Chromosomal translocations and their role in the pathogenesis of non-Hodgkin’s lymphomas

Vega, Francisco; Orduz, Rocío; Medeiros, L. Jeffrey

doi:10.1080/0031302021000009306

Cited by 36 publications

(50 citation statements)

References 126 publications

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“…CD10 positivity (which must be confirmed by morphology to be on tumor cells and not on residual reactive or colonized follicles) indicates FL, and this diagnosis can be confirmed further by staining for BCL6 and BCL2, and detection of t(14;18) by FISH or PCR, because BCL2 resulting from t(14;18) is overexpressed in 90% of cases of FL. 51 FL is also CD20+, CD5-, and cyclin D1-, and nodular aggregates of CD21+ or CD23+ follicular dendritic cells (FDCs) will usually be found. When CD10 is negative, the differential diagnosis includes marginal zone lymphomas, lymphoplasmacytic lymphomas, and HCL; immunophenotypic analysis of CD103 and CD25 can be used to identify HCL.…”

Section: Immunophenotyping Algorithmmentioning

confidence: 99%

“…In adults, when Burkitt's lymphoma is suspected, FISH for MYC, BCL2, and possibly BCL6 should be performed to confirm the presence of MYC rearrangement and assess for the presence of a dual rearrangement of MYC and BCL2 (double hit), particularly if BCL2 is expressed. 51 If MYC is positive and BCL2 and BCL6 are not rearranged, Burkitt's lymphoma may be diagnosed. If BCL2 or BCL6 is rearranged, with or without MYC, the diagnosis could be U-DLBCL/Burkitt's lymphoma.…”

Section: Immunophenotyping Algorithmmentioning

confidence: 99%

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Non-Hodgkin’s Lymphomas

Ad¹,

Js²,

Rh³

et al. 2010

J Natl Compr Canc Netw

223

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OverviewNon-Hodgkin's lymphomas (NHLs) are a heterogeneous group of lymphoproliferative disorders originating in B-, T-, or natural killer (NK) lymphocytes. In the United States, B-cell lymphomas represent 80% to 85% of all cases, with 15% to 20% being T-cell lymphomas; NK lymphomas are very rare. In 2009, an estimated 65,980 new cases of NHL will be diagnosed and 19,500 will die of the disease.1 NHL is the sixth leading site of new cancer cases among men and fifth among women, accounting for 4% to 5% of new cancer cases and 3% to 4% of cancer-related deaths. Non-Hodgkin's Lymphomas Clinical Practice Guidelines in OncologyKey Words NCCN Clinical Practice Guidelines, non-Hodgkin's lymphoma, chronic lymphocytic leukemia, follicular lymphoma, diffuse large B-cell lymphoma, mantle cell lymphoma, peripheral T-cell lymphoma, cutaneous T-cell lymphoma, mycosis fungoides, Sézary syndrome, marginal zone lymphoma, mucosaassociated lymphoid tissue lymphoma, diagnosis, treatment, hematopathology, immunohistochemistry, treatment guidelines, staging evaluation, lymphoma pathology (JNCCN 2010;8:288-334) NCCN Categories of Evidence and ConsensusCategory 1: The recommendation is based on high-level evidence (e.g., randomized controlled trials) and there is uniform NCCN consensus. Category 2A: The recommendation is based on lowerlevel evidence and there is uniform NCCN consensus. Category 2B: The recommendation is based on lowerlevel evidence and there is nonuniform NCCN consensus (but no major disagreement). Category 3: The recommendation is based on any level of evidence but reflects major disagreement. Please NoteThese guidelines are a statement of consensus of the authors regarding their views of currently accepted approaches to treatment. Any clinician seeking to apply or consult these guidelines is expected to use independent medical judgment in the context of individual clinical circumstances to determine any patient's care or treatment. The National Comprehensive Cancer Network makes no representation or warranties of any kind regarding their content, use, or application and disclaims any responsibility for their applications or use in any way.These guidelines are copyrighted by the National Comprehensive Cancer Network. All rights reserved. These guidelines and the illustrations herein may not be reproduced in any form without the express written permission of the NCCN © 2010. Disclosures for the NCCN Non-Hodgkin's Lymphomas Guidelines PanelAt the beginning of each NCCN guidelines panel meeting, panel members disclosed any financial support they have received from industry. Through 2008, this information was published in an aggregate statement in JNCCN and online. Furthering NCCN's commitment to public transparency, this disclosure process has now been expanded by listing all potential conflicts of interest respective to each individual expert panel member.Individual disclosures for the NCCN Non-Hodgkin's Lymphomas Guidelines Panel members can be found on page 334. (To view the most recent version of these guideli...

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Section: Immunophenotyping Algorithmmentioning

confidence: 99%

Section: Immunophenotyping Algorithmmentioning

confidence: 99%

Non-Hodgkin’s Lymphomas

Ad¹,

Js²,

Rh³

et al. 2010

J Natl Compr Canc Netw

223

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“…Approximately 80-90% of follicular lymphomas and 20-30% of diffuse large B-cell lymphomas carry this translocation. 1,2 As a result of the t(14;18), the BCL2 gene at 18q21 is juxtaposed with the immunoglobulin heavy chain (IGH) gene on the derivative chromosome 14, resulting in overexpression of BCL-2, an antiapoptotic molecule.…”

mentioning

confidence: 99%

“…[1][2][3] Via these translocations, the c-MYC gene is juxtaposed with the IGH gene on the derivative chromosome 14, or the immunoglobulin light chain genes are juxtaposed with c-MYC on the derivative chromosome 8. This results in overexpression of c-MYC, driving cell proliferation and expression of other genes involved in cell growth.…”

mentioning

confidence: 99%

Lymphoid neoplasms associated with concurrent t(14;18) and 8q24/c-MYC translocation generally have a poor prognosis

et al. 2006

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We identified 14 B-cell neoplasms with concurrent t(14;18) and chromosome 8q24 or c-MYC translocations shown by conventional cytogenetics or fluorescence in situ hybridization analysis. All cases assessed by conventional cytogenetics had a complex karyotype. There were 10 men and four women, with a median age of 55 years (range, 29-72). None of these patients had a history of follicular lymphoma. The biopsy specimens were obtained from bone marrow, lymph node, and extranodal sites. Morphologically, nine neoplasms had features of Burkitt or atypical Burkitt lymphoma/leukemia and three were diffuse large B-cell lymphoma with high-grade cytologic features. The remaining two cases were plasmablastic myeloma and low-grade B-cell lymphoma, respectively. All cases expressed BCL-2. The proliferation index assessed by using Ki-67 (MIB1) was 5% in the low-grade B-cell lymphoma, 80% in the plasmablastic myeloma, 90-95% in three cases of diffuse large B-cell lymphoma, and ranged from 90 to 499% in most Burkitt and atypical Burkitt neoplasms. The patient with low-grade B-cell lymphoma was treated with rituximab. All other patients received intensive combination chemotherapy. Two of these patients underwent bone marrow transplantation, and one patient received radiation therapy in addition to transplantation. The median follow-up period was 9 months (range, 3-81). In all, 10 patients died with a median survival of 9 months (range, 3-81). We conclude that most B-cell lymphomas with concurrent t(14;18) and 8q24/c-MYC translocations fall within the morphologic spectrum of diffuse large B-cell and Burkitt lymphoma. These neoplasms are high-grade and are associated with a poor prognosis. However, this combination of molecular abnormalities can also rarely occur in other neoplasms, such as the cases of low-grade B-cell lymphoma and plasmablastic myeloma in this study.

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“…The precise molecular mechanisms leading to chromosomal translocations remain largely unknown. In cases where IGH or TCR loci are involved, there is compelling evidence that the translocation is caused by mistakes in normal V(D)J recombinase activity, as evidenced by the presence of cryptic heptamer/nonamer sequences, the addition of nontemplated nucleotides at breakpoints, and exonucleolytic deletion of germline nucleotides at these breakpoint junctions (Ferguson and Alt, 2001;Vega and Medeiros, 2003). In other translocations, homologous recombination between Alu repeats has been implicated as in the case of partial tandem duplications of MLL (Strissel et al, 1998;Strout et al, 1998;Whitman et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

ReviewLeukemia/lymphoma-associated gene fusions in normal individuals

Ms¹

2008

Genet. Mol. Res.

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ABSTRACT. Hematopoietic neoplasias are characterized by recurrent chromosomal aberrations that result in the formation of gene fusions and the subsequent expression of chimeric proteins with unique properties. However, in recent years, different lymphoma/leukemia-associated rearrangements, such as BCR/ABL, IGH/BCL2, ETV6/RUNX1 and MLL duplications, have been detected in healthy individuals. The presence of these rearrangements indicates that such translocations can be generated in normal hematopoietic cells without apparent oncogenic consequences. This article reviews and discusses the data available in the literature.

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Chromosomal translocations and their role in the pathogenesis of non-Hodgkin’s lymphomas

Cited by 36 publications

References 126 publications

Non-Hodgkin’s Lymphomas

Non-Hodgkin’s Lymphomas

Lymphoid neoplasms associated with concurrent t(14;18) and 8q24/c-MYC translocation generally have a poor prognosis

ReviewLeukemia/lymphoma-associated gene fusions in normal individuals

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