Post-transplant molecularly defined Burkitt lymphomas are frequently MYC-negative and characterized by the 11q-gain/loss pattern

Ferreiro, Julio Finalet; Morscio, Julie; Dierickx, Daan; Marcelis, Lukas; Verhoef, Gregor; Vandenberghe, Peter; Tousseyn, Thomas; Włodarska, Iwona

doi:10.3324/haematol.2015.124305

Cited by 79 publications

(61 citation statements)

References 13 publications

(8 reference statements)

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“…Instead, they have a chromosome 11q alteration characterized by proximal gains and telomeric losses. 82,83 Compared with BL, these lymphomas have more complex karyotypes, lower levels of MYC expression, a certain degree of cytological pleomorphism, occasionally a follicular pattern, and frequently a nodal presentation. The clinical course seems to be similar to BL, but the number of cases reported is still limited.…”

Section: -81mentioning

confidence: 99%

The 2016 revision of the World Health Organization classification of lymphoid neoplasms

Swerdlow

Campo

Pileri

et al. 2016

Blood

6,688

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A revision of the nearly 8-year-old World Health Organization classification of the lymphoid neoplasms and the accompanying monograph is being published. It reflects a consensus among hematopathologists, geneticists, and clinicians regarding both updates to current entities as well as the addition of a limited number of new provisional entities. The revision clarifies the diagnosis and management of lesions at the very early stages of lymphomagenesis, refines the diagnostic criteria for some entities, details the expanding genetic/molecular landscape of numerous lymphoid neoplasms and their clinical correlates, and refers to investigations leading to more targeted therapeutic strategies. The major changes are reviewed with an emphasis on the most important advances in our understanding that impact our diagnostic approach, clinical expectations, and therapeutic strategies for the lymphoid neoplasms.

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Section: -81mentioning

confidence: 99%

The 2016 revision of the World Health Organization classification of lymphoid neoplasms

Swerdlow

Campo

Pileri

et al. 2016

Blood

6,688

6,518

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“…Recently, a subgroup of germinal center-derived B-cell (GCB) lymphomas has been described that resembles Burkitt lymphoma (BL) with regard to morphology, immunophenotype, and gene-expression profile but it lacks the IG-MYC translocation typical for BL. [1][2][3][4][5] Instead, these cases are cytogenetically characterized by a peculiar pattern of an 11q aberration consisting of a gain in 11q23.2-23.3 followed by a telomeric loss in 11q24.1-qter. According to the revised 4th edition of the WHO Classification of Tumours of Haematopoietic and Lymphoid Tissue, these lymphomas have been described as a new provisional entity called "Burkitt-like lymphoma with 11q aberration" (abbreviated herein as "mnBLL,11q,").…”

Section: Introductionmentioning

confidence: 99%

The mutational landscape of Burkitt-like lymphoma with 11q aberration is distinct from that of Burkitt lymphoma

Wagener

Seufert

Raimondi³

et al. 2019

Blood

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The new recently described provisional lymphoma category Burkitt-like lymphoma with 11q aberration comprises cases similar to Burkitt lymphoma (BL) on morphological, immunophenotypic and gene-expression levels but lacking the IG-MYC translocation. They are characterized by a peculiar imbalance pattern on chromosome 11, but the landscape of mutations is not yet described. Thus, we investigated 15 MYC-negative Burkitt-like lymphoma with 11q aberration (mnBLL,11q,) cases by copy-number analysis and whole-exome sequencing. We refined the regions of 11q imbalance and identified the INO80 complex-associated gene NFRKB as a positional candidate in 11q24.3. Next to recurrent gains in 12q13.11-q24.32 and 7q34-qter as well as losses in 13q32.3-q34, we identified 47 genes recurrently affected by protein-changing mutations (each ≥3 of 15 cases). Strikingly, we did not detect recurrent mutations in genes of the ID3-TCF3 axis or the SWI/SNF complex that are frequently altered in BL, or in genes frequently mutated in germinal center–derived B-cell lymphomas like KMT2D or CREBBP. An exception is GNA13, which was mutated in 7 of 15 cases. We conclude that the genomic landscape of mnBLL,11q, differs from that of BL both at the chromosomal and mutational levels. Our findings implicate that mnBLL,11q, is a lymphoma category distinct from BL at the molecular level.

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“…The mBL signature confirmed the presence of rare cases of histologically BL lacking c-MYC rearrangement, but instead had chromosome 11q aberrations characterized by interstitial gains at 11q23.2-q23.3 and telomeric losses of 11q24.1-qter [74,75]. Gains at 11q23 are associated with overexpression of genes including platelet-activating factor acetylhydrolase IB subunit beta ( PAFAH1B2) , while telomeric losses contained a focal homozygous deletion in 11q24.2-q24.3 including the ETS proto-oncogene 1 ( ETS1) gene.…”

Section: C-myc In Burkitt Lymphomamentioning

confidence: 88%

The Role of c-MYC in B-Cell Lymphomas: Diagnostic and Molecular Aspects

Nguyen

Papenhausen

Shao

2017

Genes

137

101

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c-MYC is one of the most essential transcriptional factors, regulating a diverse array of cellular functions, including proliferation, growth, and apoptosis. Dysregulation of c-MYC is essential in the pathogenesis of a number of B-cell lymphomas, but is rarely reported in T-cell lymphomas. c-MYC dysregulation induces lymphomagenesis by loss of the tight control of c-MYC expression, leading to overexpression of intact c-MYC protein, in contrast to the somatic mutations or fusion proteins seen in many other oncogenes. Dysregulation of c-MYC in B-cell lymphomas occurs either as a primary event in Burkitt lymphoma, or secondarily in aggressive lymphomas such as diffuse large B-cell lymphoma, plasmablastic lymphoma, mantle cell lymphoma, or double-hit lymphoma. Secondary c-MYC changes include gene translocation and gene amplification, occurring against a background of complex karyotype, and most often confer aggressive clinical behavior, as evidenced in the double-hit lymphomas. In low-grade B-cell lymphomas, acquisition of c-MYC rearrangement usually results in transformation into highly aggressive lymphomas, with some exceptions. In this review, we discuss the role that c-MYC plays in the pathogenesis of B-cell lymphomas, the molecular alterations that lead to c-MYC dysregulation, and their effect on prognosis and diagnosis in specific types of B-cell lymphoma.

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Post-transplant molecularly defined Burkitt lymphomas are frequently MYC-negative and characterized by the 11q-gain/loss pattern

Cited by 79 publications

References 13 publications

The 2016 revision of the World Health Organization classification of lymphoid neoplasms

The 2016 revision of the World Health Organization classification of lymphoid neoplasms

The mutational landscape of Burkitt-like lymphoma with 11q aberration is distinct from that of Burkitt lymphoma

The Role of c-MYC in B-Cell Lymphomas: Diagnostic and Molecular Aspects

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