BCL3 rearrangement and t(14;19)(q32;q13) in lymphoproliferative disorders

Michaux, Lucienne; Mecucci, Cristina; Stul, Michel; Włodarska, Iwona; Hernández, Jesús M.; Meeus, Peter; Michaux, Jean‐Louis; Scheiff, Jean-Marie; Noël, H.; Lodwagie, Andries; Criel, A.; Boogaerts, Marc; Orshoven, Angeline Van; Cassiman, Jean‐Jacques; Berghe, Herman Van den

doi:10.1002/(sici)1098-2264(199601)15:1<38::aid-gcc6>3.0.co;2-5

Cited by 56 publications

(39 citation statements)

References 32 publications

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“…2,7,12,[27][28][29] In these reported cases, aberrant immunophenotype (CD11c expression), atypical morphology, young patient age, and progressive disease were common. 2,12,28 In this study, BCL-3 positivity was found in one of 17 small lymphocytic lymphoma/chronic lymphocytic leukemia cases assessed. In the BCL-3 positive case, the patient was 65 years old and the morphology was typical.…”

Section: Bcl-3 In Lymphomasmentioning

confidence: 94%

Immunohistochemical detection of BCL-3 in lymphoid neoplasms: a survey of 353 cases

et al. 2004

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The bcl-3 gene at chromosome 19q13 encodes a member of the IjB family involved in regulating the NFjB pathway. Originally identified by its involvement in the rare t(14:19)(q32;q13), BCL-3 expression has never been analyzed in a wide variety of lymphomas. We assessed BCL-3 expression in 353 cases of non-Hodgkin lymphoma and Hodgkin lymphoma using formalin-fixed, paraffin-embedded tissue specimens, a monoclonal antibody specific for BCL-3, and immunohistochemical methods. Of 172 B-cell lymphomas, 10 (6%) were positive for BCL-3, including six of 23 (26%) diffuse large B-cell lymphoma, one of 17 (6%) small lymphocytic lymphoma, one of 26 (4%) follicular lymphoma, and two of 49 (4%) mantle cell lymphoma. All other B-cell neoplasms were negative, including marginal zone lymphoma (n ¼ 24, 11 extranodal, nine nodal, four splenic), Burkitt lymphoma (n ¼ 10), lymphoplasmacytic lymphoma (n ¼ 10), lymphoblastic lymphoma (n ¼ 8), and plasmacytoma (n ¼ 5). Of 111 T/NK-cell lymphomas, 25 (23%) were positive for BCL-3, including 13 of 40 (32%) anaplastic large-cell lymphoma, three of 10 (30%) angioimmunoblastic T-cell lymphoma, two of eight (25%) extranodal NK/T-cell lymphoma of nasal type, three of 12 (25%) mycosis fungoides, one of five (20%) enteropathy-type T-cell lymphoma, and two of 21 (10%) peripheral T-cell lymphoma unspecified. All other T-cell neoplasms were negative, including lymphoblastic lymphoma (n ¼ 6), prolymphocytic leukemia (n ¼ 6), and subcutaneous panniculitis-like T-cell lymphoma (n ¼ 3). Of 70 Hodgkin lymphomas, of all types, 29 (41%) were positive for BCL-3. The relatively high frequency of BCL-3 expression in some non-Hodgkin and Hodgkin lymphoma types raises the possibility that BCL-3 is involved in the pathogenesis of these tumors, and may be a target of new therapies.

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Section: Bcl-3 In Lymphomasmentioning

confidence: 94%

Immunohistochemical detection of BCL-3 in lymphoid neoplasms: a survey of 353 cases

et al. 2004

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“…The 5 0 end of the BCL-3 gene can be located quite near to the breakpoint or up to 16 kbp away; however, inevitably the translocation results in increased expression of BCL-3 mRNA and protein (McKeithan et al, 1997). In addition, t(14;19) translocations involving BCL-3 have been identified in some lymphomas (Nakagawa et al, 1995;Yano et al, 1995;McKeithan et al, 1997;Au et al, 2002;Soma et al, 2006) and occasionally in lymphoproliferative disorders (Michaux et al, 1996); furthermore, other genetic alterations on chromosome 19 may also lead to increased BCL-3 expression (Schlette et al, 2005). The hypothesis that increased expression of BCL-3 contributes to human B-cell malignancies is supported by several findings: (1) transgenic mice in which BCL-3 is under the control of the m heavy chain enhancer develop splenomegaly and have excess mature B cells in their bone marrow and lymph nodes (Ong et al, 1998); (2) overexpression of BCL-3 can transform mouse 3T3 cells in culture (Viatour et al, 2004); (3) overexpression of BCL-3 can enhance the survival of activated T cells (Mitchell et al, 2001) and (4) elevated levels of BCL-3 are seen in many lymphoid and non-lymphoid human tumor samples (Cogswell et al, 2000;Rassidakis et al, 2003;Canoz et al, 2004;Pallares et al, 2004;Ohno et al, 2005;Schlette et al, 2005).…”

Section: Multiple Familial Trichoepitheliomamentioning

confidence: 99%

Mutations in the NF-κB signaling pathway: implications for human disease

2006

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“…Non-CLL-type B-cell malignancies with t(14;19)(q32;q13) have been diagnosed as FL, diffuse large B-cell lymphoma (DLBCL), Burkitt-like lymphoma, splenic B-cell lymphoma (SBCL), splenic marginal zone lymphoma (SMZL) and even classical Hodgkin lymphoma (cHL). 1,11,[13][14][15][16][17][18] However, according to our diagnostic experience, t(14;19)-positive lymphomas are difficult to diagnose. Thus, it seems that the presence of a t(14;19)(q32;q13) is not associated with a clearly defined entity in the World Health Organization classification, 11 although B-CLL is the predominant diagnosis.…”

Section: Introductionmentioning

confidence: 99%

A comprehensive genetic and histopathologic analysis identifies two subgroups of B-cell malignancies carrying a t(14;19)(q32;q13) or variant BCL3-translocation

et al. 2007

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The biologic and pathologic features of B-cell malignancies bearing a translocation t(14;19)(q32;q13) leading to a fusion of IGH and BCL3 are still poorly described. Herein we report the results of a comprehensive cytogenetic, fluorescence in situ hybridization (FISH), molecular and histopathological survey of a large series of B-cell malignancies with t(14;19) or variant translocations. A total of 56 B-cell malignancies with a FISHproven BCL3 involvement were identified with the translocation partners being IGH (n ¼ 51), IGL (n ¼ 2), IGK (n ¼ 2) and a non-IG locus (n ¼ 1). Hierarchical clustering of chromosomal changes associated with the t(14;19) indicated the presence of two different groups of IG/BCL3-positive lymphatic neoplasias. The first group included 26 B-cell malignancies of various histologic subtypes containing a relatively high number of chromosomal changes and mostly mutated IgVH genes. This cluster displayed three cytogenetic branches, one with rearrangements in 7q, another with deletions in 17p and a third one with rearrangements in 1q and deletions in 6q and 13q. The second group included 19 cases, mostly diagnosed as B-cell chronic lymphocytic leukemia (B-CLL), and characterized by few additional chromosomal changes (e.g. trisomy 12) and unmutated IgVH genes. In conclusion, our study indicates that BCL3 translocations are not restricted to B-CLL but present in a heterogeneous group of B-cell malignancies.

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BCL3 rearrangement and t(14;19)(q32;q13) in lymphoproliferative disorders

Cited by 56 publications

References 32 publications

Immunohistochemical detection of BCL-3 in lymphoid neoplasms: a survey of 353 cases

Immunohistochemical detection of BCL-3 in lymphoid neoplasms: a survey of 353 cases

Mutations in the NF-κB signaling pathway: implications for human disease

A comprehensive genetic and histopathologic analysis identifies two subgroups of B-cell malignancies carrying a t(14;19)(q32;q13) or variant BCL3-translocation

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