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)

We used an indirect immunofluorescence technique to detect a surface antigen that may be associated with Hodgkin's disease (HD). A heteroantiserum raised in a rabbit given an injection of cells obtained from an HD lymph node (Stage I, classification of Lukes and Butler) allowed us to detect an antigen on the surfaces of HD-derived cells in 25 of 27 instances. Benign and malignant non-HD-type lesions (both lymph node and spleen) did not have this antigen. The nature of this antigen and the type of cells bearing it are unknown.
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PMID:A surface antigen associated with Hodgkin's disease: brief communication. 7 26

Absorbed serum of a rabbit immunized with a suspension of cells of Hodgkins origin, allowed us to demonstrate a surface antigen on cells of Hodgkin origin. Where this antigen is situated in relation to those already described, notably in respect to the possible carcinoembryonic character, has yet to be determined.
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PMID:[Evidence for surface antigens on Hodgkin's disease cells]. 80 58

The haemopoietic origins of the Hodgkin's disease (HD)-derived cell lines L428, KM-H2 and HDLM-2 remain controversial. Analysis of T-cell receptor (TcR) and Ig rearrangements cannot resolve this, and lineage promiscuity limits the interpretation of isolated surface antigen expression. Nonetheless the cell marker profile of L428 has similarities with human dendritic cells (DC), and L428 strongly stimulates in the mixed leucocyte reaction (MLR). We therefore undertook an extended immunophenotypic comparison of the HD lines with that recently defined for DC, prior to examining their ability to stimulate allogenic T lymphocytes, and comparing the molecular interactions involved with those of primary MLR stimulatory cells. The immunophenotype of the HD lines failed to establish either a lymphoid or monocytoid derivation. The profile of L428 appeared similar to the human DC. All three lines were potent stimulators in the primary MLR, and each expressed relevant adhesion and signal-transducing molecules important for co-stimulating T lymphocytes. Inhibition studies using monoclonal antibodies indicated similar contributions within HD line-T cell MLR to that documented in human tonsil DC-T cell MLR. The HD lines produced no detectable interleukin-1 (IL-1) by biological or immunological analysis. Moreover they stimulated allogeneic T lymphocytes in the presence of anti-IL-1 antibodies. Thus although IL-1 mRNA can be detected in both HDLM-2 and KM-H2 by polymerase chain reaction, these lines, and L428, share with DC the ability to stimulate allogeneic T lymphocytes in an IL-1-independent manner [corrected]. HD lines, particularly L428, may provide a standardized, reproducible, IL-1-independent model for dissection of the co-stimulatory requirements of the human primary MLR.
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PMID:Hodgkin's disease cell lines: a model for interleukin-1-independent accessory cell function. 147 81

Among 262 inpatients with hematologic diseases who were referred for chemotherapy or immunosuppressive therapy between January, 1985, and December, 1989, nine (3.4%) patients, including two with Hodgkin's disease (HD), three with acute myeloblastic leukemia, one with chronic myelogenous leukemia, two with multiple myeloma and one with aplastic anemia, were found to be hepatitis B virus (HBV) carriers before their chemotherapy began. All six HBV carriers who received chemotherapy containing glucocorticoid showed mild-to-moderate elevations in serum transaminase levels after the chemotherapy. Five showed a rise in titer of the hepatitis B surface antigen, HBsAg. In contrast, three HBV carriers not receiving glucocorticoid showed no change in serum transaminase after chemotherapy. One HBV carrier with HD suffered from severe icteric hepatitis after the withdrawal of multiagent chemotherapy containing glucocorticoid. The HBV-DNA polymerase rose markedly and was accompanied by a marked rise in titer of HBsAg. The results warn us to keep in mind the possibility of glucocorticoid inducing an activation of HBV infection, which may result in severe hepatitis in some HBV carriers. Although further investigation is required, it is recommended that HBsAg-positive patients with hematologic malignancies should, if possible, be treated without glucocorticoid.
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PMID:Activation of hepatitis B virus infection by chemotherapy containing glucocorticoid in hepatitis B virus carriers with hematologic malignancies. 175 16

One hundred and four patients with malignant lymphoproliferative disorders and 5,690 control subjects were screened for the presence of Hepatitis B surface antigen (HBsAg) in their sera. Lymphoproliferative disorders included in the study were acute lymphoblastic leukaemia (ALL), non Hodgkin's Lymphoma (NHL), chronic lymphocytic leukaemia (CLL), Hodgkin's disease (HD), Burkitt's lymphoma (BL) and multiple myeloma (MM). Screening was done by the Reverse Passive Haemagglutination method using the Welcome kit. The percentage antigenaemia in the patients and control subjects were 35.6 and 7.7% respectively (p less than 0.0001). Using the Odds ratio the relative risk was found to be 6.75. The Odds ratio for individual disorders ranged from 2.8 to 9.17. The results suggest an association between Hepatitis B surface antigenaemia and malignant lymphoproliferative disorders and highlights the risk involved in handling specimens from the patients.
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PMID:Hepatitis B surface antigenaemia in patients with malignant lymphoproliferative disorders. 181 50

The proliferative potential of multinucleated Reed-Sternberg-like cells and the process of multinuclear formation were studied on the Hodgkin's-disease-derived cell line HDLM-2. No difference in surface antigen expression was found between mono- and multinucleated cells as determined by immunolabelling with characteristic markers. After sorting and reculture of purified mononucleated cells, polykaryons emerged subsequently in these cultures, indicating that mononucleated cells give rise to multinucleated variants. The morphological observation of mitotic figures and immunostaining with the cell cycle indicators Ki-67 and BrdU provided evidence of DNA synthesis and nuclear division in multinucleated cells. The presence of mitotic figures demonstrated that multinucleated cells are able to undergo synchronous nuclear division. However, while polykaryons were clearly mitotically active and capable of DNA synthesis, the absence of telophases and the failure of active replication suggest a disturbed cytokinesis. Co-cultivation of BrdU-labelled and unlabelled populations did not lead to hybrid polykaryons with negative and positive nuclei. Therefore, multinucleated giant cell formation of HDLM-2 cells appears to involve nuclear endomitosis without cell division rather than cell fusion.
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PMID:Formation of multinucleated cells in a Hodgkin's-disease-derived cell line. 265 41

The T1 surface antigen (CD5,p67) expression on blood lymphocytes (PBL) and lymphoid cells from lymph node biopsies (LN) from 31 patients with B-cell chronic lymphocytic leukemia (B-CLL) and 79 with B non-Hodgkin lymphoma (B-NHL), was detected in 25 B-CLL (80 per cent) and in 11 B-NHL (13 per cent) belonging to the following histologic subtypes: lymphocytic of CLL type (DLWD) one case, lymphoplasmacytoid (DLWD) four cases, centrocytic (DLPD) five cases, immunoblastic (DH) one case. All B-CLL and the T1 + B-NHL were also tested with monoclonal antibodies against the Common Acute Lymphoblastic Leukemia Antigen, B cells (FMC7, FMC8, BA1, Y29-55), T cells (OKT11a), HLA-DR and HLA-DQ monomorphic determinants. All the B-CLL and the T1+ B-NHL were CALLA-, BA1+, Y29.55+. FMC7+ cells were detected in large numbers six B-CLL (three T1+ and three T1-) and in four centrocytic lymphomas. FMC8 reacted with 70 per cent of leukemias (where it stained 30 per cent of neoplastic cells) and with 8/9 T+ B-NHL. HLA-DR and HLA-DQ molecules were detected in 100 per cent and 90 per cent of cases respectively. In vitro treatment of HLA-DQ- or T1- B-CLL with phorbol ester TPA led to the expression of these antigens as well as of the receptors for Interleukin 2 and MLR3 activation antigen. Surface membrane Ig (SIg) was detected in 79 per cent of cases, its density measured by FACS analysis varied, even markedly, from case to case. Among the B-CLL, cells with high SIg content were either T1+ or T1- and more likely FMC7+. The SIg- cases were seven B-CLL (five T1+ and two T1-) and two B-NHL, in which, however, cytoplasmic IgM was detected. This study reveals the existence of four major B-CLL subgroups: T1- SIg-, T1+ SIg+, T1+ SIg+, T1- SIg+. It also indicates that the T1 antigen may be transitionally present during B-cell differentiation and that its expression may precede that of SIg as supported by the in vitro studies. In addition, the finding that some B-NHL are T1+ suggests that they derive similarly to the B-CLL from a common progenitor.
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PMID:Expression of the T1 (CD5, p67) surface antigen in B-CLL and B-NHL and its correlation with other B-cell differentiation markers. 309 11

T-cell acute lymphoblastic leukemia (ALL) comprises a third of the cases of childhood ALL in Israel. This high proportion of T-ALL is most probably due to a deficiency in pre-B/common ALL. The T-ALL patients had significantly worse 4-yr survival compared to standard risk or non-T high risk patients. In view of these special epidemiologic and clinical features a study of the immunophenotype of all consecutive cases of T-ALL and T-non Hodgkin's lymphoma (NHL) observed in our medical center was performed. Twenty-eight ALL and 3 NHL patients were studied and their cells characterized using a panel of monoclonal antibodies, TdT reactivity and E-rosette formation. Assays of the activities of adenosine deaminase (ADA) and purine nucleoside phosphorylase (NP) were also performed. Based on the surface antigen expression, the tumor cells could be classified into one of the three known developmental stages of T cells. It was found that the immunophenotype of the T-ALL cases in Israel was similar to that observed in other countries. Considerable heterogeneity of surface antigen expression was found and in a number of cases the phenotype analysis was not easily reconciled with models of T-cell ontogeny. The activities of ADA and NP were correlated with the developmental stage, as defined by the surface antigenic expression. Contrary to observations on normal T-cells, where ADA activity decreases and NP activity increases as T-cells mature and differentiate, this was not found in the malignant T cells. These findings as well as the existence of atypical immunophenotypes suggest that the leukemic T cell has an abnormal gene expression.
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PMID:T-cell acute lymphoblastic leukemia in Israel: clinical and laboratory features. 309 94

The surface antigens of Hodgkin cells and Reed-Sternberg cells (H- and R-S cells), including lacunar cells, were analyzed with a large panel of monoclonal and polyclonal antibodies by an immunohistochemical method and an immunoelectron microscopic technique. H- and R-S cells in each histologic subtype of nodular sclerosis, mixed cellularity and lymphocyte depletion were stained similarly with anti-Leu-M1, anti-Leu-11b, TG8, anti-HLA-DR, anti IL-2R, RSC-1 (Ki-1) and anti-alpha-1-antitrypsin, but not with other antibodies examined. These findings suggest the following: (1) H- and R-S cells of nodular sclerosis, mixed cellularity and lymphocyte depletion are not heterogeneous, at least in terms of surface antigen expression, and (2) H- and R-S cells may be lymphoid cells which simultaneously express activated lymphoid cell-associated antigens (e.g., HLA-DR, RSC-1 and IL-2R) and granulocytic cell-associated antigens (e.g., Leu-M1 and TG8).
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PMID:Simultaneous expression of activated lymphoid cell-associated and granulocytic cell-associated antigens on Hodgkin's and Reed-Sternberg cells in Hodgkin's disease. 318 42

Purified peripheral blood lymphocytes (PBL) from nine untreated patients with Hodgkin's disease (HD), two HD patients in complete remission and 17 healthy donors were studied for natural killer (NK) cell activity against the K-562 cell line using a single cell cytotoxic assay, which allowed enumeration of effector cells and characterization of their surface membrane phenotypes after staining with monoclonal antibodies. The frequency of NK cells was significantly lower in HD patients than in controls (mean % +/- s.d., 1.9 +/- 0.9 and 2.8 +/- 1.2, respectively), while the fraction of target binding cells was similar in the two groups. The fraction of cytotoxic lymphocytes increased after pre-treatment of PBL with 500 iu leucocyte interferon in all tested control donors (n = 12) and the two patients in remission but only in four of seven untreated patients. No relation between the impaired NK cell frequency and age, tumour histology and clinical stage could be revealed. Subtyping of the target cell binding NK cells by monoclonal antibodies disclosed a marked heterogeneity of effector cells. NK effector cells reactive with M1 and anti-Ia antibodies were enriched while T3+ and T4+ NK lymphocytes tended to be reduced as compared to PBL. There was no difference between patients and healthy donors with regard to the surface antigen patterns of NK cells. Interferon treatment did not alter significantly the phenotypic characteristics of cytotoxic lymphocytes in patients and controls. It is concluded that the impairment of NK cell activity in HD is partly attributed to a lower frequency of cytotoxic effector cells among a normal number of target binding cells. The defect could not be attributed to a selective defect of effector cell subsets.
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PMID:Surface markers and cytotoxic activity of blood natural killer cells studied at the single cell level in Hodgkin's disease. 404 22


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