagnoses included other non-Hodgkin lymphomas, Hodgkin lymphoma, and benign infectious lymphadenopathy. Conclusions.—Accuracy of clinical diagnosis of BL was reduced by inclusion of other diseases with similar clinical presentations. Local pathology, using morphology alone, only marginally improved clinical accuracy and often could not support outside pathology review due to inadequate laboratory procedures. There is an urgent need to improve pathology services in Uganda before conducting high-quality clinical and epidemiologic studies.

APA, Harvard, Vancouver, ISO, and other styles

48

Mundo, Lucia, Leonardo Del Porro, Massimo Granai, Maria Chiara Siciliano, Virginia Mancini, Raffaella Santi, Lynnette Marcar, et al. "Frequent traces of EBV infection in Hodgkin and non-Hodgkin lymphomas classified as EBV-negative by routine methods: expanding the landscape of EBV-related lymphomas." Modern Pathology 33, no. 12 (June 1, 2020): 2407–21. http://dx.doi.org/10.1038/s41379-020-0575-3.

Full text

Abstract:

AbstractThe Epstein–Barr virus (EBV) is linked to various B-cell lymphomas, including Burkitt lymphoma (BL), classical Hodgkin lymphoma (cHL) and diffuse large B-cell lymphoma (DLBCL) at frequencies ranging, by routine techniques, from 5 to 10% of cases in DLBCL to >95% in endemic BL. Using higher-sensitivity methods, we recently detected EBV traces in a few EBV-negative BL cases, possibly suggesting a “hit-and-run” mechanism. Here, we used routine and higher-sensitivity methods (qPCR and ddPCR for conserved EBV genomic regions and miRNAs on microdissected tumor cells; EBNA1 mRNA In situ detection by RNAscope) to assess EBV infection in a larger lymphoma cohort [19 BL, 34 DLBCL, 44 cHL, 50 follicular lymphomas (FL), 10 T-lymphoblastic lymphomas (T-LL), 20 hairy cell leukemias (HCL), 10 mantle cell lymphomas (MCL)], as well as in several lymphoma cell lines (9 cHL and 6 BL). qPCR, ddPCR, and RNAscope consistently documented the presence of multiple EBV nucleic acids in rare tumor cells of several cases EBV-negative by conventional methods that all belonged to lymphoma entities clearly related to EBV (BL, 6/9 cases; cHL, 16/32 cases; DLBCL, 11/30 cases), in contrast to fewer cases (3/47 cases) of FL (where the role of EBV is more elusive) and no cases (0/40) of control lymphomas unrelated to EBV (HCL, T-LL, MCL). Similarly, we revealed traces of EBV infection in 4/5 BL and 6/7 HL cell lines otherwise conventionally classified as EBV negative. Interestingly, additional EBV-positive cases (1 DLBCL, 2 cHL) relapsed as EBV-negative by routine methods while showing EBNA1 expression in rare tumor cells by RNAscope. The relapse specimens were clonally identical to their onset biopsies, indicating that the lymphoma clone can largely loose the EBV genome over time but traces of EBV infection are still detectable by high-sensitivity methods. We suggest EBV may contribute to lymphoma pathogenesis more widely than currently acknowledged.

APA, Harvard, Vancouver, ISO, and other styles

49

Kirimunda, Samuel, Murielle Verboom, Isaac Otim, Mark Ssennono, Ismail D. Legason, Hadijah Nabalende, Martin D. Ogwang, et al. "Variation in the Human Leukocyte Antigen system and risk for endemic Burkitt lymphoma in northern Uganda." British Journal of Haematology 189, no. 3 (February 18, 2020): 489–99. http://dx.doi.org/10.1111/bjh.16398.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Olowu, Wasiu A., Kayode A. Adelusola, Kabir B. Badmos, and Obafemi J. A. Aina. "AUTOPSY DIAGNOSIS OF ENDEMIC BURKITT LYMPHOMA AS THE PRIMARY ETIOLOGY OF ACUTE RENAL FAILURE IN CHILDREN." Pediatric Hematology and Oncology 22, no. 4 (January 2005): 315–21. http://dx.doi.org/10.1080/08880010590935211.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!