Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Large-cell anaplastic malignant lymphoma of T-type (T-LCAL) as an original form among human non-Hodgkin's malignant lymphomas in Updated Kiel Classification (1988) was defined. In human pathology T-LCAL presents a considerable diagnostic difficulties and is not associated with HTLV except some cutaneous forms. Comparative examination was carried out in 5 cases of baboon T-LCAL as a part of long-term investigation of the lymphoma outbreak in Sukhumi monkey stock. In tumor-bearing baboons routine morphological methods, immuno-morphological phenotyping of lymphoma cells with panel of MoAT and polyclonal antibodies to T- and B-lymphoid cell antigens and antigens of cell activation, including CD30 antigen, in cell suspension and on cryostate sections were used. STLV-provirus integration in DNA of lymphoma cells in PCR was determined. Diagnostically important morphological features of baboon and human T-LCAL include pronounced anaplasia and anisocytosis of CD30-positive large blast cells, tumour cell tendency to infiltrate sinuses and vascular walls. The presence of T-cell markers (CD2, CD3, CD4, CD8 in our cases) and antigens of cell activation (CD25, HLA-DR) were found. In DNA of baboon lymph node lymphomas (also in the cases without skin involvement) env- and tax-fragments of STLV-1 provirus were detected.
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PMID:[Large-cell anaplastic malignant CD30/Ki-1-positive T-type lymphoma, associated with STLV-1 virus (baboon malignant lymphoma model]. 761 47

The cure of human Hodgkin's tumors heterotransplanted into SCID mice can be achieved by two bispecific monoclonal antibodies (Bi-mAb) directed against the tumor-associated CD30 antigen and CD3 and CD28, respectively, and normal peripheral human blood T cells. We investigated the role of lymphocyte subsets and adhesion molecules in this Bi-mAb-mediated cytolysis. CD4+ lymphocytes were the most rapidly expanding subpopulation, but Bi-mAb-directed cytotoxicity was mediated preferentially by CD8+ lymphocytes and effector cells belonging to the CD45RO+ "memory" pool. Blocking of the LFA-1/ICAM-1 or CD2/LFA-3 adhesion pathways by mAb decreased Bi-mAb-mediated cytotoxicity. This was not due to inhibition of aggregate formation between Bi-mAb-coated T lymphocytes and target cells. Cross-linking of LFA-1 or CD2 molecules on lymphocytes prestimulated with Bi-mAb bound to CD3 and CD28 antigen lead to a more pronounced and prolonged rise in the intracellular concentration of free Ca2+. Additional CD2 cross-linking resulted in the tyrosine phosphorylation of distinct proteins. These findings indicate that adhesion molecules play a critical role and function as co-stimulatory signals rather than as cellular contact mediators in CD3 and CD28 Bi-mAb-stimulated T lymphocytes.
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PMID:The role of lymphocyte subsets and adhesion molecules in T cell-dependent cytotoxicity mediated by CD3 and CD28 bispecific monoclonal antibodies. 762 76

Epstein-Barr virus (EBV) has been implicated in the pathogenesis of a variety of lymphoproliferative disorders (LPDs) including endemic Burkitt's lymphoma, Hodgkin's disease (HD), HIV-associated non-Hodgkin's lymphomas (NHLs), and LPDs arising in immunosuppressed transplant patients. More recently, EBV has been associated with Ki-1-positive anaplastic large cell lymphoma (ALCL), a recently described NHL that shares with HD expression of the CD30 antigen Ki-1. Because EBV has been shown to induce Ki-1 expression in vitro, and ALCL has been diagnosed in patients with prior or concurrent HD or NHL, it has been proposed that EBV may mediate progression of a "primary" lymphoma to a "secondary" ALCL. We report a case in which an AIDS-associated, Ki-1-negative, large-cell immunoblastic lymphoma progressed to a Ki-1 positive ALCL. Analysis of the immunoglobulin heavy chain locus revealed a clonal relationship between these morphologically and immunophenotypically distinct tumors. Although EBV was absent from the original large-cell immunoblastic lymphoma as assessed by in situ hybridization for EBV-encoded small RNA1 (EBER1), polymerase chain reaction for EBNA-1, immunocytochemistry for latent membrane protein 1, and Southern blot hybridization for EBV terminal repeat sequences, all for techniques confirmed the presence of EBV in the secondary ALCL. Moreover, analysis of EBV terminal repeat sequences indicated that the ALCL resulted from expansion of a single EBV-infected clone. These data suggest that EBV may mediate progression of NHL to Ki-1-positive ALCL, and that in some instances, EBV may be involved in the later stages of clonal progression of NHL.
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PMID:Epstein-Bar virus and progression of non-Hodgkin's lymphoma to Ki-1-positive, anaplastic large cell phenotype. 767 77

Cross-linking of specific tumor antigens with the T-cell-associated CD3 and CD28 antigens can increase IL-2 secretion, proliferation and antigen-specific cytotoxicity in resting T cells. This cross-linking can be achieved effectively by bispecific monoclonal antibodies (BiMAb) with specificity for both the tumor antigen and CD3 or CD28 antigen, respectively. To take advantage of the enhanced activation of CD3 pre-activated T cells by additional activation via the CD28 antigen, BiMAb OKT3/HRS-3 with reactivity to both CD3 and the Hodgkin's-lymphoma-associated CD30 antigen and the BiMAb 15E8/HRS-3 with reactivity to both CD28 and CD30 antigen were generated by hybridoma fusion. Resting T cells, represented by Jurkat cells (CD3+/CD28+) were specifically activated to produce IL-2 by co-cultivation with an EBV-transformed B-cell line (LAZ509, CD30+/CD19+) only in the presence of the CD30/CD28 cross-linking BiMAb and an additional cross-linking anti-CD3/CD19 BiMAb (OKT3/6A4). Neither the cross-linking BiMAbs alone nor any combination of the monospecific parental MAbs induced a comparable IL-2 production by Jurkat cells in the presence of LAZ509. In addition, using a combination of these BiMAbs, an antigen-dependent cytotoxicity was induced by targeting APC-depleted peripheral blood lymphocytes to CD30+ L540 cells. T cells, previously specifically activated by CD3/CD30 in the presence of CD30 antigen, were cytotoxic to CD30+ cell lines only after incubation with BiMAb anti-CD28/CD30. Neither of the BiMAbs nor any of the parental antibodies induced a comparable effect. Our results indicate that such BiMAbs may offer a new approach for specific immunotherapy of Hodgkin's lymphoma, which takes advantage of cytokine secretion and cytotoxicity of activated T cells.
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PMID:CD30-antigen-specific targeting and activation of T cells via murine bispecific monoclonal antibodies against CD3 and CD28: potential use for the treatment of Hodgkin's lymphoma. 768 89

The expression, serological detection, and possible functional role of the CD30 antigen in Hodgkin's disease and anaplastic large cell lymphoma is well documented. In embryonal carcinoma (EC), the expression of this cytokine receptor has been demonstrated only by immunohistology. Because the CD30 monoclonal antibody Ki-1 was found to cross-react with an unrelated molecule, we examined by in situ hybridization testicular germ cell neoplasms for the presence of CD30-specific transcripts. CD30 mRNA was detectable in the tumor cells of 9 of 9 cases of EC or mixed germ cell tumors with an EC component but in no other nonlymphoid tumors. Thus, the CD30 transcript expression pattern proved to be identical to the immunostaining pattern seen with the CD30-specific monoclonal antibody Ber-H2. By Northern blot analysis, CD30 transcripts could be demonstrated in the EC cell line Tera-2. Employing a highly sensitive second generation sandwich enzyme-linked immunosorbent assay, we could detect the soluble CD30 molecule in 8 of 8 sera from patients with a diagnosis of EC but not in 8 of 10 sera from patients with other testicular germ cell tumors. In fetal tissue, no CD30-expressing germ cells or epithelial cells could be observed. Thus, the cellularly expressed CD30 marker for testicular neoplasms of EC type. Moreover, the serum levels of soluble CD30 antigen seem to be a promising parameter for monitoring patients with EC.
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PMID:CD30 antigen in embryonal carcinoma and embryogenesis and release of the soluble molecule. 785 55

Primary cutaneous large cell anaplastic non-Hodgkin lymphomas positive for Ki-1-antigen are rarely described. There are 100 published cases worldwide. Typically large cell anaplastic lymphomas have an inflammatory appearance, which often leads to false diagnosis and unsuccessful treatment with antibiotics. Histological examination reveals a highly malignant non-Hodgkin lymphoma. The tumour is composed of large pleomorphic lymphoid cells composed of T-cells in 80% of the cases and of B-cells in 10%. The immunological phenotype in the remaining 10% remains unclear. Crucial for the diagnosis is the expression of CD30 antigen in > 70% of the tumour cells. This article presents 5 cases of cutaneous Ki-1-positive lymphoma seen in our Berlin department during the last 10 years. In 4 patients the diagnosis was established in clinical stage I of cutaneous lymphoma without further manifestation; 1 patient had lymph node involvement and was in stage II. Total excision of the primary tumour in stage I with adjuvant polychemotherapy in stages II-IV led to complete remission in all cases. Long-term remissions were seen in case 1 (2 years) and in case 5 (1 year), whilst 2 patients showed local relapse, and 1 patient showed generalized lymphogenic and hematogenic metastasis. After repeated surgical removal or irradiation of the tumour and adjuvant polychemotherapy, further complete remission was achieved in 2 patients (up to now lasting 1 and 4 years). another patient has been in partial remission for the last 2 years. Our observations underline the high relapse rate of large cell anaplastic lymphoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Large cell anaplastic Ki-1 positive lymphoma of the skin. 5 personal cases and review of the literature]. 787 68

The Epstein-Barr virus (EBV) is associated with an increasing range of reactive and neoplastic lesions. There is a need for a sensitive and specific method for detecting latent EBV in routine histological sections. We report the use of a highly sensitive paraffin section RNA/RNA in situ hybridization (ISH) technique using digoxigenin-labelled antisense riboprobes for demonstrating EBV encoded small RNAs (EBERs), EBV gene products that are transcribed in abundance during latent EBV infection. We applied EBER-ISH to 846 paraffin embedded specimens, including cases of reactive lymphoid hyperplasia (n = 28), infectious mononucleosis (16), Burkitt's lymphoma (44), immunodeficiency-associated lymphomas in transplant recipients (9) and AIDS patients (128), Hodgkin's disease (130), CD30 antigen positive lymphomas (106), peripheral T-cell lymphomas (104), sporadic B-cell non-Hodgkin's lymphomas (162), undifferentiated nasopharyngeal carcinoma (86), salivary gland lymphoepithelioma (11), and oral hairy leukoplakia (5). Strong, reproducible EBER staining was seen in EBV latently infected cells in archival surgical biopsy and autopsy specimens. EBER-ISH is specific, has a sensitivity comparable to that of the polymerase chain reaction, and is now the method of choice for the in situ detection of latent EBV infection.
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PMID:Detection of Epstein-Barr virus small RNAs in routine paraffin sections using non-isotopic RNA/RNA in situ hybridization. 798 72

Expression of the CD30 antigen in lymphoid neoplasms and reactive lesions were examined immunohistologically using the monoclonal antibody BerH2. CD30 antigen was expressed in 17 of 18 patients with Hodgkin's disease (HD), all of three anaplastic large cell lymphomas (ALCL), 11 of 52 T-cell malignant lymphomas (TML) including ALCL, 13 of 153 B-cell malignant lymphomas (BML) including ALCL, two of three malignant histiocytosis and one of four plasmacytomas. Although a single case of small cell lymphoma was positive, in cases of mixed cellular morphology, neoplastic cells of larger or more pleomorphic nuclei tended to be stained more extensively and intensively. This antigen is expressed in TML significantly more often than in BML (P < 0.05). CD30 antigen was expressed less frequently at clinical stage I than those of stages II to IV. There was no significant relationship between CD30 antigen expression and that of proliferating cell nuclear antigen or CD43 antigen in non-Hodgkin's lymphomas (NHL). The CD30 antigen expression did not affect the prognosis of NHL overall, but in high grade TML, CD30 antigen-positive individuals tended to have a more favorable prognosis than those that were negative. In reactive diseases, some plasma cells, immunoblasts, interdigitating cells, follicular center cells and histiocytes were stained positively, but not always, and with variable intensity. These results suggest that CD30 antigen is expressed in various cell lineages to some extent and may relate to cellular activation in some instances. When making the histopathologic diagnosis of HD or NHL including ALCL, CD30-positive cell should be carefully interpreted.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:CD30 antigen in non-Hodgkin's lymphoma. 805 9

Reactive immunoblastic proliferations may be confused with certain types of non-Hodgkin's lymphoma and Hodgkin's disease on morphologic grounds. In addition, a characteristic antigen, CD30 (Ki-1; BerH2) on these neoplastic entities may be observed in morphologically atypical yet reactive florid immunoblastic proliferations such as those associated with acute infectious mononucleosis. Although it has been documented, a large series determining the frequency and extent of CD30 antigen expression on a variety of nonneoplastic immunoblastic proliferations is lacking. The authors studied 14 florid immunoblastic proliferations (9 in lymph nodes and 5 in tonsils) for CD30 antigen expression and for B- and T-cell paraffin markers. In situ hybridization to determine the presence of Epstein-Barr virus (EBV) genomes also was performed. Cases were classified into monospot-positive acute infectious mononucleosis (4 cases), EBV-related lymphoproliferative disorder suggestive of acute infectious mononucleosis (5 cases), and other etiologies (5 cases). CD30 Antigen expression was found on the immunoblasts in cases from all three categories and overall in 9 (64%) of 14 specimens. CD30 reactivity in the positive cases varied from occasional to numerous positive cells; 4 samples (3 EBV-related lymphoid proliferations and 1 vaccine-related lymphadenopathy) had numerous CD30-reactive immunoblasts. Expression of CD30 antigen on B or T cells and prominence of B or T cells within a proliferation were variable. Significant "atypia" of immunoblasts was found only in EBV-related disorders and correlated with B-cell prominence of the infiltrate. Appropriate clinical correlation and ancillary laboratory data are necessary to assist in differentiating these CD30(+)-reactive disorders from similar-appearing malignant lymphomas. Most important, a fresh tissue sample should be procured and adequately processed to allow for comprehensive determination of clonality and cellular lineage.
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PMID:CD30 antigen expression in florid immunoblastic proliferations. A clinicopathologic study of 14 cases. 808 51

CD30 is a member of the tumor necrosis factor receptor superfamily. CD30 was originally described as a cell surface antigen on primary and cultured Hodgkin's and Reed-Sternberg cells. In this study, recombinant human CD30 ligand was expressed on the surface of CV-1/EBNA cells and tested for biologic activities on a variety of different CD30+ human lymphoma cell lines. CD30 ligand enhanced Ig secretion of Epstein-Barr virus (EBV)-immortalized, CD30+ lymphoblastoid B-cell lines, but not Burkitt lymphoma lines. Recombinant CD30 ligand enhanced proliferation of "T-cell-like" Hodgkin's disease-derived cell lines and an adult T-cell leukemia cell line, but not "B-cell-like" Hodgkin's disease-derived cell lines, CD30+, EBV-immortalized lymphoblastoid B-cell lines, or CD30+ and EBV+ tumor B-cell non-Hodgkin's lymphoma cell lines. In addition, CD30 ligand mediated reduction of proliferation and viability, by induction of cytolytic cell death, of CD30+, large-cell anaplastic lymphoma cell lines. Two new antibodies, M44 and M67, against the CD30 antigen demonstrated similar biologic activities to the CD30 ligand. Taken together, these data demonstrate pleiotropic biologic activities of the CD30 ligand on different CD30+ lymphoma cell lines and indicate that the CD30-CD30 ligand interaction might have a pathophysiologic role in Hodgkin's and some non-Hodgkin's lymphomas.
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PMID:Pleiotropic effects of the CD30 ligand on CD30-expressing cells and lymphoma cell lines. 816 76


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