Translocation (14;19)(q32;q13) detected by spectral karyotyping and lack of BCL3 rearrangement in CD5-positive B-cell lymphoma associated with hemophagocytic syndrome

Yamamoto, Katsuya; Nakamura, Yūichi; Arai, Honoka; Aoyagi, Masakuni; Saito, Kenji; Furusawa, Shinpei; Mitani, Kinuko

doi:10.1016/s0165-4608(01)00466-6

Cited by 9 publications

(8 citation statements)

References 14 publications

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“…19 Thus, it is possible that some t(14;19)(q32;q13) translocations detected by chromosome banding are mistakenly assumed to represent IGH/ BCL3 fusions. This highlights the importance of demonstrating BCL3 involvement in t(19q13)-positive cases by molecular methods, including fluorescence in situ hybridization (FISH).…”

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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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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“…Given that most children with ALL are between 1 and 5 years old, it is interesting that all four children in our series and the four mentioned in the literature (Heerema et al, 1985;Prigogina et al, 1988;Pui et al, 1993;Yamamoto et al, 2001) were between 9 and 15 years old. Although the number of cases is small, there is no indication that patients with the t(14;19) have the poor prognosis that their age would otherwise indicate (Secker-Walker et al, 1997;Hann et al, 2001).…”

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confidence: 64%

“…The translocation t(14;19)(q32;q13), an alternative of the more widespread t(14;18)(q32;q21), has been reported in patients with chronic B-cell lymphoproliferative disorders, especially atypical chronic lymphocytic leukemia (CLL), and results in up-regulation of the B-cell CLL/lymphoma 3 (BCL3) gene, located at 19q13 (McKeithan et al, 1997;Michaux et al, 1997). A search of the Mitelman Database of Chromosome Aberrations in Cancer (Mitelman et al, 2003) revealed four sporadic reports of t(14;19)(q32; q11ϳq13) in ALL; however, none had been tested for the involvement of the IGH@ or BCL3 genes (Heerema et al, 1985;Prigogina et al, 1988;Pui et al, 1993;Yamamoto et al, 2001). In this report, we document six patients with common ALL and a t(14;19)(q32;q13) translocation that involves the IGH@ locus and a novel molecular breakpoint at 19q13.…”

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confidence: 99%

t(14;19)(q32;q13): A recurrent translocation in B‐cell precursor acute lymphoblastic leukemia

Robinson

Taylor

Jalali

et al. 2003

Genes Chromosomes & Cancer

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The recurrent t(14;19)(q32;q13) translocation associated with chronic B-cell lymphoproliferative disorders, such as atypical chronic lymphocytic leukemia, results in the juxtaposition of the IGH@ and BCL3 genes and subsequent overexpression of BCL3. We report six patients with B-cell precursor acute lymphoblastic leukemia who have a cytogenetically identical translocation with different breakpoints at the molecular level. Fluorescence in situ hybridization with locus-specific probes confirmed the involvement of the IGH@ gene but showed that the breakpoint on 19q13 lay outside the region documented in t(14;19)(q32;q13)-positive chronic lymphocytic leukemia. This newly described translocation constitutes a distinct cytogenetic subgroup that is confined to older children and younger adults with B-cell precursor acute lymphoblastic leukemia.

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“…As the latter case was associated with hepatosplenomegaly, pancytopenia, bone marrow infiltration of large lymphoma cells, and HPS, but no superficial lymphadenopathy, the lymphoma may actually have been an IVLBCL, raising the possibility that t(14;19)(q32;q13) is a recurring translocation of IVLBCL. As suggested by Yamamoto et al (14), another oncogene, independent of BCL3, could be localized on 19q13 and deregulated by juxtaposition to IgH, playing a role in the pathogenesis of a fraction of this particular type of lymphoma.…”

Section: Discussionmentioning

confidence: 87%

“…A literature review showed two cases of B-cell lymphoma that had t(14;19)(q32;q13) by cytogenetic analysis but lacked rearrangement of BCL3 by Southern blot using probes for the gene; i.e., an aggressive small non-cleaved cell lymphoma (13) and a CD5-positive DLBCL (14). As the latter case was associated with hepatosplenomegaly, pancytopenia, bone marrow infiltration of large lymphoma cells, and HPS, but no superficial lymphadenopathy, the lymphoma may actually have been an IVLBCL, raising the possibility that t(14;19)(q32;q13) is a recurring translocation of IVLBCL.…”

Section: Discussionmentioning

confidence: 99%

Intravascular Large B-Cell Lymphoma Associated with t(14;19)(q32;q13) Translocation

Kobayashi

Ohno

2011

Intern. Med.

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We report a 59-year-old man with intravascular large B-cell lymphoma (IVLBCL) associated with hemophagocytic syndrome, disseminated intravascular coagulopathy, and lung involvement. G-banding analysis of the metaphase spreads obtained from the bone marrow showed that the lymphoma cells were near-tetraploid and included two homologues of the 14q+ chromosome. Spectral karyotyping revealed that complex translocations occurred among chromosomes 3, 12, 14, and 19, and additional materials of 14q+ were from chromosome 19 with the breakpoint at 14q32 and 19q13. To the best of our knowledge, this is the first report describing t(14;19)(q32;q13) in IVLBCL.

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Translocation (14;19)(q32;q13) detected by spectral karyotyping and lack of BCL3 rearrangement in CD5-positive B-cell lymphoma associated with hemophagocytic syndrome

Cited by 9 publications

References 14 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

t(14;19)(q32;q13): A recurrent translocation in B‐cell precursor acute lymphoblastic leukemia

Intravascular Large B-Cell Lymphoma Associated with t(14;19)(q32;q13) Translocation

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