Loss of MHC class II gene and protein expression in diffuse large B-cell lymphoma is related to decreased tumor immunosurveillance and poor patient survival regardless of other prognostic factors: a follow-up study from the Leukemia and Lymphoma Molecular Profiling Project.

The Leukemia and Lymphoma Molecular Profiling Project recently published results from DNA microarray analyses of 240 diffuse large B-cell lymphomas (DLBCLs). Four gene expression "signatures" were identified as correlated with patient outcome, including the major histocompatibility complex (MHC) class II genes (eg, HLA-DRA) which correlated with better survival. We further analyzed the effects of HLA-DRA on survival and correlated gene expression with protein status and tumor-infiltrating lymphocytes.

Confirmation of the molecular classification of diffuse large B-cell lymphoma by immunohistochemistry using a tissue microarray.

Diffuse large B-cell lymphoma (DLBCL) can be divided into prognostically important subgroups with germinal center B-cell-like (GCB), activated B-cell-like (ABC), and type 3 gene expression profiles using a cDNA microarray. Tissue microarray (TMA) blocks were created from 152 cases of DLBCL, 142 of which had been successfully evaluated by cDNA microarray (75 GCB, 41 ABC, and 26 type 3). Sections were stained with antibodies to CD10, bcl-6, MUM1, FOXP1, cyclin D2, and bcl-2.

Molecular diagnosis of primary mediastinal B cell lymphoma identifies a clinically favorable subgroup of diffuse large B cell lymphoma related to Hodgkin lymphoma.

Using current diagnostic criteria, primary mediastinal B cell lymphoma (PMBL) cannot be distinguished from other types of diffuse large B cell lymphoma (DLBCL) reliably. We used gene expression profiling to develop a more precise molecular diagnosis of PMBL. PMBL patients were considerably younger than other DLBCL patients, and their lymphomas frequently involved other thoracic structures but not extrathoracic sites typical of other DLBCLs.

Nodular lymphocyte-predominant Hodgkin lymphoma with nodules resembling T-cell/histiocyte-rich B-cell lymphoma: differential diagnosis between nodular lymphocyte-predominant Hodgkin lymphoma and T-cell/histiocyte-rich B-cell lymphoma.

Nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL) and T-cell/histiocyte-rich B-cell lymphoma (T/HRBCL) are distinct tumors and are treated differently. They are linked by a morphologic and probably a biologic continuum, which renders the differential diagnosis difficult. To develop criteria to distinguish the entities along the morphologic continuum, we correlated the lymph node architecture and immunophenotype of both tumor cells and reactive components of 235 neoplasms in the spectrum of NLPHL and T/HRBCL with clinical data.

The proliferation gene expression signature is a quantitative integrator of oncogenic events that predicts survival in mantle cell lymphoma.

We used gene expression profiling to establish a molecular diagnosis of mantle cell lymphoma (MCL), to elucidate its pathogenesis, and to predict the length of survival of these patients. An MCL gene expression signature defined a large subset of MCLs that expressed cyclin D1 and a novel subset that lacked cyclin D1 expression. A precise measurement of tumor cell proliferation, provided by the expression of proliferation signature genes, identified patient subsets that differed by more than 5 years in median survival.

Splenic marginal zone lymphoma with villous lymphocytes shows on-going immunoglobulin gene mutations.

Splenic marginal zone lymphoma (also splenic lymphoma with villous lymphocytes) is a B-cell non-Hodgkin's lymphoma with a characteristic morphology and phenotype. We studied the pattern of somatic hypermutation of the rearranged immunoglobulin heavy chain genes on 23 cases and have correlated these data with survival as well as immunophenotypic and genetic characteristics of the cases. Two-thirds of the cases show immunoglobulin gene mutations, half of which show evidence of antigen selection, whereas one-third of the cases show no significant mutations.

Clustering of the SOM easily reveals distinct gene expression patterns: results of a reanalysis of lymphoma study.

Background: A method to evaluate and analyze the massive data generated by series of microarray experiments is of utmost importance to reveal the hidden patterns of gene expression. Because of the complexity and the high dimensionality of microarray gene expression profiles, the dimensional reduction of raw expression data and the feature selections necessary for, for example, classification of disease samples remains a challenge. To solve the problem we propose a two-level analysis.

The value of anti-pax-5 immunostaining in routinely fixed and paraffin-embedded sections: a novel pan pre-B and B-cell marker.

Whereas L26 (anti-CD20) is well established as a B-cell marker of high specificity for use in paraffin-embedded tissues and JCB117 (anti-CD79a) is increasingly used, a comparable additional pan-B-cell antibody has hitherto not yet been identified. Here we have studied the use of a novel anti-pan-B-cell marker Pax-5 for use in diagnostic pathology. Pax-5 encodes for BSAP (Pax-5), a B-cell-specific transcription factor, the expression of which is detectable as early as the pro-B-cell stage and subsequently in all further stages of B-cell development until the plasma cell stage where it is downregulated.

M-FISH cytogenetic analysis of non-Hodgkin lymphomas with t(14;18)(q32;q21) and add(1)(p36) as a secondary abnormality shows that the extra material often comes from chromosome arm 17q.

The most common translocation in non-Hodgkin lymphomas (NHL) is a t(14;18)(q32;q21) recombining the immunoglobulin heavy-chain gene (IGH) on chromosome 14 with the B cell leukemia/lymphoma 2 (BCL2) gene on chromosome 18. Although NHLs carrying a t(14;18) typically begin as low-grade, follicular lymphomas, they have a tendency towards transformation to more aggressive disease, something that is accompanied, presumably caused, by the acquisition of secondary chromosomal changes. One such common change is add(1)(p36), in which material of unknown origin is added to the tip of the short arm of chromosome 1.

The use of molecular profiling to predict survival after chemotherapy for diffuse large-B-cell lymphoma.

Background: The survival of patients with diffuse large-B-cell lymphoma after chemotherapy is influenced by molecular features of the tumors. We used the gene-expression profiles of these lymphomas to develop a molecular predictor of survival.

Methods: Biopsy samples of diffuse large-B-cell lymphoma from 240 patients were examined for gene expression with the use of DNA microarrays and analyzed for genomic abnormalities.

High-dose therapy in patients with Hodgkin's disease: the use of selected CD34(+) cells is as safe as unmanipulated peripheral blood progenitor cells.

Register data suggest that patients with Hodgkin's disease (HD) given high-dose therapy (HDT) with peripheral blood progenitor cells (PBPC) have a less favourable prognosis as compared to those given bone marrow as stem cell support. Since this can be due to infusion of tumour cells contaminating the PBPC grafts, we initiated a feasibility study in which PBPC grafts from HD patients were purged by CD34(+) cell enrichment. Controversy exists about whether the use of CD34(+) enriched stem cells leads to a delayed haematological and immune reconstitution.

Loss of chromosome 11q21-23.1 and 17p and gain of chromosome 6p are independent prognostic indicators in B-cell non-Hodgkin's lymphoma.

Comparative genomic hybridization (CGH) was employed to study chromosomal aberrations in relation to cell proliferation, apoptosis, and patient survival in 94 cases of B-cell non-Hodgkin's lymphoma diagnosed between 1983 and 1993. Eighty cases had aberrations by CGH. Chromosomal regions 1p21-31.

The transcription factor PU.1, necessary for B-cell development is expressed in lymphocyte predominance, but not classical Hodgkin's disease.

Hodgkin's disease (HD) is a lymphoproliferative disease of predominantly B-cell origin. However, the reasons for the incomplete development of the B-cell phenotype and lack of immunoglobulin expression in classical HD (cHD) have not been fully explained. We examined the expression of PU.

Chemical profiles, division of labor and social status in Pachycondyla queens (Hymenoptera: formicidae).

Queens of the neotropical ponerine ant Pachycondyla cf. 'inversa' may co-operate during colony founding. One of several co-founding queens specializes in foraging, whereas the others remain in the nest and guard the brood.

High-dose therapy with autologous stem cell transplantation in patients with peripheral T cell lymphomas.

Peripheral T cell lymphomas (PTCL) have a poorer prognosis after conventional treatment than do high-grade B cell lymphomas. The place for high-dose therapy (HDT) with autologous stem cell support in these patients is still not clear. Forty patients, 10 women and 30 men, median age 41.

Lymphocyte predominance Hodgkin disease is characterized by recurrent genomic imbalances.

Single-cell polymerase chain reaction (PCR) has been used as a tool to demonstrate clonality and B-cell origin of Reed-Sternberg (RS) cells in Hodgkin disease (HD). An analogous approach was used to investigate genomic imbalances in a (cyto)genetically poorly characterized subentity: lymphocyte predominance Hodgkin disease (LPHD). Nineteen cases of LPHD were selected for a comparative genomic hybridization (CGH) study.

Proliferative myositis in a child.

A case of proliferative myositis in the lumbar paraspinal muscles in a 14-year-old boy is presented. Imaging investigations including plain radiograph, ultrasound, computed tomography (CT), magnetic resonance imaging (MRI), bone scan and positron emission tomography (PET) were suggestive of an inflammatory process such as myositis ossificans. The diagnosis was made by incisional biopsy.

Revision of the diagnosis of T-zone lymphoma in the father of a patient with autoimmune lymphoproliferative syndrome type II.

Autoimmune lymphoproliferative syndrome (ALPS) is a disease of childhood characterized by typical clinical and laboratory findings. Here we describe an adult patient presenting with lymph node enlargement and splenomegaly. Pathological examination of an adenopathy supported the diagnosis of malignant T-zone lymphoma.

Different gastritis features are linked to different gastric neoplasms.

Objectives: Helicobacter pylori infection induces gastritis, which may evolve to carcinoma or lymphoma. Whether duration of infection and inflammation pattern determine the outcome of the neoplastic process is not known. The aim of this study was to investigate the features of the gastritis associated with neoplasia.

Primary diffuse large B cell lymphoma of the stomach: analysis of somatic mutations in the rearranged immunoglobulin heavy chain variable genes indicates antigen selection.

Gastric low grade MALT lymphomas show a pattern of somatic mutations in their rearranged immunoglobulin genes, indicative of antigen selection. This provides evidence for antigen stimulation in the lymphomagenesis. Gastric diffuse large B cell lymphomas develop secondary to low grade MALT lymphoma or de novo.