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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 surface of lymphocytes obtained from fresh biopsy specimens from 41 patients with malignant lymphoma and from 30 normal subjects or patients with non-neoplastic lymphadenopathy were investigated. Immunoglobulin on the cell surface was used to identify B cells, whereas T cells were recognized by their reactivity with an antithymocyte antiserum and their ability to form rosettes with sheep erythrocytes. Normal and inflammatory lymph nodes were composed predominantly of T lymphocytes, as were nodes from 14 patients with Hodgkin's disease. Two thymomas were T cell proliferations, whereas a node from a patient with ataxia-telangiectasia was devoid of T lymphocytes. The presence of immunoglobulin on the cell surface indicated that 19 of 21 lymphocytic lymphomas were B cell proliferations, whereas the cells from 3 histiocytic lymphomas (reticulum cell sarcomas) and 1 mixed histiocytic and lymphocytic lymphoma were devoid of surface immunoglobulin. In immunoglobulin-positive tumors, one predominant heavy chain and one predominant light chain could usually be identified, thus establishing the clonal character of the neoplastic proliferation. Ten of 11 diffuse poorly differentiated lymphocytic lymphomas were composed of cells with large amounts of surface immunoglobulin, whereas only 1 of 5 diffuse well differentiated lymphocytic tumors contained such abundant surface immunoglobulin. The surface immunoglobulin data indicate the existence of at least two subspecies of B cell neoplasms. A small lymphocyte with sparse surface immunoglobulin proliferates as diffuse well differentiated lymphocytic lymphoma and chronic lymphocytic leukemia, whereas a larger lymphocyte with abundant surface immunoglobulin proliferates as diffuse poorly differentiated lymphocytic lymphoma and lymphosarcoma cell leukemia.
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PMID:Lymphocyte surface characteristics in malignant lymphoma. 109 Jan 57

Since 26 years Hodgkins disease is classified according to the Rye classification into 4 types. This classification is based on morphology and has turned out to be clinically relevant. However, sometimes the classification on morphological and immunohistochemical ground can be difficult to put a special case in a defined category of the 4 types. In addition, there seems to be no sharp, or well defined borders between Hodgkin's disease and Non-Hodgkin's lymphomas, especially T-cell lymphomas. Immunophenotyping of small lymphocytes and detection of follicular dendritic cells can demonstrate typical patterns in different types of Hodgkin's disease. In all types of Hodgkin's disease there is the same amount of proliferating small T-cells present. Hodgkin cells are lymphoid cells with B- or T-cell markers. Hodgkin cells of nodular para-granuloma (lymphocyte predominant type of Hodgkin's disease) show m-RNA for one light chain in the cytoplasm which can be visualized by in situ-hybridization. A new technique called "molecular histology" is applied to Hodgkin's disease. This is a single cell PCR of immunostained cells extracted from tissue sections by a micromanipulator. This technique enables us for the first time to demonstrate light chain and heavy chain gene rearrangements in Hodgkin cells of nodular sclerosis and mixed cellularity type. Hodgkin's disease seems to be no single entity but a heterogenous group of B- and possibly T-cell lymphomas. In the B-cell types Hodgkin cells are probably pre-B and B-cells.
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PMID:[Hodgkin's disease--an entity?]. 128 67

The utility of staining for Leu M1 (CD15) as a diagnostic aid in Hodgkin's disease has been questioned because of a relative lack of specificity and sensitivity. Furthermore, interpretation is often made difficult by staining that tends to be weak and focal. Because the murine monoclonal anti-Leu M1 antibody is of immunoglobulin M type, it is reasonable to wonder whether improved immunohistochemical staining might result from use of a secondary goat antibody specific for the mouse mu heavy chain instead of the traditional one against mouse immunoglobulin. The two methods were compared, using a biotin-avidin detection system, on paraffin sections from 15 cases of Hodgkin's disease: 9 nodular sclerosing, 1 mixed cellularity, and 5 of nodular lymphocytic and histiocytic (L&H) type. In the nodular sclerosing/mixed cellularity group, the mu-specific detection method resulted in a greater number of cases with reactive Hodgkin's cells (7 versus 5), stained an average of more than three times as many neoplastic cells in each case (49% versus 14%), and usually produced staining that was distinctly more intense, often in a membrane and paranuclear distribution characteristic of Leu M1 in Hodgkin's cells. In the noLeu M1 in Hodgkin's cells. In the nodular L&H group, 1 case showed weak, focal staining with the newer method. None of the L&H cases stained using the traditional technique. It is concluded that use of a second-stage antibody that is directed specifically against mu heavy chains results in an improvement in immunohistochemical staining for Leu M1 in paraffin sections, which is of practical significance.
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PMID:Enhanced staining for Leu M1 (CD15) in Hodgkin's disease using a secondary antibody specific for immunoglobulin M. 134 92

This is a report on our attempt to use polymerase chain reaction (PCR) to detect rearrangement of the immunoglobulin gene in the tissue specimens obtained from 30 patients with non-Hodgkin's lymphomas. There were 20 B-cell lymphomas and 10 T-cell. All 20 B-cell lymphomas but none of the 10 T-cell lymphomas had JH rearrangement by Southern analysis. Two pairs of primers (V670/OL-4 and VH26/OL-4) were designed to amplify the CDR3 region of the immunoglobulin gene heavy chain. The PCR analysis was positive using either one or both pairs of primers in 11 of the the 20 cases (55 per cent) of B-cell lymphomas which all had positive rearrangement by Southern analysis. The two pairs of primers seemed to produce complementary results as the specimens may be positive to one pair but negative to the other. The false negative rate of 45 per cent is however much higher than the respective figures of 18 per cent and 0 per cent observed in our patients with acute lymphoblastic leukemia and chronic lymphocytic leukemia in a previous study. Peripheral blood and bone marrow biopsy specimens obtained at the time of initial diagnosis were available from 10 patients with B-cell lymphomas whose lymph node biopsy specimens at the time of diagnosis were positive by both Southern analysis and PCR. All these peripheral blood and marrow specimens had no microscopic evidence of involvement by lymphoma cells and JH rearrangement was not detected by Southern analysis. However, rearranged bands identical to that of the lymph node biopsy specimen were detected by PCR in the peripheral and marrow blood of one of them. This PCR technique has been shown to have a sensitivity of 0.1 per cent in our previous report and may be more useful than morphology alone or Southern analysis in detecting minimal lymphomatous involvement in the peripheral blood and bone marrow at the time of initial diagnosis. Further clinical correlation is required to confirm the finding.
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PMID:Detection of immunoglobulin gene rearrangement in B-cell lymphomas by polymerase chain reaction gene amplification. 139 11

The presence of the translocation t(8;14)(q24;q32) has not been well described in follicular lymphoma (FL). In a consecutive series of 278 karyotypically abnormal non-Hodgkin's lymphomas (NHL), six patients with FL showing a t(8;14) without a t(14;18)(q32;q21) were identified. They ranged in age from 45 to 73 years. The cell type was mixed in four patients, small-cleaved in one, and large-cleaved in one; four cases also contained diffuse areas. All cases tested displayed monoclonal surface Ig. The clinical courses were consistent with the histologic subtypes, being less aggressive than other t(8;14)-bearing NHL. In five cases, frozen tissue was available for Southern blotting. The BCL2 gene showed a germline configuration when studied with the MBR, MCR, and 5' cDNA probes. The MYC gene also appeared unrearranged using an exon-1 probe with EcoRI or HindIII digestion. Analysis of the Ig heavy chain (IgH) gene with a JH region probe and BamHI or EcoRI digestion showed only one rearranged band in all cases, indicating that the 14q32 breakpoint did not lie in either the J or switch-mu (SM) regions. In four cases, the exon-1/intron-1 border of the MYC gene, a target area for point mutations in cases of t(8;14) that do not display rearrangements of the MYC gene, was enzymatically amplified and sequenced; no point mutations were identified. The indolent behavior of our six cases, and the finding that the molecular structure of the t(8;14) in these cases does not follow the pattern of breakpoint sites and point mutations defined in other histologic subtypes of NHL with this translocation, suggest that the t(8;14) in these cases is cytogenetically and molecularly distinct from the t(8;14) seen in high-grade NHLs, and is relatively ineffectual in terms of MYC deregulation, or that other genetic elements at these chromosomal sites may be involved. Further analysis of these tumors may provide insights into MYC deregulation and BCL2-independent FL.
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PMID:Follicular lymphoma with t(8;14)(q24;q32): a distinct clinical and molecular subset of t(8;14)-bearing lymphomas. 156 38

Anti-BLA.36 is an antibody that recognizes a glycoprotein with an apparent molecular weight of 36 kilodaltons, termed B lymphocyte antigen (BLA.36). By using an immunochemical staining technique, BLA.36 was found to be specifically expressed on Hodgkin's and human B cell lines including early B progenitor cells. Other cell lines representing T cell lymphomas, non-B large cell lymphomas, melanomas and carcinomas were consistently negative. BLA.36 is distinct from the previously identified antigens of hematopoietic cell lineage. The specificity of expression of BLA.36 in tissue sections mirrored that of cell lines. In normal tissues, BLA.36 was detectable predominantly on cells in the germinal center and mantle zone of reactive follicles in lymph nodes and spleens. In hematopoietic malignancy, the antigen was expressed on the surface of Reed-Sternberg cells, mononuclear Hodgkin's cells and also on malignant cells of B cell lineage. BLA.36 was also observed on lymphoid cells of 10 to 24 week fetal liver: a double-antibody-staining method revealed that these BLA.36-positive cells also contained immunoglobulin mu heavy chain consistent with identification as early B cells. Under these conditions, T lymphocytes, histiocytes, granulocytes, macrophages, stromal cells in lymphoid tissue, and both normal and neoplastic epithelial cells were consistently negative for the expression of the antigen, with the single exception of a variable proportion of Kupffer cells in normal liver. The antibody has already established its usefulness for the identification of Reed-Sternberg and Hodgkin's cells, and also normal and malignant B lymphocytes in frozen as well as formalin-fixed tissue sections. Furthermore, binding of F(ab)2 fragments of anti-BLA.36 to antigen-positive cell lines specifically inhibited the proliferation of cells. Such an effect was eliminated by the removal of the antibody from the culture-medium, suggesting a possible growth-related function of the antigen in Hodgkin's and B cells.
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PMID:BLA.36: a glycoprotein specifically expressed on the surface of Hodgkin's and B cells. 169 46

Detailed immunophenotypic analyses of immunologically classified leukemias and lymphomas showed that CD40 displays an exquisite B-lineage specificity within the human lymphopoietic system. Notably, 82% of B-lineage chronic lymphocytic leukemias (CLLs), 82% of B-lineage hairy cell leukemias (HCLs), 86% of B-lineage non-Hodgkin's lymphomas (NHLs), and 29% of B-lineage acute lymphoblastic leukemias (ALLs) were CD40+. Quantitative analyses of the correlated expression of CD40 and other B-lineage differentiation antigens on fetal lymphoid precursor cells by multiparameter two-color/three-color flow cytometry, combined with analyses of sequential antigen expression on fluorescence-activated cell fluorescence activated cell sorter (FACS) isolated immunologically distinct fetal B-cell precursor subpopulations during in vitro proliferation and differentiation, provided evidence that the acquisition of CD40 antigen in human B-cell ontogeny occurs subsequent to the expression of CD10 and CD19 antigens but before the surface expression of CD20, CD21, CD22, CD24, and surface immunoglobulin M (sIgM). Some leukemic pro-B cells from ALL patients as well as normal pro-B cell clones from fetal livers displaying germline Ig heavy chain genes were CD40+, indicating that the acquisition of CD40 antigen likely precedes the rearrangement of Ig heavy chain genes. CD40+ FACS-sorted malignant cells from B-lineage ALL as well as B-lineage NHL patients were capable of in vitro clonogenic growth, indicating the CD40 antigen is expressed on clonogenic leukemia and lymphoma cells. This hypothesis was confirmed by the ability of an anti-CD40 immunotoxin that we used as an antigen-specific cytotoxic probe to effectively kill clonogenic B-lineage ALL and NHL cells.
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PMID:Temporal association of CD40 antigen expression with discrete stages of human B-cell ontogeny and the efficacy of anti-CD40 immunotoxins against clonogenic B-lineage acute lymphoblastic leukemia as well as B-lineage non-Hodgkin's lymphoma cells. 170 26

The molecular structure of reciprocal translocations associated with low grade and high grade non-Hodgkin's lymphomas occurring together was analysed in two tumors. Sequential biopsies documented histological transformation of a large cell lymphoma to an immunoblastic lymphoma bearing t(14;18)(q32;q21) and t(8;22)(q24;q11). A second tumor, a small non-cleaved cell lymphoma, demonstrated a t(8;14)(q24;q11) as well as t(18;22)(q21;q11). DNA analysis from these tumors showed rearrangements at the Ig heavy chain, kappa and lambda light chains, BCL2 and c-MYC loci. Utilizing multiple enzyme digests and different probes spanning the BCL2, c-MYC and Ig genes, mapping of DNA break-points was performed. In both these tumors primary translocation events dysregulating the BCL2 or c-MYC were identified to have occurred in a pre-B-cell. Based on these results and those published previously, a sequence of B-cell development during which somatic recombination errors lead to the genesis of specific translocations is proposed. From these studies it is inferred that secondary dysregulation of a c-MYC in a lymphoma tumor carrying dysregulated BCL2 gene leads to rapid progression to high grade disease.
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PMID:Molecular structure of double reciprocal translocations: significance in B-cell lymphomagenesis. 199 41

We searched for the presence of IL2 receptor (CD25) on T cells as an activation marker in lymph nodes involved by B-cell non-Hodgkin's lymphomas (B-NHL). In 26 malignant lymph nodes studied, the number of CD25+ T cells among total T cells was usually low when assessed by immunofluorescence analysis (mean +/- SD: 6.7% +/- 11.2%), but greatly increased when an immunomagnetic rosette method was used (mean +/- SD: 17.5% +/- 16.6%). In six cases, CD25-/CD25/CD25+ cells were isolated by immunomagnetic separation, with a purity greater than 97% for both populations. Expansion of CD25-/CD25+ T cells was obtained with IL2 and PHA, then conditioned media (CM) were prepared. No IL2 activity was found in CM from both CD25-/CD25+ T cells when tested on CTLL2 cells. BCGF and BCDF mu/gamma activities were assayed on normal B cells stimulated with soluble or insolubilized anti-mu antibodies(BCGF) or with Cowan I (BCDF). Results of production of all these activities were comparable for both populations, and thus do not favour the possibility that CD25+ T cells closely associated with malignant B-NHL cells in lymph nodes may influence their proliferation (BCGF) or expression/secretion of heavy chain isotype (BCDF mu/gamma).
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PMID:Detection, isolation and functional studies of CD25+ T cells in lymph nodes involved by B-cell non-Hodgkin's lymphomas. 206 35

Two atypical human non-Hodgkin's lymphomas (NHLs) that exhibited unusual genotypic and in situ immunophenotypic abnormalities are described. Immunophenotypically, both NHLs lacked surface Ig heavy chains. With the exception of the MB2 B-cell-associated antigen, no B- and T-cell differentiation antigen was detected in case 1. NHL 2 failed to show evidence of clonality by immunohistochemical analysis but revealed the presence of many B-lymphocytes with an abnormal phenotypic profile: CD19+, CD20+, CD22+, kappa-, lambda-, CD9-, CD10-, CD21-, and CD24-. Genotypic analysis indicated that both lymphomas derived from anomalously matured pre-B-cells that had rearranged the lambda or kappa light chain genes but not the Ig heavy chain gene. The neoplastic cells of the two NHLs resemble the light chain-only B-cells recently discovered, following Epstein-Barr virus immortalization, in the human bone marrow. The authors' data confirm, therefore, the existence of the light chain-only B-cells in the human hematopoietic compartment. Moreover, their results emphasize the conclusive role of the immunogenotypic analysis in defining clonality, lineage, and maturation abnormalities of such atypical NHLs.
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PMID:Genotypic and immunophenotypic characterization of two human light chain-only B-cell non-Hodgkin's lymphomas. 212 Oct 20


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