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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 recurrent Hodgkin's disease of the "sarcomatoid" or "syncytial variant" type was seen that occurred as an extension from the mediastinum to a previously uninvolved extranodal site (breast) and pericardium after treatment of classical nodular sclerosing Hodgkin's disease based in the lymph nodes. This histologic variant was composed of sheets of large, undifferentiated neoplastic cells with few, if any, diagnostic features of nodular sclerosing Hodgkin's disease. For this reason, the differential diagnosis of this variant was difficult and included non-Hodgkin's lymphoma (peripheral T-cell lymphoma), Ki-1-positive lymphoma, medullary carcinoma, metastatic carcinoma, melanoma, and granulocytic sarcoma. Immunologic analysis by immunoperoxidase technique showed a phenotype consistent with "syncytial variant" Hodgkin's disease: Leu-M1+, Ki-1+, IL-2+, HLA-DR+, T11-, pan B-, K-, lambda-, cytokeratin-, S-100-, muramidase-.
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PMID:Recurrent "syncytial variant" of Hodgkin's disease: an immunohistologic diagnosis. 359 90

Atypical cells resembling Reed-Sternberg cells are a characteristic histologic feature of lymphomatoid papulosis. Thus far no consistent data are available on the nature of these cells, or a possible antigenic relationship between them and Reed-Sternberg cells. Twenty-four biopsy specimens from 14 patients with lymphomatoid papulosis were immunolabeled with antibodies against Ki-1 and other Reed-Sternberg cell-associated antigens. In all cases a proportion of the large, atypical cells expressed the Ki-1 antigen. In contrast, in 20 biopsy specimens of benign inflammatory skin lesions or mycosis fungoides, Ki-1-positive cells were absent or only occasionally present. Furthermore, the large atypical cells of lymphomatoid papulosis also expressed other antigens (for example, T3, T4, HLA-DR, IL-2 receptors) that have previously been demonstrated on Reed-Sternberg cells. Our findings, together with the observation that the Ki-1 antigen can be induced on peripheral blood lymphocytes after prolonged phytohemagglutinin stimulation, suggest that the Ki-1-positive cells in lymphomatoid papulosis are activated T cells closely related to the Reed-Sternberg cells of Hodgkin's disease.
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PMID:Monoclonal antibody patterns in lymphomatoid papulosis. 384 52

Ki-1 is a monoclonal antibody (raised against a Hodgkin's disease-derived cell line) that, in biopsy tissue affected by Hodgkin's disease, reacts selectively with Reed-Sternberg cells. The expression of Ki-1 antigen has been analyzed by immunocytochemical techniques in a wide range of human tissue and cell samples, including fetal tissue, malignant lymphomas (290 cases), and mitogen- and virus-transformed peripheral blood lymphocytes. The antigen was detectable on a variable proportion of cells in all cases of lymphomatoid papulosis and angio-immunoblastic lymphadenopathy and in 28% of the cases of peripheral T cell lymphomas (including lympho-epithelioid lymphomas). It was also expressed (more strongly) on tumor cells in 45 cases of diffuse large-cell lymphoma, most of which had originally been diagnosed as malignant histiocytosis or anaplastic carcinoma, because of their bizarre morphology. However, all of these cases lacked macrophage and epithelial antigens. Thirty-five cases expressed T cell-related antigens (associated in nine cases with the coexpression of B cell-related antigens), seven bore B cell-related antigens alone, and three were devoid of T and B cell markers. DNA hybridization with a JH specific probe showed a germline configuration in 11 cases of T cell phenotype, in two cases lacking T and B cell antigens, and in one case of mixed T/B phenotype, while rearrangement was found in two cases of clear B cell type and in one mixed T/B case. Expression of the Ki-1 antigen could be induced, together with interleukin 2 (IL 2) receptor, on normal lymphoid cells of both T and B cell type by exposure to phytohemagglutinin, human T leukemia viruses, Epstein-Barr virus, or Staphylococcus aureus. The results obtained indicate that Ki-1 antigen is an inducible lymphoid-associated molecule that identifies a group of hitherto poorly characterized normal and neoplastic large lymphoid cells. Tumors comprised solely of these cells show both morphological and immunological similarities to the neoplastic cells in Hodgkin's disease. This suggests that both disorders represent the neoplastic proliferation of activated lymphoid cells of either T cell or, less commonly, B cell origin. Disorders in which only a minority of cells express Ki-1 antigen (lymphomatoid papulosis, angio-immunoblastic lymphadenopathy, and certain T cell lymphomas) probably represent lesions in which only some of the abnormal cells have transformed into an "activation state." In direct support of this view is the finding that the Ki-1 expression in these lesions is accompanied by the expression of HLA-DR and IL 2 receptors.
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PMID:The expression of the Hodgkin's disease associated antigen Ki-1 in reactive and neoplastic lymphoid tissue: evidence that Reed-Sternberg cells and histiocytic malignancies are derived from activated lymphoid cells. 387 24

A series of immune parameters were available covering the period before, during, and after tumor appearance in ten patients who developed tumors after renal transplantation. Results were obtained using monoclonal antibodies OKT3, OKT4, OKT8, and the ratio OKT4/OKT8, and surface membrane fluorescence microscopy (SMIg) for B-lymphocytes, E-rosetting and blast transformation. A much lower immune responder state was indicated at the time of transplantation in patients who later developed a tumor, as compared to a control group, and a much lower immune responder state was seen before than after tumor appearance. A low OKT4/OKT8 ratio was found before the diagnosis of Hodgkin's disease in one patient, and an increase in the immune responder state was seen after treatment of a patient developing spinocellular carcinoma at the site of a former herpes labialis. Using a monoclonal antibody against Hodgkin and Sternberg-Reed cells (Ki-1), it was possible to demonstrate that these were present before transplantation, with an increase before the appearance of the first clinical symptoms and, perhaps activated by the transplantation and the following immunosuppression, in the patient who developed Hodgkin's disease.
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PMID:Immune monitoring of tumor development after renal transplantation. 388 Nov 64

Cryostat sections from fully developed papular lesions of lymphomatoid papulosis (histologic subtype A or B) have been examined by immunoenzymatic staining with 24 monoclonal antibodies against lymphoid cells and their subsets. The lesions demonstrated essentially identical cellular compositions and consisted of T-lymphocytes with a peripheral phenotype (Lyt3+, anti-Leu-4+, OKT6-), macrophages (HLA-DR+, EB11+, OKM1+), and Langerhans cells (HLA-DR+, OKT6+). T-helper/inducer cells (anti-Leu-3+) usually dominated over T-suppressor/cytotoxic cells (anti-Leu-2+). In all cases, proportions of the infiltrating T-cells expressed markers associated with activation (HLA-DR, the OKT1O antigen, interleukin-2 receptor) or proliferation (transferrin receptor, the Ki-67 antigen) of lymphoid cells. Furthermore, the infiltrates contained clusters and/or sheets of large cells reactive with antibodies (Ki-1, Ki-24, Ki-27), which recognize Hodgkin's and Reed-Sternberg cells. These data indicate an origin of the cellular infiltrate from transformed or activated lymphoid cells and suggest an interrelationship of lymphomatoid papulosis to Hodgkin's disease.
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PMID:Lymphomatoid papulosis. Characterization of skin infiltrates by monoclonal antibodies. 390

This report describes the phenotypic analysis of a cell line obtained from a female patient with the nodular sclerosing subtype of Hodgkin's disease (HD). The cell line has a neoplastic karyotype and is stable in culture in the absence of feeder layers or growth factors. Phenotypic analysis of this cell line shows that it cannot easily be characterized as either a lymphocyte, macrophage or granulocyte but resembles in its characteristics certain HD lines already described in the literature. The cell line carries the antigen defined by the Ki-1 monoclonal antibody, shows myeloid markers on a proportion of cells and has cytoplasmic UCH-T1.
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PMID:Phenotypic analysis of an established cell line derived from a patient with Hodgkin's disease (HD). 401 43

A Hodgkin cell-specific antigen detected by the monoclonal antibody Ki-1 was found on T helper lymphocytes after activation by autologous and allogeneic stimulator cells. About 50% of lymphoblasts generated by auto- and alloactivation reacted with the antibody. In contrast, only less than 6% of lymphoblasts stimulated with Con-A, phytohemagglutinin (PHA), or protein A, and none of lymphoblasts activated by oxidative mitogenesis, expressed this antigen. Among several permanent cell lines tested, the K562, MOLT-4, HL-60, and EBV transformed B lymphoblastoid cells reacted with the Ki-1 antibody. The results may indicate possible relationships between the autoreactive subset of T lymphocytes and the pathogenesis of Hodgkin's disease.
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PMID:A Hodgkin cell-specific antigen is expressed on a subset of auto- and alloactivated T (helper) lymphoblasts. 620 42

To clarify the origin of Hodgkin (H) and Sternberg-Reed (SR) cells, frozen sections of lymph nodes from 30 patients with Hodgkin's disease were immunostained with a large panel of monoclonal antibodies reactive with cells of lymphoid tissue and granulopoiesis. The results showed that: (a) H and SR cells are devoid of markers specific to, or characteristic of B cells, macrophages, dendritic reticulum cells, interdigitating cells, or cells of erythropoietic or thrombopoietic origin; (b) the vast majority of H and SR cells contain granulocyte-related antigens detectable with the monoclonal antibodies TU9 and 3C4, but constantly lack other granulocytic cell markers (such as peroxidase and chloroacetate esterase). Monoclonal antibodies raised against a Hodgkin's disease-derived cell line included one, Ki-1, that was found to be selectively reactive with H and SR cells and a minute, but distinct cell population in normal lymphoid tissue and bone marrow. The latter, as yet unidentified cell population appears to be the normal equivalent of H and SR cells.
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PMID:Evidence for the detection of the normal counterpart of Hodgkin and Sternberg-Reed cells. 667 60

The consistency of the breakpoint on chromosome 5 at band 5q35 occurring in Ki-1 non-Hodgkin's lymphomas is highly suggestive of the involvement of a locally altered gene in this disease. In this study, we analyzed the potential involvement, in the translocation, of two receptor tyrosine kinase genes and putative oncogenes, FLT4 and FGFR4, previously localized near this breakpoint. Fluorescence in situ chromosomal hybridization allowed us to refine their localization to sub-band 5q35.3 and to show that both genes are translocated to the derivative chromosomes in Ki-1 cell lines containing either a t(2;5) or a t(3;5). Pulsed-field gel electrophoresis showed that the FLT4 and FGFR4 genes are not physically linked, nor are they altered by the translocation. Finally, Northern blot analysis showed that neither FLT4 nor FGFR4 is expressed in the Ki-1 cell lines, suggesting that they are not implicated in the genesis of Ki-1 lymphomas.
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PMID:Localization of two tyrosine kinase receptor genes with respect to the 5q35 chromosomal breakpoint of Ki-1 lymphoma cell lines. 750 15

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


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