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Kawakami, Keiki; Amakawa, Ryuichi; Miyanishi, Setsuko; Okumura, Atsuko; Hayashi, T; Kurata, Morito; Ohno, Hitoshi; Ohno, Y; Fukuhara, Suguru

doi:10.1016/s0925-5710(97)00109-6

Cited by 10 publications

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“…DNA from the present case in addition to the KIS-1 cell line and another t(9;14)(p13;q32)-carrying DLBCL (#895) [9,10] was subjected to PCR amplification of the region for EBER [11]. As shown in Fig.…”

Section: Presence Of Ebv Genomementioning

confidence: 99%

Epstein–Barr virus-positive diffuse large B-cell lymphoma carrying a t(9;14)(p13;q32) translocation

et al. 2009

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We, herein, report a 75-year-old man with lymphoma who initially presented with disseminated disease involving the lung, followed by temporal regression, and finally died of disease progression. Lymph-node biopsy showed a morphology of diffuse large B-cell lymphoma (DLBCL), containing CD30(+) Reed-Sternberg-like cells. The lymphoma cells were stained by in situ hybridization (ISH) for Epstein-Barr virus (EBV)-encoded RNA, and the presence of the EBV genome was confirmed by the polymerase chain reaction. A cytogenetic study showed that the lymphoma cells carried a t(9;14)(p13;q32) translocation, and rearrangement of the PAX5 gene was determined by fluorescence ISH using a split signal probe. This case report is the first to identify t(9;14)(p13;q32) in EBV(+) DLBCL of the elderly, which was very recently listed among subtypes of DLBCL.

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Section: Presence Of Ebv Genomementioning

confidence: 99%

Epstein–Barr virus-positive diffuse large B-cell lymphoma carrying a t(9;14)(p13;q32) translocation

et al. 2009

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PAX5/IGH rearrangement is a recurrent finding in a subset of aggressive B‐NHL with complex chromosomal rearrangements

Poppe

Paepe

Michaux

et al. 2005

Genes Chromosomes & Cancer

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We present an extensive characterization of 10 B-cell lymphomas with a t(9;14)(p13;q32). The presence of the PAX5/IGH gene rearrangement was demonstrated by fluorescence in situ hybridization (FISH) using a validated probe set, whereas complex karyotypic changes were reassessed by multiplex-FISH (M-FISH). Pathologic and clinical review revealed the presence of this rearrangement in 4 histiocyte-rich, T-cell-rich B-cell lymphomas (HRTR-BCLs) and 2 posttransplantation diffuse large B-cell lymphomas (PTLD-DLBCLs). In contrast to initial observations describing this translocation in lymphoplasmacytic lymphoma (LPL) and LPL-derived large B-cell lymphoma, our data showed a wide morphologic and clinical spectrum associated with the PAX5/IGH rearrangement, pointing to an association between this aberration and a subset of de novo DLBCLs presenting with advanced disease and adverse prognosis. In addition, the recurrent incidence of this rearrangement in both HRTR-BCL (4 cases) and PTLD-DLBCL (2 cases) was previously unrecognized and is intriguing.

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Diffuse large B‐cell lymphoma carrying t(9;14)(p13;q32)/PAX5‐immunoglobulin heavy chain gene is characterized by nuclear positivity of MUM1 and PAX5 by immunohistochemistry

Ohno

Nakagawa

Kishimori

et al. 2020

Hematological Oncology

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We described four patients with diffuse large B‐cell lymphoma (DLBCL) carrying t(9;14)(p13;q32) that places the PAX5 adjacent to the immunoglobulin heavy chain (IGH) gene. Ages ranged between 63 and 80, and three were female. One developed a nodal disease, and the other three involved extranodal organs. The lymphoma cells were CD10−/BCL6−/MUM1+ in three and CD10+/BCL6+/MUM1+ in one. BCL2 was weak or negative. All had t(9;14)(p13;q32), and three had additional 14q32/IGH translocations or +der(14)t(9;14)(p13;q32). Fluorescence in situ hybridization using the PAX5 break‐apart probe showed that the locus was disrupted between the 5′ and 3′ probes or within the 5′ probe. Immunohistochemistry (IHC) using a monoclonal antibody against PAX5 showed strong nuclear positivity in all four patients. Cell block IHC of a CD30+ DLBCL cell line, KIS‐1, which carried the t(9;14)(p13;q32) and PAX5‐IGH fusion gene, reproduced the CD10−/BCL6−/MUM1+ immunophenotype, low‐level BCL2, and strong nuclear PAX5. Uniform nuclear positivity of MUM1 in all four cases and KIS‐1 cells suggest that these lymphomas arose at a late stage of B‐cell differentiation, where expression of PAX5 physiologically becomes downregulated. It is therefore possible that high‐level PAX5 resulting from t(9;14)(p13;q32) at this stage of differentiation perturbs the plasma cell differentiation program initiated by PAX5 repression, thereby contributing to the development of a fraction of DLBCL.

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Cited by 10 publications

References 0 publications

Epstein–Barr virus-positive diffuse large B-cell lymphoma carrying a t(9;14)(p13;q32) translocation

Epstein–Barr virus-positive diffuse large B-cell lymphoma carrying a t(9;14)(p13;q32) translocation

PAX5/IGH rearrangement is a recurrent finding in a subset of aggressive B‐NHL with complex chromosomal rearrangements

Diffuse large B‐cell lymphoma carrying t(9;14)(p13;q32)/PAX5‐immunoglobulin heavy chain gene is characterized by nuclear positivity of MUM1 and PAX5 by immunohistochemistry

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