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

A case of syncytial variant of nodular sclerosing Hodgkin's disease in a 34-year-old woman is reported. Histologically, numerous Reed-Sternberg (RS) cells and their variants were seen in sheets. They were positive for CD30, CD15, CD25, and HLA-DR antigens. In addition, they expressed CD45 antigen and T-cell antigens (CD2, CD4). Molecular genetic analysis showed that this case had a germ line configuration for T-cell receptor (TCR) beta chain, TCR gamma chain, and immunoglobulin heavy chain genes. The percentage of the neoplastic cells in the specimen identified by CD30 positive cells was about 20% which was far above sensitivity of the molecular genetic analysis. Such analysis is reliable as to judgement of the results. Thus, these findings suggest that the RS cells and their variants in the present case are not derived from mature T cell in spite of their T-cell antigens expression.
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PMID:[Syncytial variant of nodular sclerosing Hodgkin's disease expressing T-cell antigens]. 206 87

Surface IgG expression of 29 cases of hairy cell leukemia (HCL) was assessed using IgG-subclass-specific monoclonal and F(ab)'2 polyclonal antibodies. A marked preference for the IgG3 subclass was found, as 16 of 19 IgG-positive HCL's expressed IgG3. In 10 cases, IgG3 was concurrently expressed with other heavy chains. No preferential IgG3 expression was observed in 11 IgG-positive non-Hodgkin's lymphomas. The marked predominance of IgG3 in HCL suggests a deviation in heavy chain class switching that may be related to the characteristically very low expression of LFA-1 and ICAM-1 molecules on hairy cells, and hence a defect in T-cell hairy cell interaction.
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PMID:Hairy cell leukemia preferentially expresses the IgG3-subclass. 213 55

There is a wide spectrum of lymphoid hyperplasias and neoplasias that may arise in salivary gland tissue. Some lesions arise in the extranodal mucosal-associated lymphoid tissue (MALT) located in the salivary gland; others arise within the lymph nodes embedded in the gland parenchyma. It is difficult to distinguish the site and cell of origin in many salivary gland lymphoid lesions, but recent advances in the identification of specific gene rearrangements in lymphomas corresponding to normal follicular center cells have provided a molecular marker for these tumors. The genes involved are the immunoglobulin heavy chain gene (located on chromosome 14) and the blc-2 gene (located on chromosome 18). This specific chromosomal translocation [t(14;18)] has been sought in extranodal lymphomas of skin, stomach, and intestine. To date, primary lymphomas in these sites have lacked the t(14;18) translocation. We investigated the t(14;18) using molecular techniques in a series of morphologically and immunophenotypically defined malignant non-Hodgkin's lymphomas presenting in the salivary gland. Of the seven cases we examined, three had molecular evidence of a t(14;18) translocation. All three lesions had a nodular growth pattern. The four cases lacking bcl-2 rearrangement had diffuse growth patterns. In addition, all four bcl-2 germline cases had morphologic or clinical findings consistent with a MALT origin. In contrast to the data published to date for primary lymphomas of the stomach, skin, and intestine, our findings indicate that salivary gland lymphomas frequently contain bcl-2 gene rearrangement. In addition, there appear to be differences in the clinical findings of bcl-2 rearranged and bcl-2 germline salivary gland lymphomas.
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PMID:bcl-2 gene rearrangement in salivary gland lymphoma. 206 17

In addition to conventional morphological, histological and immunological marker studies, cells from 150 children with leukemia or non Hodgkin's lymphoma were analysed using the Southern blot hybridization technique to examine immunoglobulin- (Ig) and T-cell receptor (TCR) gene rearrangements. Patients with B-lineage leukemia or NHL demonstrated in 90% an Ig heavy chain gene rearrangement, 6% with an additional light chain kappa gene rearrangement. Combined Ig- with TCR-beta-gene rearrangements were mainly found in patients with common ALL: 19% at first presentation, and 33% in relapse. Moreover, 6 c-ALL patients showed rearrangements in all 3 gene loci (JH-, Ck- and TCR). Based on the developmental hierarchy of Ig- and TCR gene rearrangements it was possible to further subclassify c-ALL into different stages of B cell development. No correlation could be established between the different constellations of gene rearrangements, the number of rearranged fragments and the course of illness. All patients with T-lineage leukemia or NHL demonstrated TCR rearrangements of the beta-, g- and delta-gene loci, two with an additional Ig gene rearrangement. These data confirm recent reports indicating that immunoglobulin heavy chain gene rearrangements are not restricted to B-lineage neoplasms. Furthermore, non-germline configuration was found in tumor cells of every patient with AUL, O-ALL and AHL, permitting a classification to B- or T-cell lineage. Noteworthy is that every AML patient with Ig- and/or TCR gene rearrangements showed a poor or non-response towards therapy. Specimens of individual patients with differently involved tissues at diagnosis always showed an identical rearrangement. The intensity depended on the number of infiltrating blast cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical applications of the study of immunoglobulin and T-cell receptor gene rearrangements in acute leukemia and non-Hodgkin's lymphoma in children]. 239 11

We present two patients with human immunodeficiency virus-1 (HIV-1) infection in whom T-cell non-Hodgkin lymphoma developed, based on pathologic diagnosis, immunophenotyping, and T-cell receptor gene rearrangement. Both cases were positive for human immunodeficiency virus-1 by enzyme-linked immunosorbent assay and immunoblot methods. Histologic sections from each patient showed a high-grade pleomorphic T-cell non-Hodgkin lymphoma, and immunophenotyping demonstrated a prevalence of reactivity for CD4 (helper) over CD8 (suppressor) antigens. T-cell receptor beta-chain gene rearrangement studies revealed a rearranged pattern with either the HindIII or BamHI enzymes, whereas immunoglobulin heavy chain genes retained a germ-line configuration. Viral sequences specific for human T-cell leukemia virus-I, human T-cell leukemia virus-II, or HIV-1 were not detected. Thus, although rare, T-cell non-Hodgkin lymphoma may be observed in HIV-1-infected individuals.
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PMID:T-cell non-Hodgkin lymphoma in human immunodeficiency virus-1-infected individuals. 250 Aug 50

We analyzed the rearrangement of T-cell receptor (TcR) delta chain gene in 88 cases of lymphoproliferative disorders; 31 acute lymphoblastic leukemias/lymphoblastic lymphomas (ALL/LBL); 27 adult T-cell leukemias/lymphomas, 9 angioimmunoblastic lymphoadenopathies (AILD); 10 T-cell lymphomas (non-Hodgkin's lymphoma); and 11 Hodgkin's disease. All of 9 T-ALL/LBL cases, of which 4 cases have neither beta nor gamma gene rearrangement, had a new rearranged band of TcR delta locus. Ten of 16 B-lineage ALL/LBL had rearranged band(s) or deletion of TcR delta locus. The rearranged bands were recognized in 2 cases of AILD and 1 case of T-cell lymphoma. All cases of adult T-cell leukemias/lymphomas, 4 of AILD, 4 of T-cell lymphoma, and 8 of Hodgkin's disease had deleted TcR delta locus. Heterogeneous findings of TcR delta locus analysis were observed in AILD, T-cell lymphoma, and Hodgkin's disease. In 16 cases with TcR delta rearrangement, the J delta 1 region was frequently used and the J delta 2 region was rearranged in one AILD. It is suspected that J delta 3 was used in one T-ALL/LBL. There was no correlation between the phenotypic pattern of CD3, CD4, CD8 in T-cell disorders and the rearrangement of the TcR delta gene. These findings suggest that the newly identified TcR delta chain gene rearranges at a very early stage of T-cell ontogeny; prior to the other TcR genes and perhaps at almost the same stage with CD7 expression. The TcR delta gene is useful in assessing clonality for the most immature T-cell neoplasms not showing rearrangement of the other TcR genes. This gene is not lineage specific; however, when used in conjunction with immunoglobulin heavy chain gene, it may be a useful tool to distinguish lymphoid lineage of ALL/LBL.
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PMID:Rearrangement of T-cell receptor delta chain gene as a marker of lineage and clonality in T-cell lymphoproliferative disorders. 250 Oct 27

Each of three individuals with acquired immunodeficiency syndrome (AIDS) developed a pleomorphic malignant neoplasm in which a precise histopathologic diagnosis could not be rendered. In each case, the tumor cells expressed leukocyte common antigen and a variable constellation of antigens associated with B- and T-cell activation (HLA-DR, T9, T10, BL2, BL3, Ki-24, BLAST-2). They lacked all B cell, T cell, myeloid, and monocyte lineage-restricted antigens, resulting in their classification as hematopoietic neoplasms of uncertain lineage. However, antigen receptor gene rearrangement analysis demonstrated that each of these three neoplasms exhibited clonal immunoglobulin heavy chain and kappa light chain gene rearrangements and lacked T-cell receptor beta chain gene rearrangements and therefore were B cell-derived non-Hodgkin's lymphomas (NHL) representative of an equivalent, relatively mature stage of B-cell differentiation. In contrast with most AIDS-associated NHLs, each of these three neoplasms lacked c-myc gene rearrangements and contained Epstein-Barr virus (EBV) proteins and/or sequences. These studies demonstrate that these three AIDS-associated neoplasms of uncertain lineage exhibit a strikingly similar constellation of distinctly uncommon morphologic, immunophenotypic, and molecular genetic characteristics that distinguishes them substantially from the vast majority of NHLs that have been reported to occur in association with AIDS. The consistent presence of EBV proteins and/or DNA sequences suggests that the Epstein-Barr virus played a pathogenetic role in the development of these three AIDS-associated neoplasms. Finally, these studies further illustrate the utility of antigen receptor gene rearrangement analysis in the diagnosis and classification of hematopoietic neoplasms of uncertain lineage.
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PMID:Molecular genetic analysis of three AIDS-associated neoplasms of uncertain lineage demonstrates their B-cell derivation and the possible pathogenetic role of the Epstein-Barr virus. 253 19

A new cell line, SUP-HD1, was established from the pleural effusion of a patient with nodular sclerosing Hodgkin's disease (NSHD). The SUP-HD1 cells had the characteristic morphology of Reed-Sternberg cells and contained acid phosphatase and nonspecific esterase. The cells lacked the Epstein-Barr virus (EBV) genome and reacted with monoclonal antibodies (MoAbs) against CD15 (Leu-M1), CD25 (Tac), CD71 (OKT9), Ki67, and HLA-Dr. However, the SUP-HD1 cells were nonreactive with MoAbs that specifically identify T lymphocytes, B lymphocytes, and macrophage/myeloid cells. Karyotype analysis of the cell line showed clonal abnormalities involving 1p13, 7p15, 8q22, and 11q23, chromosomal locations, at which breakpoints have been reported in HD. Southern blot analysis demonstrated rearrangement of the immunoglobulin heavy chain and kappa light chain genes as well as the gene for the beta chain of the T-cell receptor (TCR). Transcriptional analysis showed expression of RNAs for kappa light chain, interferon-gamma (IFN-gamma), and interleukin-2 receptor (IL-2R) but not IL-2. The SUP-HD1 cells lacked cytoplasmic and surface immunoglobulin heavy chain, but a small amount of cytoplasmic kappa light chain was detected. The presence of nuclear factor kappa B (NF kappa B), a B-lymphocyte-associated transcription factor, was demonstrated in stimulated and unstimulated cells. In addition, the SUP-HD1 cell line, produced IFN-gamma, a T-lymphocyte-associated lymphokine. Based on these data, the SUP-HD1 cells appear to be aberrant lymphocytes with characteristics of both activated B and T lymphocytes. Elaboration of lymphokines such as IFN-gamma by the malignant cells may represent one explanation for the unique clinical and pathologic features of HD.
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PMID:SUP-HD1: a new Hodgkin's disease-derived cell line with lymphoid features produces interferon-gamma. 232 24

The cell line HDLM-2 was established from the pleural effusion of a patient with Hodgkin's disease. Here, we describe the morphological, cytochemical, enzymological, immunological, molecular biological, and functional characteristics of the cell line. The results of this multiparameter profile show that HDLM-2 is different from other well-studied leukemia-lymphoma cell lines including other Hodgkin's disease derived cell lines. HDLM-2 cultures contain mainly mono- or binucleated cells, but also prominent giant cells with two to ten nuclei. HDLM-2 cells do not express an immunophenotype characteristic of a given cell lineage. However, the cells are positive for Ki-1, HeFi-1, Leu-M1, Tac, and HLA class II markers. Cytochemical, enzymological, and functional data are equally inconclusive, but are definitely not compatible with a monocyte/macrophage profile. Analysis of the gene status documents that T-cell receptor beta- and gamma-chain genes are rearranged while immunoglobulin heavy chain genes are in germline configuration. The combined results indicate a T-cell origin of HDLM-2 cells. The evidence available from this and other established Hodgkin's disease derived cell lines suggests a lymphoid origin of Hodgkin and Reed-Sternberg cells.
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PMID:Characterization of Hodgkin's disease derived cell line HDLM-2. 260 52

We have studied a remarkable family with seven cases of malignant lymphoma extending through three generations wherein five sisters and their mother had histopathologically documented non-Hodgkin's lymphoma, while a granddaughter had Hodgkin's disease. An immunological study of three lymphoma survivors, nine of their first degree relatives, and four spouse controls was undertaken. Significant findings consisted of a depressed serum IgG3 level in four of the nine first-degree relatives; in two of these four, lymphocyte stimulation by both pokeweed mitogen and concanavalin A were significantly depressed. The subtle immunological abnormalities present in this kindred may be associated with the pathogenesis of the lymphomas.
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PMID:Genetic and immunopathological findings in a lymphoma family. 271 49


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