IGH switch breakpoints in Burkitt lymphoma: Exclusive involvement of noncanonical class switch recombination

Guikema, Jeroen E. J.; Boer, Conny de; Haralambieva, Eugenia; Smit, Laura A.; Noesel, Carel J. M. van; Schuuring, Ed; Kluin, Philippus

doi:10.1002/gcc.20345

Cited by 20 publications

(10 citation statements)

References 40 publications

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“…Nevertheless, all these methods can fail to detect IG-M yc fusions [65]. The most reliable method is cytogenetic analysis by fluorescence in situ hybridization (FISH).…”

Section: Resultsmentioning

confidence: 99%

MYC chromosomal aberration in differential diagnosis between Burkitt and other aggressive lymphomas

Aquino

Marra

Cantile

et al. 2013

Infect Agents Cancer

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Myc oncogenetic deregulation is abundantly described in several solid human cancer and lymphomas. Particularly, Burkitt's lymphoma belongs to the family of B Non Hodgkin aggressive lymphomas. Although it is morphologically characterized, immunophenotypic and cytogenetic diagnosis remains complex. In 2008, the WHO has introduced a new diagnostic class of aggressive B-cell lymphomas with features intermediate between BL and DLBCL. This diagnostic class represents a temporary container of aggressive B-cell lymphomas, not completely belonging to the BL and DLBCL categories. The importance of establishing a correct diagnosis would allow a better prognostic classification and a better therapeutic approach. In this review, we summarize the main diagnostic approaches necessary for appropriate diagnoses and we emphasize the importance of cytogenetic analysis of the oncogene Myc in the histopathological diagnosis and the prognostic/predictive stratification. In this contest, Myc represents the more involved gene in the development of these lymphomas. Therefore, we analyze the genetic aberrations causing its over-expression and the concomitant deregulation of molecular pathways related to it. We also propose a FISH approach useful in the diagnosis of these lymphomas.

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“…Nevertheless, all these methods can fail to detect IG-M yc fusions [65]. The most reliable method is cytogenetic analysis by fluorescence in situ hybridization (FISH).…”

Section: Resultsmentioning

confidence: 99%

MYC chromosomal aberration in differential diagnosis between Burkitt and other aggressive lymphomas

Aquino

Marra

Cantile

et al. 2013

Infect Agents Cancer

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“…Interestingly however, Myc, is typically expressed only when positively selected centrocytes are moving back to the DZ, where it is again suppressed [64,65]. Myc translocation patterns in sporadic BL suggest derivation from CSR events [66,67]. Therefore, one possibility is that low levels of AID activity [59,60,68] [34].…”

Section: Physiological Role Of E and Id Proteins In B Cell Developmentmentioning

confidence: 99%

Paradoxical role of Id proteins in regulating tumorigenic potential of lymphoid cells

Roy

Zhuang

2018

Front. Med.

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A family of transcription factors known as Id proteins, or inhibitor of DNA binding and differentiation, is capable of regulating cell proliferation, survival and differentiation, and is often upregulated in multiple types of tumors. Due to their ability to promote self-renewal, Id proteins have been considered as oncogenes, and potential therapeutic targets in cancer models. On the contrary, certain Id proteins are reported to act as tumor suppressors in the development of Burkitt's lymphoma in humans, and hepatosplenic and innate-like T cell lymphomas in mice. The contexts and mechanisms by which Id proteins can serve in such contradictory roles to determine tumor outcomes are still not well understood. In this review, we explore the roles of Id proteins in lymphocyte development and tumorigenesis, particularly with respect to inhibition of their canonical DNA binding partners known as E proteins. Transcriptional regulation by E proteins, and their antagonism by Id proteins, act as gatekeepers to ensure appropriate lymphocyte development at key checkpoints. We re-examine the derailment of these regulatory mechanisms in lymphocytes that facilitate tumor development. These mechanistic insights can allow better appreciation of the context-dependent roles of Id proteins in cancers and improve considerations for therapy.

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“…In the endemic cases, EBV-positive MYC/Ig breakpoints originate from aberrant somatic hypermutation, while in the EBV-negative sporadic cases, MYC translocations mostly involve the Ig switch regions of the IGH locus. 191,192 In EBV-positive tumor cells, the growth-transforming program of viral gene expression (latency III) is extinguished, and only the EBV nuclear antigen (EBNA)1 is expressed via the alternative latency I program. Gene expression profiling studies in EBV-positive and -negative BL found significant differences in the expression of viral micro-RNAs and in selected target genes: LIN28B, CGNL1, GCET2, MRAS, PLCD4, SEL1L, SXX1, STK10/STK33L.…”

Section: Diffuse Large B-cell Lymphomamentioning

confidence: 99%

Clinical utility of recently identified diagnostic, prognostic, and predictive molecular biomarkers in mature B-cell neoplasms

2017

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Genomic profiling studies have provided new insights into the pathogenesis of mature B-cell neoplasms and have identified markers with prognostic impact. Recurrent mutations in tumor-suppressor genes (TP53, BIRC3, ATM), and common signaling pathways, such as the B-cell receptor (CD79A, CD79B, CARD11, TCF3, ID3), Toll-like receptor (MYD88), NOTCH (NOTCH1/2), nuclear factor-κB, and mitogen activated kinase signaling, have been identified in B-cell neoplasms. Chronic lymphocytic leukemia/small lymphocytic lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, mantle cell lymphoma, Burkitt lymphoma, Waldenström macroglobulinemia, hairy cell leukemia, and marginal zone lymphomas of splenic, nodal, and extranodal types represent examples of B-cell neoplasms in which novel molecular biomarkers have been discovered in recent years. In addition, ongoing retrospective correlative and prospective outcome studies have resulted in an enhanced understanding of the clinical utility of novel biomarkers. This progress is reflected in the 2016 update of the World Health Organization classification of lymphoid neoplasms, which lists as many as 41 mature B-cell neoplasms (including provisional categories). Consequently, molecular genetic studies are increasingly being applied for the clinical workup of many of these neoplasms. In this review, we focus on the diagnostic, prognostic, and/or therapeutic utility of molecular biomarkers in mature B-cell neoplasms.

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IGH switch breakpoints in Burkitt lymphoma: Exclusive involvement of noncanonical class switch recombination

Cited by 20 publications

References 40 publications

MYC chromosomal aberration in differential diagnosis between Burkitt and other aggressive lymphomas

MYC chromosomal aberration in differential diagnosis between Burkitt and other aggressive lymphomas

Paradoxical role of Id proteins in regulating tumorigenic potential of lymphoid cells

Clinical utility of recently identified diagnostic, prognostic, and predictive molecular biomarkers in mature B-cell neoplasms

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