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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The wide clinicopathologic heterogeneity of non-Hodgkin's lymphoma is reflected by the various molecular pathways underlying non-Hodgkin's lymphoma pathogenesis, including activation of dominantly acting oncogenes, deletion and inactivation of tumor-suppressor genes, viral infection, deregulation of cytokine networks, and chronic antigenic stimulation. Molecular lesions involving protooncogenes include activation of bcl-2 and bcl-1 in specific subsets of low-grade non-Hodgkin's lymphomas and c-myc in a proportion of intermediate- and high-grade non-Hodgkin's lymphomas. The deregulation of these genes promotes cell growth or protects the tumor population from programmed cell death, or both. Additional genetic abnormalities representing putative sites of novel oncogenes contributing to lymphomagenesis include chromosomal breaks at 3q27 in intermediate-grade non-Hodgkin's lymphoma and at 9p13 in small lymphocytic lymphoma. The role of inactivation of tumor-suppressor loci is best exemplified by the frequent inactivation of p53 in Burkitt's lymphoma and by the recurrent deletion of 6q25-q27 and 6q21-q23 in intermediate- and high-grade non-Hodgkin's lymphoma, respectively. Infection by Epstein-Barr virus occurs in a variable fraction of high-grade non-Hodgkin's lymphomas, whereas it is usually absent in other types of non-Hodgkin's lymphoma. Other mechanisms supporting non-Hodgkin's lymphoma growth and development include autocrine or paracrine cytokine loops, or both, and clonal expansion through antigen receptor stimulation. The heterogeneity of non-Hodgkin's lymphoma pathogenesis provides a framework for the development of novel classification methods of potential clinical relevance.
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PMID:Biologic and molecular characterization of non-Hodgkin's lymphoma. 821 89

Twenty-five reactive lymph nodes, 10 palatine tonsils, and 72 B-cell non-Hodgkin's lymphomas (NHLs) of supposed follicular origin were investigated in an immunohistologic study of fixed, paraffin-embedded tissues using a panel of monoclonal antibodies reactive with antigens resistant against fixation and paraffin-embedding techniques together with polyclonal antibodies. The results concerning the microenvironmental organization of reactive lymphoid follicles confirmed that the distribution of CD21+ and CD23+ dendritic reticulum cells, vimentin+ fibroblastic reticulum cells, and CD68+ tingible-body macrophages is heterogeneous with reference to their immunostaining patterns and topographic localization within the germinal center and mantle zone. Moreover, a close microenvironmental similarity between the follicular lymphomas of supposed germinal center or mantle zone origin and their normal counterparts was noted. The study of the microenvironment of the B-zone small lymphocytic lymphoma cases, showing the same distribution patterns for the nonlymphoid cells as seen in mantle zone lymphomas, corroborated the supposed follicular origin of this unusual variant of small lymphocytic lymphoma. In conclusion, this study shows that monoclonal antibodies recognizing CD21, CD23, and CD68 antigens may be valuable additions to vimentin, S-100 protein, laminin, and type IV collagen antibodies for investigating the microenvironmental organization of lymphoid tissues in both normal and neoplastic conditions.
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PMID:The nonlymphoid microenvironment of reactive follicles and lymphomas of follicular origin as defined by immunohistology on paraffin-embedded tissues. 841 15

Analysis of incidence of different types of malignancies during 15 years showed occurrence of malignant lymphoma in 192 cases (4.1%). There were 82 cases (42.7%) of non-Hodgkin's lymphoma and 110 cases (57.3%) of Hodgkin's disease. Lymphocytic lymphoma, the major type observed among the non-Hodgkin's lymphoma with 58 cases (30.21%), showed a preponderance of well differentiated type (40 cases). Other cases in this group comprised mixed cellularity (2.08%), histiocytic (3.64%) and unclassified one (6.77%). Analysis of the Hodgkin's disease cases showed majority in it belonged to the mixed cellularity type (44.5%) followed by the lymphocytic predominant type (27.3%), lymphocytic depletion type (18.2%) and nodular sclerosing type (10%). The incidence of 14 cases of extranodal lymphomas was 7.3% among the lymphomas with maximum occurrence in the gastrointestinal tract (42.8%).
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PMID:Malignant lymphoma--a 15-year study report. 850 10

CD26 and CD40 ligand (CD40L) are surface molecules on human activated T lymphocytes that play a critical role in the regulation of lymphopoiesis. Both molecules are expressed on a restricted fraction of human T-cell non-Hodgkin's lymphomas (NHL)/leukemias; however, little is known about their functional and/or clinical significance in these disorders. In this study, the pattern of expression of CD40L was compared with that of the CD26 molecule. A series of 67 human T-cell NHL/leukemias and a panel of leukemia/lymphoma T-cell lines were evaluated by immunohistochemistry, flow cytometry, and RNA studies. The overall frequency of CD26+ and CD40L+ samples was rather similar (25/67 [37%] v 18/67 [27%]). However, the majority of CD26-expressing cases clustered in the lymphoblastic lymphomas (LBL)/T-acute lymphoblastic leukemias (ALL; 12/23) and CD30+ anaplastic large-cell (ALC) lymphomas (5/8), whereas CD40L+ lymphomas included a large fraction of mycosis fungoides (11/21 [52%]). CD26 and CD40L coexpression was found only in 2 myocosis fungoides cases and 1 small lymphocytic lymphoma. Thus, the expression of the two antigens was mutually exclusive in almost all T-cell lymphomas/leukemias. Accordingly, lymphoma cell lines expressed either one of the molecules or the relative amounts of CD26 and CD40L were inversely proportional. In contrast, reactive T lymphocytes from patients with non-neoplastic T-cell expansions and in vitro activated CD3+ or CD4+ normal T cells were found to coexpress CD40L and CD26. Results of a multivariate analysis showed that the expression of CD26 in T-cell LBL/ALL patients was associated to a worse outcome in terms of survival, as compared with patients with CD26- tumors (P < or = .0001). Based on our results, it can be concluded that, (1) as opposed to activated or reactive normal T cells, the expression of CD26 and of CD40L is mutually exclusive in human T-cell lymphomas/leukemias; (2) expression of CD26 is restricted to aggressive pathologic entities, such as T-cell LBL/ALL and T-cell CD30+ ALC lymphomas, whereas CD40L is expressed on slow progressing diseases such as mycosis fungoides; and (3) within the T-cell LBL/ALL group of tumors, CD26 may identify a subset of poor prognosis patients.
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PMID:The expression of CD26 and CD40 ligand is mutually exclusive in human T-cell non-Hodgkin's lymphomas/leukemias. 854 53

BCL1/PRAD1 gene rearrangements involving the cyclin D1 gene are a feature of about 70% of centrocytic/mantle-cell lymphomas (CC/MCL) but are identified in only a small proportion of other B-cell non-Hodgkin's lymphomas. Of 37 lymphomas found to have BCL1/cyclin D1 (PRAD1, CCND1) gene rearrangements, 30 fit the morphologic and immunophenotypic criteria for typical CC/MCL. Seven cases with morphologic features atypical for CC/MCL were identified. CD5+ monoclonal B cells were documented in all these cases. Six cases were subsequently stained for cyclin D1 protein, and all showed nuclear positivity. Five cases had variably sized foci of cells with moderately abundant pale cytoplasm resembling parafollicular/monocytoid B cells, marginal zone cells, hairy cells, or even proliferation centers. Transformed-appearing cells were also present in some lymphomas. In one case, striking follicular colonization created a markedly nodular growth pattern mimicking a follicular lymphoma. A sixth case had a marked predominance of small, round lymphocytes at some sites, mimicking a small lymphocytic lymphoma. Five of these six cases also had areas more typical of CC/MCL. The seventh case was a CD5-positive splenic marginal zone-like lymphoma (SMZL) with plasmacytic differentiation and circulating villous lymphocytes consistent with a splenic lymphoma with villous lymphocytes (SLVL). These cases illustrate the morphologic spectrum of small B-cell lymphoid neoplasms that have BCL1/cyclin D1 gene rearrangements and overexpression of cyclin D1. Despite the BCL1 translocation and cyclin D1 overexpression, the splenic lymphoma with plasmacytic differentiation was definitely not a CC/MCL and fit the clinicopathologic entity of SMZL/SLVL. The other six cases are best considered CC/MCL variants based on a combined morphologic, immunophenotypic, and genotypic evaluation. Genotypic or immunophenotypic studies to identify cyclin D1 rearrangements and overexpression, although not pathognomonic, are useful in recognizing these variant CC/MCL cases, which can mimic almost any of the other well-described but more indolent low-grade B-cell lymphomas and leukemias. Some of the variant CC/MCL cases had features in common with the CD5+ cyclin D1+ SMZL/SLVL, suggesting a possible relationship between these two otherwise distinct entities.
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PMID:The morphologic spectrum of non-Hodgkin's lymphomas with BCL1/cyclin D1 gene rearrangements. 861 27

A case of primary intracerebral non-Hodgkin's lymphoma in a 67-yr-old immunocompetent female is presented. The histopathological diagnosis was supported by immunohistochemical, flow cytometric and electron microscopic findings, and by clinical staging. This tumor is unusual in its morphological features of a low grade, small lymphocytic lymphoma with plasmacytoid differentiation (Working Formulation Classification), and its association with extensive, local, extracellular, proteinaceous deposits. Primary central nervous system non-Hodgkin's lymphomas are briefly discussed and it is postulated that the extracellular proteinaceous deposits in this case originated from immunoglobulins secreted by the neoplastic cells. To our knowledge the massive degree of local immunoglobulin deposition present in this primary central nervous system lymphoma has not been previously reported in the literature.
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PMID:Primary intracerebral small lymphocytic non-Hodgkin's lymphoma with plasmacytoid differentiation, associated with prominent extracellular proteinaceous deposits. 871 83

Mantle cell lymphoma (formerly known as intermediate lymphocytic lymphoma, diffuse centrocytic lymphoma, or diffuse small cleaved lymphoma) is one of the small cell non-Hodgkin lymphoma entities that is clinically more aggressive than small lymphocytic lymphoma, and needs to be separated from it. Mantle cell lymphoma is strongly associated with the t(11;14) chromosomal translocation that rearranges the bcl-1 oncogene (PRAD-1 gene) and immunoglobulin heavy chain gene. In this study, we developed a nested polymerase chain reaction system to evaluate the t(11;14) translocation. The study material consisted of 10 mantle cell lymphomas fulfilling the criteria suggested by other authors (P. M. Banks et al. Surg Pathol 16:637, 1992). A novel nested polymerase chain reaction system was used to evaluate the bcl-1 breaks in the major translocation cluster using two successive polymerase chain reaction amplifications. This reaction yielded a background-free single product of the size of 200 to 300 base pairs in four of 10 mantle cell lymphomas. The identity of the product from the nested polymerase chain reaction was confirmed by Southern blotting followed by hybridization with a specific probe. The amplification products were also evaluated by Sst-I, Alu-I, Dde-I, and Ita-I restriction enzymes and showed different patterns of digestion reflecting individual differences between the MTC/ IgH junctions. A selection of other low-grade lymphomas, including lymphocytic, follicular, and mucosa-associated lymphoid tissue lymphoma, and hairy cell leukemia and 29 hyperplastic lymph nodes were negative. This nested polymerase chain reaction system for the t(11;14) translocation involving major translocation cluster offers a convenient specific identification for mantle cell lymphoma. However, this test has a limited diagnostic power because only about half of the mantle cell lymphomas show the bcl-1 breaks in the major translocation cluster. The test performs well in formaldehyde-fixed and paraffin-embedded material, allowing the study of large numbers of retrospective cases of mantle cell lymphomas.
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PMID:Molecular diagnosis of mantle cell lymphoma in paraffin-embedded tissue. 872 72

CD95 (APO-1/Fas) is a member of the superfamily that includes the nerve growth factor and tumor necrosis factor receptors, OX40, CD27, CD30, and CD40. Present on a minority of resting blood lymphocytes, CD95 expression is upregulated on activated T and B lymphocytes and natural killer cells, where binding of the antigen by anti-Fas and anti-APO-1 antibodies has been shown to induce apoptosis. This CD95-mediated apoptosis is at least partially inhibited by expression of the Bcl-2 protooncogene. To evaluate possible roles of CD95 and Bcl-2 in growth regulation of lymphoid neoplasms, we studied by immunohistochemistry the expression of CD95 and Bcl-2 in 67 B- and 5 T-cell lymphomas, and 10 cases of Hodgkin's disease. In all, 29 B and 2 T cell lymphomas, and 9 cases of Hodgkin's disease expressed CD95. Compared with diffuse large B-cell and Burkitt-like lymphomas, lowgrade B-cell lymphomas more frequently expressed CD95 (52% versus 26%; P < .005). None of the B-cell small lymphocytic lymphomas or mantle cell lymphomas expressed CD95, whereas the majority of follicle center lymphomas, extranodal marginal zone B-cell lymphomas, and immunocytomas were CD95+. Of the 29 CD95+ B-cell lymphomas, only 33% of the high-grade group coexpressed Bcl-2, compared with 87% of the low-grade group (P < .04). Two of three peripheral T-cell lymphomas--including one anaplastic large cell lymphoma--expressed CD95. Staining for CD95 was seen in 9 of 10 cases of Hodgkin's disease. The infrequent expression of CD95 in high-grade B-cell lymphomas suggests an association between loss of CD95 expression/function and a more aggressive tumor grade. Whereas frequent coexpression of Bcl-2 with CD95 may protect low-grade B-cell lymphomas against CD95-mediated apoptosis, in the high-grade group such coexpression is infrequent, and other regulators besides Bcl-2 may be involved in modulating the apoptosis signal delivered by CD95.
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PMID:Expression of CD95 antigen and Bcl-2 protein in non-Hodgkin's lymphomas and Hodgkin's disease. 877 39

Specimens of lymphoid and splenic tissue with reactive changes or involvement by non-Hodgkin's lymphomas or Hodgkin's disease were examined for low-affinity nerve growth factor receptor (NGFR) immunoreactivity of dendritic reticulum cells (DRCs) in frozen tissue and paraffin sections. The DRCs in 13 of 13 specimens with reactive follicular hyperplasia were uniformly immunoreactive with the NGFR-specific antibody NGFR5 and with the DRC-specific antibody DRC-1. We also found that the DRCs associated with 30 of 30 cases of follicular non-Hodgkin's lymphoma were immunoreactive with NGFR5 in a pattern similar to that seen with DRC-1, in contrast to a previous study. Our results were similar in frozen tissue and microwave-treated paraffin sections. Four of four cases of diffuse large cell non-Hodgkin's lymphoma, six of six cases of immunoblastic large cell non-Hodgkin's lymphoma and three of three cases of small noncleaved cell non-Hodgkin's lymphoma did not exhibit significant tumor-associated NGFR5-positive DRCs. Similarly, no NGFR5 staining was observed in eight of eight cases of small lymphocytic lymphoma/chronic lymphocytic leukemia or in six of six cases of marginal zone lymphoma, except in residual germinal centers. However, in 10 of 11 cases of mantle cell lymphoma, the DRCs present in a loose tumor-associated meshwork were reactive with NGFR5; this finding is of potential utility in the differential diagnosis of low-grade lymphoproliferative disorders. In four of four cases of nodular lymphocyte predominance Hodgkin's disease, tumor nodule-associated DRCs were immunoreactive for NGFR in a pattern similar to that seen with DRC-1, but NGFR-positive DRCs were not observed in association with other types of Hodgkin's disease. These results indicate that NGFR expression by DRCs is not lost in follicular non-Hodgkin's lymphomas and mantle cell lymphomas. Nerve growth factor and NGFR may have a role in the function of DRCs and the formation of the DRC matrix in normal and neoplastic lymphoid follicles and in other DRC-associated neoplasms.
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PMID:Dendritic reticulum cell immunoreactivity for low-affinity nerve growth factor receptor in malignant lymphomas. 890 31

Patients developing Hodgkin's disease (HD) after a diagnosis of chronic lymphocytic leukemia (CLL), are frequently included in a series of patients with Richter's syndrome (RS). We sought to determine the natural history of the association of CLL and HD. Over a 21 year period, 1374 patients with CLL have been registered in our computer data base. Seven cases of CLL and HD have been documented and confirmed. The median age of these patients was 71 years (range 44-77) and clinical features included male gender (86%), B symptomatology (86%), rapidly progressive lymphadenopathy (71%), prior CLL therapy (71%), advanced Ann Arbor stage (86%), marrow involvement with HD (43%), and autoimmune hemolytic anemia (29%). HD was documented by excisional lymph node biopsy in six cases and splenectomy in one. Mixed cellularity HD was shown in six and nodular sclerosis in one. Five of the biopsies revealed intervening areas consistent with small lymphocytic lymphoma. The Sternberg-Reed (SR) cells were CD15+ in 6/7 cases, and Ki-1+ in the 6 patients tested. CD45 and CD20 staining of the SR cells was nonreactive. The median time to development of HD was 45 months (range 0 to 96). The overall responses to different chemotherapy regimens was approximately 25% with only one CR. Six patients have died at 3, 9, 10, 13, 15 and 36 months and one patient is alive with progressive disease at 11 months. Our data suggests that CLL patients have a heightened risk for HD, features of advanced HD on presentation, and a poor response rate with short survival.
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PMID:Hodgkin's disease variant of Richter's syndrome: experience at a single institution. 903 Nov 14


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