A new case of t(14;19) (q32;q13) in a patient with follicular lymphoma in leukemic phase

Solé, Françesc; Woessner, S; Florensa, Lourdes; Pérez-Losada, A.; Bonet, Carles; Besses, Carles

doi:10.1016/0165-4608(94)90219-4

Cited by 14 publications

(12 citation statements)

References 8 publications

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“…However, case reports indicate that BCL3 translocations are present in multiple pathologies, not only B-cell non-Hodgkin lymphomas, but also Hodgkin lymphomas and T-cell lymphomas (fusing BCL3 to TCRAD instead of to IGH). [1][2][3]5,11,[13][14][15][16][17][18] In agreement with these findings, immunohistochemical studies have identified the presence of BCL3 expression in both B-and T-cell lymphomas pointing to a role of BCL3 in B-and T-cell lymphomagenesis. 33,34 The major aim of the present study was to perform a thorough cytogenetic, FISH, molecular and histopathologic study of B-cell malignancies bearing a t(14;19)(q32;q13) or variant translocations to shed further light on these pathologic associations.…”

Section: Discussionsupporting

confidence: 71%

“…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%

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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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Section: Discussionsupporting

confidence: 71%

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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“…5 The t (14;19) or bcl-3 gene rearrangement has been reported rarely in non-Hodgkin lymphomas, in approximately 35 cases, mostly in cases of chronic lymphocytic leukemia/small lymphocytic lymphoma, and less frequently in cases designated as follicular lymphoma, diffuse large B-cell lymphoma, Burkitt-like lymphoma, and one case of acute biphenotypic leukemia. [6][7][8][9][10][11][12] Although the t(14;19) is rare, BCL-3 expression has been shown in a few types of non-Hodgkin lymphoma not known to carry the t (14;19). For example, two recent studies have shown high levels of BCL-3 expression in ALKpositive anaplastic large-cell lymphoma.…”

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confidence: 99%

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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“…However, the role of bcl-2 gene and its family members remains to be fully de®ned in normal and neoplastic lymphoid tissues (Hamilton et al, 1991;Zutter et al, 1991;Yano et al, 1992) and in persons with follicular lymphoma in which other genetic translocations have been identi®ed (Frizzera et al, 1991;Hillion et al, 1991;Ladanyi et al, 1992;Rimokh et al, 1993;Straka et al, 1993;Sole et al, 1994;Wlodarska et al, 1994). Other variations in FL presentation include a transcriptionally silent rearranged bcl-2 gene (Wang et al, 1993) and the¯oral variant (Goates et al, 1994).…”

Section: Discussionmentioning

confidence: 99%

“…When evaluating the Em-N-myc mouse disease system as a possible candidate model for human FL, we must consider that numerous variant forms of human follicular lymphoma have been reported that re¯ect considerable heterogeneity in disease presentation with regard to translocations including t(14;18), t(11;14), t(2;18), t(8;14) and t(14;19), expression levels of bcl-2 protein and disruption of the c-myc gene (Frizzera et al, 1991;Hamilton et al, 1991;Hillion et al, 1991;Price et al, 1991;Zutter et al, 1991;Ladyani et al, 1992;Yano et al, 1992;Finke et al, 1993;Mitani et al, 1993;Rimokh et al, 1993;Straka et al, 1993;Wang et al, 1993;Goates et al, 1994;Marin et al, 1994;Sole et al, 1994;Wlodarska et al, 1994). The role of bcl-2 protein in human FL is not entirely clear.…”

Section: Discussionmentioning

confidence: 99%

Transgenic N-myc mouse model for indolent B cell lymphoma: tumor characterization and analysis of genetic alterations in spontaneous and retrovirally accelerated tumors

et al. 1998

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Little is known about stepwise deregulation of speci®c genes leading to lymphoid malignancy. Aberrant myc gene expression in transgenic mice is correlated with B cell lymphomagenesis. We generated a unique transgenic mouse model in which deregulated murine Em-N-myc transgene expression leads to development of indolent B cell lymphoma. Tumor cells were monoclonal, morphologically mature and surface immunoglobulin expressing B cells. Tumors arose in a disease course and exhibited a cytoarchitectural appearance reminiscent of human follicular lymphoma. Yet tumor cells were staged as preB since they failed to rearrange the immunoglobulin light chain genes. Retroviral insertion mutagenesis analyses of adult transgenic mice infected as newborns with murine leukemia virus revealed decreased disease latency, increased lymphoma incidence and a histologically more mature tumor type. Proviral insertion sites were not equivalent when accelerated Em-N-myc indolent lymphomas were compared to accelerated c-myc preB cell lymphomas. The bcl-2 gene was not disrupted in either spontaneous or provirally accelerated Em-N-myc lymphomas. These ®ndings suggest that tumor progression in N-myc-associated indolent B cell lymphoma can proceed along diverse pathways involving distinctly di erent combinations of deregulated and/or intact genes than those pathways described in highly aggressive forms of myc-related murine preB cell disease.

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A new case of t(14;19) (q32;q13) in a patient with follicular lymphoma in leukemic phase

Cited by 14 publications

References 8 publications

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

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

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

Transgenic N-myc mouse model for indolent B cell lymphoma: tumor characterization and analysis of genetic alterations in spontaneous and retrovirally accelerated tumors

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