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Genomic landscape of IG-MYC positive Burkitt lymphoma with precursor B-cell immunophenotype.

ABSTRACT: As part of the ICGC, the ICGC MMML-Seq project performed whole genome sequencing of a rare Burkitt lymphoma subtype with precursor B-cell immunophenotype. Analysis were performed in concordance with the guidelines of the ICGC.

PROVIDER: EGAS00001002968 | EGA |

REPOSITORIES: EGA

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IG-MYC + neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas.

Wagener Rabea R López Cristina C Kleinheinz Kortine K Bausinger Julia J Aukema Sietse M SM Nagel Inga I Toprak Umut H UH Seufert Julian J Altmüller Janine J Thiele Holger H Schneider Christof C Kolarova Julia J Park Jeongbin J Hübschmann Daniel D Murga Penas Eva M EM Drexler Hans G HG Attarbaschi Andishe A Hovland Randi R Kjeldsen Eigil E Kneba Michael M Kontny Udo U de Leval Laurence L Nürnberg Peter P Oschlies Ilske I Oscier David D Schlegelberger Brigitte B Stilgenbauer Stephan S Wössmann Wilhelm W Schlesner Matthias M Burkhardt Birgit B Klapper Wolfram W Jaffe Elaine S ES Küppers Ralf R Siebert Reiner R

Blood 20181003 21

The WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue notes instances of Burkitt lymphoma/leukemia (BL) with IG-MYC rearrangement displaying a B-cell precursor immunophenotype (termed herein "preBLL"). To characterize the molecular pathogenesis of preBLL, we investigated 13 preBLL cases (including 1 cell line), of which 12 were analyzable using genome, exome, and targeted sequencing, imbalance mapping, and DNA methylation profiling. In 5 patients with reads across ...[more]

PMID: 30282799

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The genomic landscape of Burkitt Lymphoma

Project description:As part of the ICGC, the ICGC MMML-Seq project performed whole genome sequencing and RNA sequencing of Burkitt Lymphomas . Burkitt lymphomas are the most common B-cell lymphomas in childhood. Analyses were performed in concordance with the guidelines of the ICGC. The results define the genomic landscape of structural variants, somatic single nucleotide variants and mutational signatures in these lymphomas.

| EGAS00001002198 | EGA

IG-MYC-positive neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas

Project description:Genome wide DNA methylation profiling of Burkitt lymphoma subsets. The Illumina Infinium HumanMethylationEPIC BeadChip was used to obtain DNA methylation profiles across approximately 85,000 CpGs in B-cell lymphoma samples. Samples included 2 primary IG-MYC-positive B-cell neoplasms with precursor B-cell phenotype and 5 Burkitt lymphoma.

2018-10-08 | GSE114210 | GEO

The genomic landscape of germinal center derived B-cell lymphomas other than follicular, diffuse-large B-cell and Burkitt lymphom

Project description:As part of the ICGC, the ICGC MMML-Seq project performed whole genome sequencing and RNA sequencing of germinal center derived B-cell lymphoma. Analyses were performed in concordance with the guidelines of the ICGC.

| EGAS00001002422 | EGA

IG-MYC + neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas.

Project description:The WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue notes instances of Burkitt lymphoma/leukemia (BL) with IG-MYC rearrangement displaying a B-cell precursor immunophenotype (termed herein "preBLL"). To characterize the molecular pathogenesis of preBLL, we investigated 13 preBLL cases (including 1 cell line), of which 12 were analyzable using genome, exome, and targeted sequencing, imbalance mapping, and DNA methylation profiling. In 5 patients with reads across the IG-MYC breakpoint junctions, we found evidence that the translocation derived from an aberrant VDJ recombination, as is typical for IG translocations arising in B-cell precursors. Genomic changes like biallelic IGH translocations or VDJ rearrangements combined with translocation into the VDJ region on the second allele, potentially preventing expression of a productive immunoglobulin, were detected in 6 of 13 cases. We did not detect mutations in genes frequently altered in BL, but instead found activating NRAS and/or KRAS mutations in 7 of 12 preBLLs. Gains on 1q, recurrent in BL and preB lymphoblastic leukemia/lymphoma (pB-ALL/LBL), were detected in 7 of 12 preBLLs. DNA methylation profiling showed preBLL to cluster with precursor B cells and pB-ALL/LBL, but apart from BL. We conclude that preBLL genetically and epigenetically resembles pB-ALL/LBL rather than BL. Therefore, we propose that preBLL be considered as a pB-ALL/LBL with recurrent genetic abnormalities.

| S-EPMC6251006 | biostudies-literature

Burkitt Lymphoma beyond MYC translocation:N-MYC and DNA methyl transferases dysregulation

Project description:Identification of miRNA differentially expressed between MYC-translocation positive and and MYC-translocation negative Burkitt Lymphoma and their impact on gene expression profile Study of microRNA profile of MYC-translocation positive and MYC-translocation negative Burkitt Lymphoma cases in order to uncover possible differences at the molecular level

2015-08-05 | E-GEOD-71471 | biostudies-arrayexpress

IG-MYC-positive neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas

Project description:IG-MYC-positive neoplasms with precursor B-cell phenotype are molecularly distinct from Burkitt lymphomas

| PRJNA470587 | ENA

Burkitt Lymphoma beyond MYC translocation:N-MYC and DNA methyl transferases dysregulation

2015-08-05 | GSE71471 | GEO

Expression data from Burkitt lymphoma cases

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

Comparing sequencing of four proto-typical Burkitt lymphomas (BL) with IG-MYC translocation.

Project description:By whole-genome, exome, transcriptome and methylome sequencing of four proto-typical Burkitt lymphomas (BL) with IG-MYC translocation we identified seven recurrently mutated genes including ID3. In an extended cohort, 36/53 (68%) molecularly-defined BL carried potentially damaging mutations of ID3 which were enriched at somatic hypermutation motifs. Only 6/47 (13%) other IG-MYC-positive B-cell lymphomas carried ID3 mutations suggesting cooperation of ID3 inactivation and IG-MYC translocation to be a hallmark of Burkitt lymphomagenesis.

| EGAS00001000271 | EGA

JNK/AP1 Pathway Regulates MYC Expression and BCR Signaling through Ig Enhancers in Burkitt Lymphoma Cells.

Project description:In Burkitt lymphoma (BL), a chromosomal translocation by which the MYC gene is fused to an immunoglobulin (Ig) gene locus is frequently found. The translocated MYC gene is overexpressed, which is the major driver of BL tumorigenesis. Studies have shown that Ig enhancers are essential for MYC overexpression, but the involved mechanisms are not fully understood. In addition, the survival of BL cells relies on B-cell receptor (BCR) signaling, which is determined by the levels of Ig molecules expressed on the cell surface. However, whether MYC has any impact on Ig expression and its functional relevance in BL has not been investigated. Herein, we show that MYC upregulates Ig kappa (Ig?) expression in BL cells through two Ig? enhancers, the intronic enhancer (Ei) and the 3' enhancer (E3'). Mechanistically, by activating the JNK pathway, MYC induces the phosphorylation of c-Fos/c-Jun and their recruitment to AP1 binding sites in the Ig? enhancers, leading to the activation of the enhancers and subsequent Ig? upregulation. The AP1-mediated activation of the Ig? enhancers is also required for the expression of the translocated MYC gene, indicating positive feedback for the MYC overexpression in BL cells. Importantly, interrupting the JNK pathway inhibits both Ig? and MYC gene expression and suppresses BL cell proliferation. Our study not only reveals a novel mechanism underlying MYC overexpression in BL but also suggests that targeting the JNK pathway may provide a unique strategy to suppress BL tumorigenesis.

| S-EPMC6959055 | biostudies-literature