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)

The Ki-1-antibody was raised against a cell-line of Hodgkin-cells, and reacts with most Hodgkin- and Reed-Sternberg-cells. By use of this antibody a new entity of non-Hodgkin's lymphomas has been identified; the anaplastic large cell lymphoma. We report our experience from studying 16 such tumours diagnosed during the period October 1986 to February 1988. In three cases the anaplastic large cell lymphoma appeared in patients who presented Hodgkin's disease as well. Of 15 cases studied using frozen section immunohistochemistry, ten showed T-, one B-, and one monocyte/macrophagephenotype, whereas three cases presented a mixed T-, B- and monocyte/macrophagephenotype. All cases showed a high proliferative activity as evaluated by presence of activation antigens. In paraffin sections six of 16 cases expressed epithelial membrane antigen (EMA). In 13 cases EMA, leucocyte common antigen (LCA) and Ber-H2 (a Ki-1-antibody) reactivity was compared in paraffin and frozen sections. The EMA reactivity was of nearly equal intensity in paraffin and frozen sections, while the reactivity of LCA and Ber-H2 was significantly reduced in paraffin sections, implying only partial preservation of the antigens. Clinically, most cases were in an advanced (III and IV) stage by the time of diagnosis. Of 14 actively treated patients, nine went into complete and two into partial remission, while three patients did not respond. Six patients are dead, five after less than one year. The coexistence of anaplastic large cell lymphoma and Hodgkin's disease and the common Ki-1 (CD30) antigen expression in these tumours suggest a possible histogenetic relationship.
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PMID:[Giant cell anaplastic anemia]. 277 96

Ki-1 (CD30) antigen expression has been considered to be restricted to hematopoietic tissues including the recently described anaplastic large cell lymphoma and Reed-Sternberg (RS) cells in Hodgkin's disease. Its presence on some activated lymphocytes in non-neoplastic lymphoid tissues has been used as evidence that such cells might represent the physiologic counterpart of RS cells. In this study expression of CD30 antigen in 117 nonhematopoietic tumors was investigated using monoclonal antibody Ber-H2. The antigen was regularly expressed in frozen section (strongly) and paraffin section (less strongly) by embryonal carcinomas (8 of 10 studied) and the embryonal elements of mixed germ cell tumors (4 of 4), but not in other types of germ cell tumors (0 of 11) or nonhematopoietic tumors (0 of 92). Normal adult, neonatal, and fetal testes were negative for CD30 antigen, as were other fetal tissues and placenta. Ki-1 antibody gives similar results in frozen section. These findings have implications for theories suggesting an origin of RS cells from activated lymphocytes. They are also important for determining the diagnostic significance of CD30 positivity in a tumor of unknown origin, and suggest possible new uses for CD30 antibodies in routine diagnostic immunohistology.
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PMID:Ki-1 (CD30) antigen is regularly expressed by tumor cells of embryonal carcinoma. 284

Endothelial cell activation and alterations of intravascular coagulation were investigated in 27 cases of Hodgkin's disease (HD), in five cases of anaplastic large cell lymphoma (ALCL), and in ten reactive lymph nodes. Lymph node sections were immunostained for E-selectin, a molecule present on cytokine-activated endothelial cells; for tissue factor (TF), a cellular initiator of the coagulation cascade; for glycoprotein (gp) II/III, a platelet-specific antigen; and for fibrin. In HD, vascular activation was particularly prominent in the nodular sclerosis subtype, as indicated by a larger number of E-selectin-positive blood vessels (72 +/- 49) compared with mixed cellularity (22 +/- 37). High expression of E-selectin was associated with alterations of intravascular coagulation, as indicated by immunostaining of some vascular endothelial cells for TF, by a higher incidence of intravascular thrombi, and by the extensive presence of areas of fibrin exudation and necrosis. In ALCL, the levels of endothelial cell activation and intravascular coagulation were comparable to those of HD nodular sclerosis. In reactive nodes, some E-selectin-positive blood vessels were observed only in 3/10 cases; immunostaining for TF was not detected on endothelial cells; and alterations of intravascular coagulation were rarely observed.
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PMID:Vascular activation in the histopathogenesis of Hodgkin's disease: potential role of endothelial tissue factor in intravascular thrombosis and necrosis. 750 70

The product of the proto-oncogene c-kit is a transmembrane receptor protein that plays an important role in the regulation of normal and neoplastic hematopoiesis via the interaction with its specific ligand termed stem cell factor. To examine whether c-kit product is possibly involved in the pathogenesis of human lymphomas, we analyzed the expression of the c-kit protein in neoplastic cells from a variety of lymphoid tumors by immunostaining of lymph node frozen sections with the 17F11 antibody, detecting an extracellular epitope of the c-kit receptor, and of c-kit RNA by Northern blot hybridization. Of 24 nonHodgkin's lymphomas (NHL) of B- and T-cell phenotype, none expressed immunodetectable c-kit protein that was also not evidenced in lymphoid cells of reactive lymph nodes and normal tonsils. In contrast, c-kit protein was expressed by Reed-Sternberg cells and their mononuclear variants from 11 of 21 Hodgkin's disease (HD) cases, and in tumor cells from 11 of 16 cases of CD30+ anaplastic large cell lymphoma (ALCL). c-kit specific mRNA was also detected in lymph node tissues from HD and ALCL cases but not in neoplastic tissues from NHL other than ALCL. In addition, c-kit/CD30+ tumor cells were evidenced by flow cytometry in a patient displaying massive bone marrow involvement by ALCL. With the exclusion of lymphocyte predominance cases of HD that resulted c-kit expression and the other histologic subtypes of HD or the immunologic phenotype of tumor cells (B, T, nonB-nonT) in both HD and ALCL. The highly restricted expression of the c-kit product among human lymphomas to HD and ALCL provides a further biologic link between these two closely related lymphoma entities.
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PMID:Expression of the c-kit receptor in human lymphomas is restricted to Hodgkin's disease and CD30+ anaplastic large cell lymphomas. 1465 71

Hodgkin's disease (HD) and Ki-1 positive anaplastic large cell lymphoma (Ki-1 ALCL) appear pathologically and immunohistochemically related, and a common histogenesis has been postulated in at least some cases. The breakpoints of the t(2;5) (p23;q35) [corrected] translocation, which is reported in about 40% of Ki-1 ALCL, have recently been cloned. They involve a novel tyrosine kinase gene, ALK, at 2p23 and the nucleophosmin gene, NPM, at 5q35. Reverse transcriptase polymerase chain reaction (RT-PCR) using NPM and ALK primers consistently detects a fusion product in Ki-1 ALCL cases with the translocation. To determine if this tumor-specific genetic alteration also occurs in HD, we performed NPM-ALK RT-PCR on RNA samples extracted from 40 lymph node biopsies of HD (25 nodular sclerosis, 11 mixed cellularity, 2 lymphocyte depleted, 2 lymphocyte predominant). Using control samples, the sensitivity of the NPM-ALK RT-PCR assay was shown to be at least 1:10(4). Amplifiable template was confirmed in all samples by RT-PCR using beta-actin primers. None of the 40 cases showed the expected 177-bp RT-PCR product indicative of the translocation. We conclude that the most common primary genetic alteration in Ki-1 ALCL, the t(2;5), is absent or very infrequent in typical cases of HD. These results further support the concept that HD and Ki-1 ALCL are pathogenetically distinct entities.
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PMID:Reverse transcriptase polymerase chain reaction for the Ki-1 anaplastic large cell lymphoma-associated t(2;5) translocation in Hodgkin's disease. 752 17

CD30 expression is found on Hodgkin and Reed-Sternberg cells, anaplastic large cell lymphoma cells and on activated B or T lymphocytes. Recently CD30 was shown to be a transmembrane receptor that is significantly homologous to the tumor necrosis factor receptor (TNFR) family. Ligands for most members of this family, including CD30, have now been identified. This review summarizes the role of the different TNFR family members in lymphocyte proliferation and differentiation in an attempt to understand more clearly the role of CD30 expression in the pathogenesis and clinical behavior of non-Hodgkin's lymphomas. We state that CD30 expression is of prognostic relevance in primary cutaneous and nodal T cell lymphomas in contrast to the absence of clinical relevance of CD30 expression in B cell lymphomas.
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PMID:CD30 expression in normal and neoplastic lymphoid tissue: biological aspects and clinical implications. 756 99

Anaplastic large cell lymphoma (ALCL) and Hodgkin's disease (HD) have some pathologic and immunohistochemical similarities, and a histogenetic relationship between them has been suggested by some investigators. By cytogenetic study, the t(2;5)(p23;q35) translocation appears to be unique for ALCL. The breakpoints of the t(2;5)(p23;q35) have recently been cloned and are reported to involve a novel tyrosine kinase gene, anaplastic lymphoma kinase (alk), on chromosome 2 and the nucleophosmin gene (npm) on chromosome 5. Therefore, we studied the frequency of npm-alk translocation in ALCL using a reverse transcriptase-polymerase chain reaction (RT-PCR) assay. We also studied HD and a variety of reactive lymphoid lesions since there is contradictory information in the literature on the occurrence of the npm-alk rearrangement in HD. We detected npm-alk hybrid mRNA in 8 of 22 cases of ALCL (36%), but none of the 21 cases of HD or the 11 cases with reactive lesions contained amplifiable template. All positive ALCL had the T or indeterminate phenotype and occurred in young adults or children. There was very good correlation between a cytogenetically detectable t(2;5) and a positive signal by RT-PCR. Our results indicate a selective but relatively infrequent association between the t(2;5) and ALCL of T or indeterminate phenotype, not shared with HD or reactive hyperplasia.
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PMID:Transcripts of the npm-alk fusion gene in anaplastic large cell lymphoma, Hodgkin's disease, and reactive lymphoid lesions. 757 58

Monoclonal antibody BLA.36 stains Reed-Sternberg (RS) cells and their mononuclear variants, as well as some benign and malignant cells of B-cell lineage, and retains its immunoreactivity in formalin- and B5-fixed tissue. The origin of the RS cell is controversial and the distinction between Hodgkin's disease (HD), anaplastic large cell lymphoma (ALCL), and lymphomatoid papulosis (LyP) (the latter two primarily T-cell in origin), can be difficult. The authors studied expression of BLA.36 in 22 cases of ALCL, 13 cases of LyP, and 15 cases of HD. Most atypical or malignant cells stained for BLA.36 in 10 of 22 cases of ALCL, 9 of 13 cases of LyP, and 9 of 15 cases of HD. Additional immunohistochemistry or gene rearrangement analysis indicated a T-cell origin for 8 of 10 BLA.36 positive ALCL, and 9 of 9 BLA.36 positive LyP cases. BLA.36 was expressed by T-cell lines derived from two ALCLs and one CD30+ cell line derived from LyP. The authors conclude that BLA.36 is not specific for lymphomas of B-cell origin and cannot be used to distinguish between HD, ALCL, and LyP with RS-like cells. These results further support a relationship between HD, ALCL, and LyP and suggest that RS cells are histogenetically related to both B- and T-lymphocytes.
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PMID:Expression of Hodgkin's disease associated antigen BLA.36 in anaplastic large cell lymphomas and lymphomatoid papulosis primarily of T-cell origin. 761 Nov 77

The authors critically review the concept of anaplastic large cell lymphoma (ALCL). In particular, they provide the guidelines to the morphologic identification of the four main varieties of the tumour: common, giant-cell-rich, lympho-histiocytic, and Hodgkin's-like. The phenotypic and molecular characteristics of the neoplasm are discussed with special emphasis to those which can assist in the differential diagnosis between ALCL and Hodgkin's disease. Finally, the clinical features are presented along with the results obtained in the course of long-term prospective therapeutical trials.
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PMID:[Anaplastic large-cell lymphoma. Conceptual and diagnostic assessment]. 761 87

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


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