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)

Transfusion-associated graft-versus-host disease (TA-GVHD) is a serious, often fatal complication to the transfusion of blood components. TA-GVHD is caused primarily by donor T lymphocytes reacting towards recipient MHC antigens. The diagnosis TA-GVHD should be considered when patients, within a month of receiving blood transfusion, develop sudden, unexpected high fever and erythematous rash, possibly accompanied by gastrointestinal symptoms and/or pancytopenia. Congenital (cellular) immune defect, intrauterine transfusion, bone marrow transplantation, Hodgkin's disease, and directed transfusions (especially from first degree relatives) all carry high risk of developing TA-GVHD. Since mortality exceeds 90% irrespective of any treatment, prevention is essential. Pretransfusion gamma-irradiation of blood components with a 25 Gy dose effectively prevents TA-GVHD, and it is therefore recommended that all blood components be irradiated prior to transfusion to patients belonging to defined groups-at-risk.
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PMID:[Transfusion-associated graft-vs-host disease]. 146 84

Canine lymphoid tumours, which share a number of features with human non-Hodgkin's lymphomas, were grafted in nude or SCID mice. Two (DL.24,DL.31) out of eight lymphomas and two (DL.31,DL.35) out of three lymphomas produced a sub-cutaneous (s.c.) tumour in nude and SCID mice respectively. In all animals, the s.c. tumours that developed at the inoculation site were regularly associated with metastasis to the regional lymph nodes, and also to the spleen, liver and bone marrow in SCID mice. The four transplanted tumours, with a pseudo-diploid canine karyotype, were diffuse large cell lymphomas as the initial dog tumours, and could be immunophenotypically characterized by surface immunoglobulins, MHC-class 2 and Thy-1 antigens. Serially transplanted lymphomas in nude and SCID mice may hence be used for further studies of these tumours.
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PMID:Transplantation of canine malignant lymphomas in the nude and SCID mouse. 162 46

We examined stimuli which are required for the induction of in vitro proliferation of follicular lymphoma cells, a low grade non-Hodgkin's B cell lymphoma characterized by a specific chromosomal translocation, t(14;18)(q32;q21), and by in vivo growth of the lymphoma cells in germinal center-like follicles infiltrated with CD4+ T cells. The purified follicular lymphoma cells, which are morphologically uniform, small, and dense, did not respond to stimulation with soluble lymphokines in the absence of T cells. Vigorous in vitro proliferation of follicular lymphoma cells was induced, however, when the follicular lymphoma cells were cultured with a CD4+ T cell clone which recognized alloantigens expressed by the lymphoma cells. This response required B-T cell contact, and was inhibited by anti-class II but not by anti-class I MHC mAb, indicating that these neoplastic B cells behaved as normal B cells and responded to normal activation and differentiation signals from T cells. After the cognate B lymphoma-T cell interaction occurred in culture, addition of IL-2 or IL-4 enhanced the proliferation of the tumor cells. These results, with a monoclonal and homogeneous population of B cells, affirm the idea that cognate interaction between B cells and Th cells is required for the effective activation of resting B cells. Moreover, these results suggest that a critical host-tumor interaction occurs in vivo, and that the polyclonal CD4+ T cells that infiltrate follicular lymphomas play a role in sustaining rather than inhibiting tumor growth in vivo. If so, therapies directed not only against the neoplastic cell but also against specific T cells and their cognate interactions with tumor cells may have a rationale.
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PMID:Induction of proliferation of human follicular (B type) lymphoma cells by cognate interaction with CD4+ T cell clones. 196 51

Of a series of 300 patients with histologically verified Hodgkin's lymphoma, six cases of familial occurrence of the disease involving three families were reported from two clinical centers. In two families the affected patients were next of kin (daughter and father in the first family and two brothers in the third one). The interval between the onset of the disease was 6 years in the first and 4 months in the third family. In the second family an aunt and her niece were affected with an 18 year interval in the onset of the disease. The histological type was identical within the families involved (1 x LP and 2 x NS). Deficiency of cellular immunity was established in all the members of the two Prague families and the expression of HLA-A and B antigens of the MHC was determined in the first family. The involvement of environmental and genetic factors in familial Hodgkin's disease was analyzed also in the light of findings reported in the literature.
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PMID:[Familial occurrence of Hodgkin's disease]. 225 44

A panel of antibodies that recognize antigens that survive fixation and conventional processing have been applied to 43 cases of Hodgkin's disease and five cases of large cell anaplastic lymphoma. Reed-Sternberg cells in all five cases of nodular lymphocyte predominance Hodgkin's disease were positive with leucocyte common (CD45) and B-cell antibodies, and negative with LeuM1 (CD15) and BerH2 (CD30) antibodies. In other types of Hodgkin's disease, Reed-Sternberg cells were positive with BerH2 in all cases, positive with LeuM1 in 63% of cases (with enzymic predigestion), positive with at least one B-cell antibody in 29% of cases and positive for CD45 in 8% of cases. In 19% of all cases, Reed-Sternberg cells were positive for epithelial membrane antigen and in 93% they were positive with TAL1B5 (anti-class II MHC). No case showed immunoreactivity with anti-T-cell antibodies. The patterns of immunoreactivity of large cell anaplastic lymphoma were similar, except that none was positive with B-cell antibodies and three were positive with T-cell antibodies. All five were positive with BerH2 (CD30) and TAL1B5. Comparison of the results with those seen in other cases of non-Hodgkin's lymphoma indicates that, with the currently available reagents, this immunohistological profile cannot be used as the sole diagnostic discriminant of these conditions; this must still be based upon careful morphological assessment.
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PMID:Paraffin section immunohistochemistry. II. Hodgkin's disease and large cell anaplastic (Ki1) lymphoma. 316 84

Reagents that recognize antigens on lymphoid cells in fixed and wax-embedded sections have been applied to a series of cases of non-Hodgkin's lymphomas. The panel consisted of MB1, 4KB5 (CD45r), LN1, L26 and MB2 which recognize antigens expressed predominantly on B-lymphocytes; UCHL1 and MT1 which recognize antigens expressed on T-lymphocytes and myeloid cells; antibodies recognizing the non-lineage antigens LeuM1 (CD15), BerH2 (CD30), anti-EMA; anti-lysozyme and MAC 387 which detect antigens present on some macrophages; and finally TAL1B5 (class II MHC), CAM 5.2 (low molecular weight cytokeratin) and PD7/26 + 2B11(CD45). Two hundred and four cases of non-Hodgkin's lymphoma have been studied, of which 158 had been fully characterized on frozen sections. The series was biased towards high-grade (n = 108) and T-cell (n = 44) tumours and these were largely prospectively accrued. It was found that discrimination between B-cell and T-cell lymphomas can be reliably achieved using these reagents and that a small panel (CD45, L26, MB2, MT1, UCHL1) is adequate for this purpose. Using the full range of reagents it is not possible to subdivide cases into groups that correspond with morphological subtypes of lymphoma. Although paraffin section immunohistochemistry is of value, the diagnosis of lymphoproliferative disorders must still be based upon the assessment of well fixed, carefully prepared tissue sections using conventional tinctorial methods.
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PMID:Paraffin section immunohistochemistry. I. Non-Hodgkin's lymphoma. 326 64

In many higher animal species, a major histocompatibility complex (MHC; in man: HLA; in mice: H-2) has been established and extensively studied. MHC products are essential in the recognition and destruction of cells carrying non-self antigenic determinants. Associations between specific HLA haplotypes and susceptibility towards nasopharyngeal carcinoma, breast cancer, acute lymphocytic leukaemia and Hodgkin's disease have been reported. A summary is made of the evidence for the involvement of H-2 genes in the development of virally induced tumours (leukaemia, mammary tumours and Rous sarcoma virus-induced fibrosarcomas). The formation of mouse lung tumours, for which there is no indication of a viral or hormonal etiology, has also proved to be significantly influenced by the H-2 haplotype. Similar results were obtained for spontaneous and chemically induced lung tumours. On closer analysis, more specific parameters, such as type of lung tumour and size, were found to be controlled by several regions of the H-2 complex.
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PMID:Tumour susceptibility in mice in relation to H-2 haplotype. 636 70

From the large amount of data pertaining to a possible relationship between MHC and susceptibility to malignancies in humans, some significant findings emerge. 1. In population studies, HLA-A2 in ALL and A1 in Hodgkin's disease are observed significantly increased in frequency in comparison to the normal controls. Some significant associations with an HLA phenotype are also observed in several cancers. 2. HLA genotyping of familial cases of Hodgkin's disease, with multiplex affected sibs, lead to the conclusions that an excess of HLA identical pairs are observed among the patients. This could indicate a linkage between the susceptibility gene and the HLA region. Another linkage might exist with familial malignant melanoma fitting with a dominant mode of transmission of the trait. These facts strongly support the role of the MHC among the polyfactorial and polygenic determinism of some malignancies. The mechanisms are discussed.
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PMID:[HLA and susceptibility to malignancies]. 712 93

Seventy-three T-cell clones (TCC) were established from tumour-infiltrating lymphocytes-T (TIL-T) derived from lymph nodes involved by B-cell non-Hodgkin's lymphomas (B-NHL) in nine patients with different histological subtypes and clinical stages. 40 TCC (55%) expressed the CD25 Ag and were also able to proliferate in the presence of irradiated autologous B-NHL cells. Among them, 23 autotumour (AuTu) proliferative TCC were found not to proliferate to autologous EBV-transformed B-cell lines, indicating that the proliferative reactivity of these TCC was preferentially directed at autologous B-NHL cells. Tested against autologous B-NHL cells, only three AuTu proliferative TCC (CD8+) showed a significant level of cytotoxicity (specific lysis > 15%). In blocking experiments, the AuTu proliferative reactivity of three TCC from one patient was strongly inhibited by anti-DR and anti-DQ mAbs, whereas that of three TCC from another patient was not affected by either anti-MHC class I or class II (DR, DP, DQ) mAbs. These findings suggest that the recognition of autologous B-NHL cells by AuTu proliferative TCC may occur through MHC-restricted as well as MHC-unrestricted mechanisms.
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PMID:Autotumour reactive T-cell clones among tumour-infiltrating T lymphocytes in B-cell non-Hodgkin's lymphomas. 766 62

The intercellular adhesion molecule 1 (ICAM-1) is the ligand for the lymphocyte function-associated antigen 1 (LFA-1). The ICAM-1/LFA-1 complex mediates cell-cell and cell-matrix interactions and is believed to be crucial for several immunological functions, including non-MHC-restricted cytotoxicity. Recently, a circulating form of the surface ICAM-1 molecule, the 82 kDa cICAM, has been identified. Using enzyme-linked immunosorbent assay (ELISA) we have examined 82 kDa cICAM-1 levels in the sera of 45 age- and sex-matched healthy subjects and 130 consecutive patients with Hodgkin's disease (HD). The mean +/- SD concentration of the 82 kDa cICAM-1 was significantly higher (p < 0.001) in HD patients (725.6 +/- 141 ng/ml) than in healthy controls (403.5 +/- 54.5 ng/ml). Patients with B-symptoms (n = 66) had higher cICAM-1 levels than patients without systemic symptoms (n = 64) (825.1 +/- 202.9 ng/ml versus 671.7 +/- 164.9 ng/ml; p < 0.001). Serum levels of cICAM-1 were also significantly higher (p < 0.05) in patients with disseminated disease (stage III and IV) than in those with localized disease (stage I and II). The HD patients in stage III and IV with B-symptoms had significantly higher (p < 0.001 and p < 0.02, respectively) cICAM-1 levels then stage III/IV patients lacking B-symptoms. The increase of cICAM-1 concentrations was positively correlated to increases of soluble receptors for interleukin-2 (sIL-2R) (r = 0.69; p < 0.001). Since cICAM-1 is functionally able to bind to LFA-1, increased serum levels of this molecule could be a mechanism for promoting de-adhesion and inability of Hodgkin and Reed-Sternberg cells (H-RS) to be recognized by cytotoxic effector cells, and could thus represent a way for these cells to escape immunosurveillance and for progression and spreading of disease.
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PMID:Serum levels of circulating ICAM-1 are increased in Hodgkin's disease. 810 18


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