Subtyping Burkitt Lymphoma by DNA Methylation
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PROVIDER: PRJNA1207511 | ENA |
REPOSITORIES: ENA
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Project description:Subtyping Burkitt Lymphoma by DNA Methylation [EPIC]
| PRJNA1207512 | ENA
Project description:Burkitt lymphoma (BL) is an aggressive germinal center B-cell-derived malignancy. Historically, sporadic, endemic, and immunodeficiency-associated epidemiological variants were distinguished which differ in the frequency of Epstein-Barr virus (EBV) association. Aiming at identifying subgroups based on DNA methylation patterns we here profiled 96 primary BL cases, 17 BL cell lines and 6 lymphoblastoid cell lines using Illumina BeadChip arrays. DNA methylation clustered the cases into each two subgroups according to EBV status, with each showing two underlying subgroups (EBV-positive: BL-mC1, BL-mC2 and EBV-negative: BL-mC3, BL-mC4). The subgroups BL-mC1/2 enriched for EBV-positive cases showed increased DNA methylation, epigenetic age and in part increased proliferation history compared to BL-mC3/4. CpGs hypermethylated in EBV-positive BLs were enriched for polycomb repressive complex 2 marks, while the CpGs hypomethylated in EBV-negative BLs were linked to B-cell receptor signaling. EBV-associated hypermethylation affected regulatory regions of genes frequently mutated in BL (e.g. CCND3, TP53), and impacted superenhancers, suggesting that hypermethylation may compensate for the lower mutation burden of oncogenic drivers in EBV-positive BLs. Though minor, but significant differences were also observed between EBV-positive endemic and sporadic cases (e.g. at the SOX11 and RUNX1 loci), our findings suggest that EBV status, rather than epidemiological variants, drive the DNA methylation-based subgrouping of BL.
2025-04-16 | GSE286028 | GEO
Project description:Burkitt lymphoma (BL) is an aggressive germinal center B-cell-derived malignancy. Historically, sporadic, endemic, and immunodeficiency-associated epidemiological variants were distinguished which differ in the frequency of Epstein-Barr virus (EBV) association. Aiming at identifying subgroups based on DNA methylation patterns we here profiled 96 primary BL cases, 17 BL cell lines and 6 lymphoblastoid cell lines using Illumina BeadChip arrays. DNA methylation clustered the cases into each two subgroups according to EBV status, with each showing two underlying subgroups (EBV-positive: BL-mC1, BL-mC2 and EBV-negative: BL-mC3, BL-mC4). The subgroups BL-mC1/2 enriched for EBV-positive cases showed increased DNA methylation, epigenetic age and in part increased proliferation history compared to BL-mC3/4. CpGs hypermethylated in EBV-positive BLs were enriched for polycomb repressive complex 2 marks, while the CpGs hypomethylated in EBV-negative BLs were linked to B-cell receptor signaling. EBV-associated hypermethylation affected regulatory regions of genes frequently mutated in BL (e.g. CCND3, TP53), and impacted superenhancers, suggesting that hypermethylation may compensate for the lower mutation burden of oncogenic drivers in EBV-positive BLs. Though minor, but significant differences were also observed between EBV-positive endemic and sporadic cases (e.g. at the SOX11 and RUNX1 loci), our findings suggest that EBV status, rather than epidemiological variants, drive the DNA methylation-based subgrouping of BL.
2025-04-16 | GSE286029 | GEO
Project description:Burkitt lymphoma is the commonest cancer in children in Africa. We compared the gene expression profiles of African Burkitt lymphoma patients with those of cases presented in Western countries in both immunocompetent (sporadic Burkitt lymphoma) and HIV-infected patients (immunodeficiency associated Burkitt lymphoma). We used microarrays to detail the global programme of gene expression in different subtypes of Burkitt lymphoma.
2011-01-20 | GSE26673 | GEO
Project description:DNA methylation epitypes of Burkitt lymphoma with distinct molecular and clinical features
| PRJNA1240817 | ENA
Project description:Burkitt lymphoma is characterized by deregulation of MYC, but the contribution of other genetic mutations to the disease is largely unknown. Here, we describe the first completely sequenced genome from a Burkitt lymphoma tumor and germline DNA from the same affected individual. We further sequenced the exomes of 59 Burkitt lymphoma tumors and compared them to sequenced exomes from 94 diffuse large B-cell lymphoma (DLBCL) tumors. We identified 70 genes that were recurrently mutated in Burkitt lymphomas, including ID3, GNA13, RET, PIK3R1 and the SWI/SNF genes ARID1A and SMARCA4. Our data implicate a number of genes in cancer for the first time, including CCT6B, SALL3, FTCD and PC. ID3 mutations occurred in 34% of Burkitt lymphomas and not in DLBCLs. We show experimentally that ID3 mutations promote cell cycle progression and proliferation. Our work thus elucidates commonly occurring gene-coding mutations in Burkitt lymphoma and implicates ID3 as a new tumor suppressor gene.
2013-07-01 | GSE48435 | GEO
Project description:Burkitt lymphoma is the commonest cancer in children in Africa. We compared the gene expression profiles of African Burkitt lymphoma patients with those of cases presented in Western countries in both immunocompetent (sporadic Burkitt lymphoma) and HIV-infected patients (immunodeficiency associated Burkitt lymphoma). We used microarrays to detail the global programme of gene expression in different subtypes of Burkitt lymphoma. Lymph-node biopsies were collected at diagnosis. Gene expression profiles were generated with the Affymetrix HG U133 2.0 plus microarray
2011-01-20 | E-GEOD-26673 | biostudies-arrayexpress
Project description:The genetic drivers of Burkitt Lymphoma (BL) have been comprehensively explored while the role of epigenetics remains unclear. Using samples from patients across four continents, we searched for sites with consistent DNA methylation changes and associations with clinical and molecular features such as Epstein-Barr virus (EBV) status and driver mutations. We identified robust methylation patterns that were not fully explained by EBV status, implying the existence of robust epitypes: HypoBL and HyperBL. The latter had distinct genomic and clinical features including global hypermethylation, a higher mutation burden, elevated aberrant somatic hypermutation, and inferior outcomes. Methylation, gene expression and mutational differences between the epitypes support a model in which each arises from a distinct cell-of-origin. These results suggest an approach for identifying BL patients with a greater risk of treatment failure and provide a basis for the exploration of new therapeutic strategies that target the unique molecular underpinnings of each group.
2025-03-26 | GSE292690 | GEO
Project description:Burkitt lymphoma is characterized by deregulation of MYC, but the contribution of other genetic mutations to the disease is largely unknown. Here, we describe the first completely sequenced genome from a Burkitt lymphoma tumor and germline DNA from the same affected individual. We further sequenced the exomes of 59 Burkitt lymphoma tumors and compared them to sequenced exomes from 94 diffuse large B-cell lymphoma (DLBCL) tumors. We identified 70 genes that were recurrently mutated in Burkitt lymphomas, including ID3, GNA13, RET, PIK3R1 and the SWI/SNF genes ARID1A and SMARCA4. Our data implicate a number of genes in cancer for the first time, including CCT6B, SALL3, FTCD and PC. ID3 mutations occurred in 34% of Burkitt lymphomas and not in DLBCLs. We show experimentally that ID3 mutations promote cell cycle progression and proliferation. Our work thus elucidates commonly occurring gene-coding mutations in Burkitt lymphoma and implicates ID3 as a new tumor suppressor gene. Gene expression profiling on 21 Burkitt lymphomas was performed using standard Affymetrix protocols as described previously. Briefly, 1 μg of total RNA was reverse transcribed, using oligo(dT) primer to synthesize cDNA. T7 primer was used for in vitro transcription, resulting in labeled cRNA, which was fragmented and hybridized to Affymetrix Whole-Genome Gene 1.0 ST microarrays. Microarrays were washed and scanned, and the data were normalized as described previously.
2013-07-01 | E-GEOD-48435 | biostudies-arrayexpress
Project description:Burkitt Lymphoma patient samples using gene expression to create a molecular definition of the disease. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Keywords: clinical history design Samples were obtained from patients with Burkitt lymphoma and gene expression profiling was used to create a molecular definition of the disease. The molecular definition was then used to predict the disease in an independent set of patients with atypical Burkitt lymphoma and diffuse large B cell lymphoma.
2006-07-04 | E-GEOD-4732 | biostudies-arrayexpress