Author:

Keywords:

Aged, Aged, 80 and over, B-Cell-Specific Activator Protein, Chromosomes, Human, Pair 14, Chromosomes, Human, Pair 9, DNA-Binding Proteins, Female, Gene Rearrangement, Humans, Immunoglobulin Heavy Chains, Karyotyping, Lymphoma, B-Cell, Male, Middle Aged, Research Support, Non-U.S. Gov't, Transcription Factors, Translocation, Genetic, Science & Technology, Life Sciences & Biomedicine, Oncology, Genetics & Heredity, IN-SITU HYBRIDIZATION, LARGE-CELL LYMPHOMA, T(9-14)(P13-Q32), DIFFERENTIATION, CLASSIFICATION, TRANSLOCATIONS, MALIGNANCIES, VIRUS, LOCUS, PAX-5, PAX5 Transcription Factor, 1112 Oncology and Carcinogenesis, Oncology & Carcinogenesis, 3105 Genetics, 3211 Oncology and carcinogenesis

Abstract:

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.