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)

A 45-year old immunocompetent man presented with multiple lesions in the brain. A histological examination of the tumors showed a diffuse infiltrate of lymphoid cells with cellular polymorphism and of multinucleated giant cells. These cells were immunolabeled with antibodies against B cell lineage and with a monoclonal antibody, Ber-H2 (CD30), which showed the presence of Ki-1 antigen. Recently, among systemic non-Hodgkin's lymphomas, attention has been given to Ki-1-positive lymphomas, which have been incorporated in the up-dated Kiel classification. We report here a case of Ki-1-positive lymphoma arising in the CNS and review previously reported cases.
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PMID:Anaplastic large cell Ki-1 lymphoma in the central nervous system: report of an autopsy case. 146 71

Epstein-Barr virus (EBV)-specific DNA sequences were detected by polymerase chain reaction analysis in 15 of 47 (32%) DNA extracts prepared from CD30-positive (Ki-1 antigen-positive) anaplastic large cell (ALC) lymphomas. EBV-encoded RNA (EBER) transcripts could be detected by in situ hybridization in the tumor cells of 9 of 11 EBV DNA-positive cases. Twenty-eight cases were examined by immunohistology on cryostat sections for the presence of the EBV-encoded latent membrane protein (LMP), the nuclear antigen 2 (EBNA2), the BZLF1 transactivator protein, and the late viral glycoprotein gp350/250. A distinct LMP-specific membrane and cytoplasmic staining was detected exclusively in lymphoma cells of five cases (18%); two of these cases additionally expressed EBNA2. BZLF1 protein and gp350/250 immunoreactivity was absent in all instances. All LMP-positive cases contained EBV DNA and EBER sequences. The pattern of EBV latent protein expression in ALC lymphomas showed heterogeneity with respect to EBNA2 expression: LMP-positive/EBNA2-negative cases displayed a pattern previously described for undifferentiated nasopharyngeal carcinomas and Hodgkin's disease, whereas LMP-positive and EBNA2-positive cases showed parallels to lymphoblastoid cell lines. Because the LMP gene has transforming potential, our findings support the concept of a pathoetiologic role for EBV in a proportion of CD30-positive ALC lymphomas.
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PMID:Epstein-Barr virus DNA and latent gene products in Ki-1 (CD30)-positive anaplastic large cell lymphomas. 166 8

Anaplastic large-cell Ki-1 lymphoma is defined by its characteristic histological appearance, reactivity with antibodies against CD30, and possibly by a chromosome marker t(2;5)(p23;q35). Because of its pleomorphic appearance, sinus distribution, and frequent reactivity with EMA, this lymphoma is often mistaken for other diseases such as metastatic carcinoma and malignant histiocytosis. The clinical features of this lymphoma are unusual and include a young median age and frequent extranodal disease with skin being a common site. Although remission is easily achieved, relapse is common and combination chemotherapy is suggested. The role of Ki-1 antigen in normal lymphocyte function, the cell of origin of anaplastic large-cell Ki-1 lymphoma, and its relationship to Hodgkin's disease are important questions that hopefully will be answered in the near future.
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PMID:Anaplastic large-cell Ki-1 malignant lymphomas. Recognition, biological and clinical implications. 184 27

The Hodgkin-associated Ki-1 antigen (CD30) consists of a 120-kDa membrane-associated glycosylated phosphoprotein (Ki-1/120) and a 57-kDa non-glycosylated phosphoprotein (Ki-1/57) which only occurs intracellularly. Both molecules are phosphorylated at serine residues. An analysis of the peptide fragments resulting from staphylococcal V8-protease digestion of the Ki-1/57 molecule revealed identical bands irrespective of the cell source. Only a few bands of the Ki-1/57 digests appeared among the peptide fragments of the Ki-1/120 membrane antigen. The protein kinase activity was tested for both forms of the Ki-1 antigen. The Ki-1/120, devoid of the Ki-1/57 molecule, was immunoprecipitated from cell lysates of Hodgkin-analogous cell lines L428 or L540, which had been loaded with the Ki-1 or the Ki-1-analogous antibodies Ber-H2, HSR-1, -2 and -3 (method 1). These other antibodies reacted with the Ki-1/120, but not with the Ki-1/57 antigen. The latter, devoid of the Ki-1/120, was isolated from L540 cells after removal of the membrane form by method 1 or from U266/Bl myeloma or Raji Burkitt lymphoma cells which only contain the smaller form. Effects of non-specific adsorption were eliminated by various control precipitates. The Ki-1/57 intracellular antigen showed autophosphorylation and could phosphorylate histones as well. In contrast, a protein kinase activity of the membrane-associated Ki-1/120 could not be demonstrated.
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PMID:Protein kinase activity of the intracellular but not of the membrane-associated form of the Ki-1 antigen (CD30). 216 Nov 15

Although several independent series of non-Hodgkin's lymphomas (NHLs) have been subjected to cytogenetic studies or analyses of lineages by assaying for clonal immunophenotypes and clonal rearrangements affecting immunoglobulin (IG) and T-cell receptor (TCR) genes, no published reports exist of series of non-B-cell NHLs on which cytogenetic, immunohistochemical, and IG and TCR gene rearrangement studies have been undertaken together. Among 343 NHLs ascertained prospectively between January 1984 and December 1988 at the Memorial Sloan-Kettering Cancer Center, 278 cases with clonal chromosome abnormalities were identified. Of the latter, 20 were non-B-cell NHLs, which in turn comprised 15 peripheral T-cell lymphomas (PTCLs) and 5 lymphomas of uncertain lineage (LULs). The LULs either were biogenotypic, had discordant immunophenotype and immunogenotype, or showed no evidence of B-cell, T-cell, or histiocytic derivation. Of the 15 PTCLs, eight expressed the Ki-1 antigen and four of these had translocations involving the band 5q35 [t(5q35)]. Of the five LULs, four expressed the Ki-1 antigen and one of these had a translocation involving band 5q35. Previous studies have associated t(5q35) with Ki-1 positive NHLs characterized histologically by a pleomorphic diffuse large cell morphology. In our series of 12 Ki-positive non-B-cell NHLs, five (42%) had a 5q35 translocation. They were histologically indistinguishable from the subset without the translocation. The frequent lineage uncertainty exhibited by Ki-1 positive NHLs of similar histology and cytogenetic abnormalities suggests their derivation from an early uncommitted lymphoid cells.
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PMID:Immunohistochemical, molecular, and cytogenetic analysis of a consecutive series of 20 peripheral T-cell lymphomas and lymphomas of uncertain lineage, including 12 Ki-1 positive lymphomas. 217 40

Lymphomatoid papulosis (LyP) is characterized by the presence of large multinucleated cells resembling Reed-Sternberg (RS) cells. Evidence of antigenic similarity between these two cell types has been sought by immunohistologic labeling of 10 biopsies from cases of LyP with monoclonal antibodies against Ki-1 and other RS and Hodgkin (H) cell-associated antigens. In all cases studied, a proportion of the large atypical cells expressed the Ki-1 antigen. On the contrary, in 20 biopsies of benign skin lesions or cutaneous T-cell lymphomas, Ki-1-positive cells were absent or only occasionally present. Furthermore the large atypical cells of LyP also expressed antigens (e.g., T3, T4, HLA-DR, IL-2 receptors) which we have previously demonstrated on RS cells in the majority of cases of Hodgkin's disease (HD). These findings, in conjunction with the observation that Ki-1 antigen expression can be induced on peripheral blood lymphocytes following exposure to phytohemagglutinin or HTLV I, provide evidence that the Ki-1 positive cells in LyP represent activated T cells as RS cells do in many cases of HD.
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PMID:Atypical cells in lymphomatoid papulosis express the Hodgkin cell-associated antigen Ki-1. 242 10

The normal precursor of the neoplastic cell in Hodgkin's lymphoma is still unknown. Previous reports on the expression of the Hodgkin's cell-associated antigen Ki-1, CD30, on normal cells have been limited to activated lymphocytes. This study demonstrates, however, that cells of the macrophage lineage also are able to express the Ki-1 antigen. The Ki-1 antigen is absent from normal blood monocytes but expressed on up to 85% of macrophage-type cells developed during subsequent in vitro differentiation on Teflon membranes. Unlike other maturation-associated antigens, Ki-1 is found only at late stages of the macrophage primary cultures. Its expression can be enhanced by human interferon-gamma in a fashion similar to that of HLA-DR molecules. In addition, freshly explanted tumor cells from three patients with histopathologic and clinical features consistent with the diagnosis of true histiocytic lymphoma or malignant histiocytosis as well as the permanent cell line SU-DHL-1 could be demonstrated to express the Ki-1 antigen. The phenotype of histiocytic malignancy was further evaluated to be HLA-DR+MAX.26+CD25+-EMA+OKT9+Ki-1+. The results could indicate either that Hodgkin's lymphoma may arise not only from the lymphocyte but also from the macrophage lineage or may emphasize a macrophage involvement in the pathogenesis of this disease.
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PMID:Human macrophages can express the Hodgkin's cell-associated antigen Ki-1 (CD30). 253 22

The Hodgkin-associated Ki-1 antigen occurs in two different molecular forms. The 120-kDa membrane-associated form is a phosphorylated glycoprotein, which is derived from a non-phosphorylated intracellular 84-kDa apoprotein that is co-translationally N-glycosylated with a carbohydrate portion of 6 kDa. The other form of the Ki-1 antigen is a non-glycosylated phosphoprotein of 57 kDa which only occurs intracellularly. Both forms of the antigen are phosphorylated at serine residues. Enzymatic cleavage with sialidase reduced the 120-kDa membrane antigen by about 15 kDa, while its 90-kDa precursor and the 57-kDa intracellular form of the Ki-1 antigen remained unaltered. Pulse-chase experiments revealed that the 57-kDa and 90/120-kDa molecules are synthesized independently of each other. Four to eight hours after synthesis, the degradation of the 120-kDa molecule to a 105-kDa membrane-associated intermediate begins. This is further processed and appears in the cell supernate as a 90-kDa molecule. Hodgkin's disease-derived, Epstein-Barr virus-transformed cell lines and the acute T cell leukemia line MOLT-4 contain both forms of the Ki-1 antigen, whereas only the 57-kDa intracellular antigen is expressed in U266/B1 myeloma cells, in the Burkitt lymphoma cell lines Raji and Daudi and in acute promyelocytic HL-60 leukemia cells.
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PMID:The Hodgkin-associated Ki-1 antigen exists in an intracellular and a membrane-bound form. 254 29

We examined an antibody against Ki-1 antigen in 161 cases of malignant lymphoma, four of histiocytic sarcoma, and six of nonspecific lymphadenitis, using monoclonal antibody Ki-1, which is known to react selectively with activated lymphocytes, Reed-Sternberg cells, and Hodgkin's cells. Among them, 12 cases of malignant lymphoma demonstrated a diffuse positive cell membrane and/or cytoplasmic reaction of tumor cells and were categorized as Ki-1-positive lymphoma. Nine of these cases exhibited large cells with indented nuclei, distinct nucleoli, and abundant basophilic or amphophilic cytoplasm. Of the remaining three cases, two were of medium-sized and one of small-cell type. Immunologically, the 12 cases of malignant lymphoma demonstrated T-helper/inducer phenotype in six cases, B-cell in two case, and non-T, non-B in four cases. Tac and HLADR were positive in 9/12 and 4/5, respectively, and markers for histiocytes (lysozyme, alpha-1 anti-chymotrypsin, and OK-M1) were usually negative. Clinically, T-cell Ki-1-positive lymphoma was most likely to occur in the elderly, at extranodal sites, and had a rather poor prognosis (mean survival 35.5 months) as compared with B-cell and non-T, non-B lymphoma (7-52 months survival).
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PMID:Clinicopathological study of Ki-1-positive lymphomas. 260 19

Stabilization of cell surface antigens and preservation of tissue morphologic characteristics are important for diagnostic immunologic studies. Current reports continue to regard unfixed frozen sections as the material of choice for immunoperoxidase studies of lymphoproliferative diseases. In this study, periodate-lysine-paraformaldehyde (PLP) is shown to be a valuable fixative for the improved detection of surface antigens in lymphoid tissue. In cases of non-Hodgkin's lymphoma and Hodgkin's disease, more frequent detection of diagnostic markers and ease of interpretation was demonstrated by use of PLP-fixed frozen tissue as compared with unfixed frozen tissue. Immunoglobulin staining was more easily interpreted in 30% of B-cell non-Hodgkin's lymphoma. In Hodgkin's disease, Ki-1 antigen, a diagnostic marker of Reed-Sternberg cells, was found in PLP-fixed tissue from two cases in which this antigen was not detected in corresponding unfixed frozen tissue. The authors have demonstrated that PLP-fixed tissue can be sent to a central reference laboratory at ambient or room temperature, avoiding the expense and inconvenience of transporting specimens on dry ice. The authors conclude that PLP fixation is the preferred method for immunopathologic study of human lymphomas.
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PMID:Improved detection of lymphoid cell surface antigens in tissues fixed in periodate-lysine-paraformaldehyde (PLP). 282 97


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