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From the Departments of Pathology and Microbiology, Internal Medicine, and Preventive and Societal Medicine, and Eppley Cancer Institute,* University of Nebraska Medical Center, Omaha, Nebraska; the Departments of Pathology and Medical Oncology, British Columbia Cancer Agency, Vancouver, British Columbia, Canada; the Department of Pathology, University of Würzburg, Würzburg, Germany; the Metabolism Branch and Laboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland; the Department of Computer Science,¶ University of Nebraska at Omaha, Omaha, Nebraska; the Department of Pathology,|| Norwegian Radium Hospital, Oslo, Norway; the Department of Pathology,** University of Oregon Health Sciences Center, Portland, Oregon; the Department of Pathology, Hospital Clinic, University of Barcelona, Barcelona, Spain; and the Department of Pathology, University of Arizona, Tucson, Arizona
Gene expression profiling of diffuse large B-cell lymphoma (DLBCL) has revealed prognostically important subgroups: germinal center B-cell-like (GCB) DLBCL, activated B cell-like (ABC) DLBCL, and primary mediastinal large B-cell lymphoma. The t(14;18)(q32;q21) has been reported previously to define a unique subset within the GCB-DLBCL. We evaluated for the translocation in 141 cases of DLBCL that were successfully gene expression profiled. Using a dual-probe fluorescence in situ hybridization assay, we detected the t(14;18) in 17% of DLBCLs and in 34% of the GCB subgroup which contained the vast majority of positive cases. In addition, 12 t(14;18)-positive cases detected by polymerase chain reaction assays on additional samples were added to the fluorescence in situ hybridization-positive cases for subsequent analysis. Immunohistochemical data indicated that BCL2, BCL6, and CD10 protein were preferentially expressed in the t(14;18)-positive cases as compared to t(14;18)-negative cases. Within the GCB subgroup, the expression of BCL2 and CD10, but not BCL6, differed significantly between cases with or without the t(14;18): 88% versus 24% for BCL2 and 72% versus 32% for CD10, respectively. In the GCB-DLBCL subgroup, a heterogeneous group of genes is overexpressed in the t(14;18)-positive subset, among which BCL2 is a significant discriminator. Interestingly, the t(14;18)-negative subset is dominated by overexpression of cell cycle-associated genes, indicating that these tumors are significantly more proliferative, suggesting distinctive pathogenetic mechanisms. However, despite this higher proliferative activity, there was no significant difference in overall or failure-free survival between the t(14;18)-positive and -negative subsets within the GCB subgroup.
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