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)

Ten cases of "undifferentiated" large-cell tumors were ultrastructurally characterized by cells with abundant filiform cytoplasmic projections without intercellular junctions. These cases were studied by means of the avidin-biotin-peroxidase complex (ABC) technique applied to formalin-fixed, paraffin-embedded sections using antibodies against high- and low-molecular weight keratins (Ker), vimentin (Vi), epithelial membrane antigen (EMA), S-100 protein, leucocyte common antigen (LCA), kappa (K) and lambda (L) light chains, Leu-M1, lysozyme (Ly), alpha-1 antitrypsin (A1AT) and alpha-1 antichymotrypsin (A1ACT). All 10 cases were negative for Ker and EMA but positive for Vi. S-100 was present only in scattered dendritic cells. LCA was identified in seven cases. In the three LCA-negative cases, two stained for Leu-M1, and one of these also showed intracytoplasmic L; one was negative for all markers but Vi. None of the tumors showed any significant staining for Ly, A1AT, or A1ACT. Our findings indicate that these tumors are nonepithelial and nonneuroectodermal, and that they are best classified as non-Hodgkin's lymphomas. The possibility that some of the filiform large-cell lymphomas may be derived from dendritic reticular cells cannot be excluded.
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PMID:Filiform large-cell lymphomas. An ultrastructural and immunohistochemical study. 243 14

Antibodies to leukocyte common antigen (LCA) are valuable in surgical pathology in the diagnostic separation of malignant lymphomas from poorly differentiated neoplasms of other types. However, several publications have reported difficulty in obtaining adequate LCA labeling in paraffin-embedded specimens. To assess this problem further, we applied an amplified version of the avidin-biotin-peroxidase complex procedure to 315 formaldehyde-fixed hematopoietic malignancies, and 420 nonhematopoietic tumors that had been similarly processed. All non-Hodgkin's lymphomas were LCA-reactive with this method, whereas none of the nonhematopoietic neoplasms were stained. Twelve of 25 cases of Hodgkin's disease displayed LCA-positivity in Reed-Sternberg cells, but all contained reactive, benign inflammatory cells. Hence, the specificity of the amplified anti-LCA/avidin-biotin-peroxidase technique was 100%, and its sensitivity was 96%. This procedure should allow surgical pathologists to obtain reliable, reproducible staining of hematopoietic neoplasms in paraffin-embedded tissues.
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PMID:Immunostaining for leukocyte common antigen using an amplified avidin-biotin-peroxidase complex method and paraffin sections. A study of 735 hematopoietic and nonhematopoietic human neoplasms. 244 89

The aim of this study was to compare the results of flow cytometric (FCM) determination of heavy and light chain cytoplasmic immunoglobulin (cIg) with those obtained by the peroxidase-antiperoxidase (PAP) method. Fifty-one patients, including five non-T-acute lymphoblastic leukemias, 16 B-chronic lymphocytic leukemias (CLL), 13 non-Hodgkin's lymphomas, seven hairy cell leukemias, four multiple myeloma/plasma cell leukemias, and six T-cell leukemia/lymphomas, as well as 12 normal controls, were studied. Saponin-permeabilized cell suspensions were indirectly stained with monoclonal antibodies and analyzed by flow cytometry. Acetone-fixed cytocentrifuge smears were stained for cIg by the PAP method. The results obtained indicate that: (a) detection of cIg by FCM is a feasible and useful technique to confirm the B-cell lineage of leukemias and lymphomas, particularly those characterized by low-density surface immunoglobulin, such as CLL; and (b) cIg detection by FCM and PAP staining are complementary methods to recognize with certainty the monoclonality of B-cell malignancies.
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PMID:Detection of intracytoplasmic immunoglobulin by flow cytometry in B-cell malignancies. 249 55

Hodgkin's disease of nodular sclerosis and mixed cellularity subtypes contains numerous eosinophils and substantial amounts of extracellular eosinophil peroxidase (EPO). To determine if the extracellular EPO retains cytotoxic activity, the authors analyzed cells from 13 cases of Hodgkin's disease and ten cases of benign lymphoid hyperplasia for their in vitro sensitivity to killing by a low concentration of hydrogen peroxide. Cells from cases of benign lymphoid hyperplasia (0.5% +/- 1% killing) and lymphocyte predominant Hodgkin's disease (4.5% +/- 6% killing) were significantly (P less than 0.05) less sensitive to killing by hydrogen peroxide than cells from nodular sclerosis Hodgkin's disease (26% +/- 13% killing) and mixed cellularity Hodgkin's disease (52% +/- 9% killing). The authors concluded that cells from Hodgkin's disease of nodular sclerosis and mixed cellularity subtypes have an increased sensitivity to killing by an otherwise nonlethal concentration of hydrogen peroxide.
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PMID:In-vitro sensitivity of Hodgkin's disease to hydrogen peroxide toxicity. Correlation with peroxidase activity. 254 83

A 46-year-old female was admitted to our hospital for fever and weight loss in September, 1986. Physical examinations were unremarkable. CBC revealed moderate anemia and leukopenia with abnormal lymphocytes. Examination of the bone marrow (BM) disclosed peroxidase negative blasts and multinucleated or multilobulated giant cells positive for CD30 (Ki-1) antigen. Chest X-ray was negative. CT scan and echography of the abdomen showed minimal enlargement of retroperitoneal lymph nodes (LN). Lymphangiography revealed mild enlargement of the LN without filling defects. Gallium scan was negative. Hence a diagnosis of Hodgkin's disease (HD) stage IVB was made. She was treated with MOPP therapy with modification and obtained a complete remission. BM involvement of HD occurs mostly in advanced stages. We assumed that this is a rare case of HD in which bone marrow metastasis occurred in a very early stage of the disease or that of bone marrow primary.
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PMID:[Hodgkin's disease diagnosed from the numerous Reed-Sternberg cells in the bone marrow]. 255 92

A Technicon H-1 hematologic analyzer was used to measure the mean leukocyte myeloperoxidase (MPX) in 160 patients seen in a hematology clinic. The normal range was -15 to +10, which included 95% of 300 consecutive hospitalized patients. No abnormalities in the MPX were found in 35 patients with beta-thalassemia minor, 8 with iron deficiency, 14 with myeloproliferative disorders, 17 with autoimmune disorders, and 37 patients with lymphoma in complete remission. On the other hand 36% (10/28) of lymphoma patients with active disease either at diagnosis or relapse had a MPX of greater than 10 compared to only 2.3% (7/300) in hospitalized patients (P less than 0.001). Increased levels of MPX were found primarily in patients with non-Hodgkin's lymphoma (NHL) of intermediate or high grades, or Hodgkin's disease [56% (9/16) compared to only 8.3% (1/12) in those with low grade NHLs, P less than 0.05]. The MPX levels returned to normal after successful treatment. Of the various chemotherapeutic agents used, only hydroxyurea led to a consistent elevation of the MPX. The authors conclude that MPX is commonly increased in patients with lymphoma and in those receiving hydroxyurea. Further studies are required to determine if the MPX is a sensitive test for relapse in patients with lymphomas who had an elevated pretreatment value.
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PMID:The mean leukocyte myeloperoxidase index in hematological patients. 255 19

The monoclonal antibody designated LN-1 was used in an attempt to identify the antigen in follicular center cell lymphomas using tissue sections fixed in formalin. The LN-1 antibody has been shown in previous studies to identify follicular center cells and give reproducible results in tissue fixed in B5. We used the ABC peroxidase technique to examined formalin-fixed, paraffin embedded sections representing 52 cases of various histologic subgroups of non-Hodgkin's lymphomas based upon the Lukes-Collins classification. Following immunostaining with LN-1 using overnight incubation of the antibody and papain treated sections, 37 cases, and all of the 38 cases previously diagnosed as follicular center cell lymphomas, gave a positive reaction to the LN-1 monoclonal antibody.
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PMID:Immunohistochemical analysis of non-Hodgkin's lymphomas with the monoclonal antibody to follicular center lymphocytes reactive in paraffin sections. 266 10

A 55-year-old woman developed a secondary leukemia following 1-year treatment of Hodgkin's disease. She was admitted to our hospital because of the celiac lymphadenopathy. Open laparotomy was performed. Biopsy specimens of the lymph node demonstrated Reed Sternberg cells with mature lymphocytes. She was diagnosed as having Hodgkin's disease (lymphocyte predominant type). She was treated by the combination chemotherapy consisting of mitoxantrone, cyclophosphamide, vincristine and prednisolone for Hodgkin's disease in November 1986. Hodgkin's disease achieved complete remission and she was regularly followed. No abnormal findings were observed in the peripheral blood and bone marrow. But thrombocytopenia and the blastoid cells appeared in the peripheral blood in February 1988. The bone marrow specimen was hypercellular and occupied by 90% of blastoid cells that were positive for peroxidase staining. She was diagnosed as having AML from the bone marrow aspiration and biopsy specimens. She did not respond to several chemotherapy regimens and now she is treated by low dose Ara C.
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PMID:[Acute myeloid leukemia after the treatment of Hodgkin's disease]. 276 76

This thesis is a survey of nine previously published articles on MPO deficient PMN. The incidences in leukaemia and allied disorders of the presence of this abnormal subpopulation of mature neutrophils and the relationship to clinical course in AML, susceptibility to infections in AML, FAB classification in AML and MDS, cytogenetically defined aberrations in MDS and morphometrical characteristics were investigated. The aims of the studies were to examine the diagnostic as well as the prognostic value of the parameter, to examine the usefulness of the parameter as an predictive indicator of CR and relapse in AML and to examine the concept that MPO deficient PMN may originate from leukaemic precursors. MPO deficient PMN were found to occur in a minor number (less than 4% of the total number of PMN) in normal humans and the incidences of an abnormal number (greater than 4%) were found to be about 40% in AML (I, II, III, IV, VIII), 60% in CML (I, VII), 30% in MPD other than CML (VII) and 30% in MDS (V). The highest incidences in AML were found in the FAB subtypes possessing the most myeloid differentiation potential i.e. FAB M2 and FAB M4 (IV). In ALL, CLL, HCL, Hodgkin's disease, anaemia not related to leukaemia and leukaemoid reactions the incidences all were 0% (I, unpublished data). The abnormal MPO deficient PMN subpopulation, if present, disappeared when CR was achieved and reappeared when relapse eventually was developed (II, VIII). In both situations serial determinations showed that the change occurred before the usual routine blood examinations predicted CR and relapse; several days and several months prior, respectively (VIII). The probability of obtaining CR was lower in the AML patients with the abnormal subpopulation and the risk of developing relapse higher than in AML patients without the anomaly (II, VIII). These differences were not statistically significant, however. AML patients, showing an increased number of MPO deficient PMN, revealed a statistically significant increased susceptibility to infections (P less than 0.01) during the preremission phase accounting for 18% to 67% of the total number of infections in this period (III). This increase was positively correlated to the extent of the anomaly (P less than 0.002). The spontaneous occurrence of a subpopulation of MPO deficient PMN in MDS went together with a simultaneous progression in cytogenetically determined clonal chromosomal aberrations and were related to progression in FAB subtype as well (VI). Morphometrically MPO deficient PMN were characterized by a decreased total cell size and an increased nucleus size of the projected images (IX).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Myeloperoxidase deficient polymorphonuclear leucocytes in leukaemia and allied disorders. 285 15

Expression of the granulocyte antigen Leu M-1 is characteristic of Reed-Sternberg cells and the related mononuclear cells of Hodgkin's Disease. Leu M-1 has been proposed as a specific immunological marker for Hodgkin's Disease which may be otherwise difficult to distinguish both morphologically and immunologically from non Hodgkin's lymphomas of peripheral T-cell type. In the present study the comparative expression of Leu M-1 in Hodgkin's Disease and peripheral T cell lymphoma was studied in a series of 43 cases including 25 cases of Hodgkin's Disease and 18 cases of immunologically documented peripheral T cell lymphoma. Leu M-1 staining by avidin-biotin-peroxidase complex technique in acetone fixed frozen sections was observed in 22 of 25 cases of Hodgkin's Diseases, (2 of 3 cases of lymphocyte predominant Hodgkin's Disease and 1 case of mixed cellularity were negative) and in 4 of 18 cases of peripheral T cell lymphoma. The pattern of staining in the peripheral T cell lymphomas was indistinguishable from that observed in Hodgkin's Disease in 2 of the cases. Leu M-1 staining appears to be of limited diagnostic value in the differential diagnosis of Hodgkin's Disease and T cell lymphoma. Absence of Leu M-1 staining in frozen tissue however, makes a diagnosis of Hodgkin's Disease (with the exception of the lymphocyte predominant form) unlikely.
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PMID:Leu M-1 antigen: comparative expression in Hodgkin's disease and T cell lymphoma. 288 52


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