Needle-core biopsy is an effective technique for the diagnosis of lymphoma and should be considered the first-line procedure for cases with suspicion for lymphoma.
The human germinal-center-associated lymphoma (HGAL) gene and its cognate protein are expressed in a germinal center (GC)-specific manner. Its expression in classic Hodgkin lymphoma (cHL) prompted us to address whether HGAL expression could distinguish biologically distinct subgroups of cHL. Tissue microarrays from 145 patients treated with curative intent showed HGAL staining in 75% and was closely correlated with MUM1/ IRF4 (92%) expression. BCL6 (26%), CD10 (0%), BCL2 (31%), Blimp1 (0.02%), and Epstein-Barr virus (EBV) (20%) showed no specific correlation; neither did phospho-STAT6, a key mediator of IL-4 and IL-13 signaling that induces HGAL and is implicated in cHL pathogenesis. In our study cohort, the 5-year overall survival (OS) correlated with young age (less than 45 years, P < .001), low stage (stage I and II, P ؍ .04), and low International Prognostic Score (P ؍ .002). In univariate analysis, HGAL expression was associated with improved OS (P ؍ .01) and failure-free survival (
Chronic lymphocytic leukemia (CLL) is a prevalent B-cell neoplasia that is often preceded by a more benign monoclonal CD5 1 B-cell lymphocytosis. We previously generated trans-
Background: Plasmacytic differentiation in mantle cell lymphoma (MCL) occurs rarely. However, no flow cytometric studies that demonstrate plasmacytic (PC) differentiation in MCL have been reported. Herein, we report a case of MCL with PC differentiation identified by flow cytometry.Methods: Morphologic review was performed by hematoxylin and eosin (H&E) stained sections from paraffin-embedded lymph node, colon and bone marrow specimens, and Wright-Geimsa stained bone marrow aspirate smears and touch imprints. Immunohistochemical stains using antibodies against CD3, CD5, CD20, and cyclin-D1, and in-situ hybridization for kappa and lambda light chains were reviewed. Multicolor flow cytometry analysis was performed on the bone marrow aspirate with monoclonal antibodies to CD3, CD4, CD5, CD8, CD14, CD19, CD20, CD23, CD38, CD45, CD56, CD138, and kappa and lambda light chains. FISH analysis for t(11;14)(q13;q32) was performed on interphase cells.
Current genomic technologies have immensely improved disease classification and prognostication of major subtypes of B-cell lymphomas. This novel genetic information has not only aided in diagnosis, but has also revealed a landscape of critical molecular events that determine the biological and clinical behavior of a lymphoma. In this review, we summarized the genetic characteristics of major subtypes of B-cell lymphomas, including diffuse large B cell lymphoma (DLBCL), follicular lymphoma (FL), Burkitt lymphoma (BL), and mantle cell lymphoma (MCL). We illustrated how genomic profiling had identified molecular subgroups in DLBCL with varied clinical outcomes, and how a subset of genes defined prognosis in MCL and aided in BL diagnoses. We also highlighted some Phase II/III clinical trials using new therapeutic agents to determine clinical efficacy in novel molecular subgroups with distinct gene expression patterns. We believe that refinement of genomic signatures will require more intensive efforts from the biomedical research community to improve targeted therapy designs and bring a substantial change in the treatment decisions. In the next era of genomic medicine, we anticipate that a clinically and biologically relevant molecular profile of each tumor will be obtained at diagnosis to guide therapy.
Lymphocyte Predominant Hodgkin’s Disease (LPHD) is a B-cell lymphoma that may require different treatment and may have a different natural history than classical Hodgkin’s disease. Although AHSCT is accepted therapy for patients with relapsed and refractory classical Hodgkin’s disease, there is little information regarding transplantation for LPHD. We performed a retrospective analysis of 19 patients who were treated with AHSCT for relapsed or refractory LPHD at the University of Nebraska Medical Center between April, 1987 and October, 2002. Biopsies of all LPHD patients were reviewed to confirm the diagnosis according to the WHO classification. Patients with a prior or concurrent diagnosis of classical Hodgkin’s disease or non-Hodgkin’s lymphoma were excluded. There were 18 men and 1 woman. Median age was 33 years (range 19–52). Thirteen patients (68%) received 1–2 chemotherapy regimens prior to AHSCT, and 6 patients (32%) received 3 or more regimens. Nine patients (47%) received radiation therapy prior to AHSCT. Five patients (26%) had extranodal disease at the time of AHSCT. Five patients (26%) were transplanted with autologous bone marrow, and 14 patients (74%) received peripheral blood stem cells. Six patients (32%) were transplanted with BEAM (carmustine, etoposide, cytarabine, melphalan), and 13 patients (68%) were treated with CBV (cyclophosphamide, carmustine, etoposide). The results of AHSCT for the 19 patients with LPHD were compared with 229 patients in our database who received AHSCT for relapsed and refractory nodular sclerosis Hodgkin’s disease during the same time period. The characteristics of the groups were similar with respect to age, disease status at the time of AHSCT, stage at AHSCT, amount of treatment prior to AHSCT, and interval between diagnosis and AHSCT. Patients with LPHD were more likely to be males (p<0.001), less likely to have received radiation prior to AHSCT (p=0.06), and more likely to have been transplanted with peripheral blood stem cells (p=0.05). The actuarial 5-year progression-free survival following AHSCT for patients with LPHD and nodular sclerosis Hodgkin’s disease was 40% (95% CI 18% to 61%) and 39% (95% CI 33% to 45%), respectively (p=0.30). The actuarial 5-year overall survival following AHSCT for patients with LPHD and classical Hodgkin’s disease was 56% (95% CI 30% to 75%) and 53% (95% CI 46% to 59%), respectively (p=0.36). A multivariate analysis comparing patients with LPHD and those with nodular sclerosis Hodgkin’s disease was performed. The relative risk of treatment failure following AHSCT for patients with nodular sclerosis histology was 1.14 (95% CI 0.62 to 2.12; p=0.67), and the relative risk of death was 1.22 (95% CI 0.62 to 2.41; p=0.56). These results demonstrate that long-term progression-free survival and overall survival can be achieved following high-dose therapy and AHSCT for patients with LPHD. Furthermore, no significant differences in progression-free survival and overall survival were identified when results of AHSCT for LPHD and nodular sclerosis Hodgkin’s disease were compared. Although none of the LPHD patients were treated with newer agents such as gemcitabine or rituximab prior to AHSCT, this analysis suggests that high-dose therapy followed by AHSCT may be used for patients with relapsed and refractory LPHD as well as classical Hodgkin’s disease.
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