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)

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

Many cases of familial aggregation of lymphoproliferative malignancy have been reported. But familial aggregation of non-Hodgkin lymphoma is less frequent than Hodgkin's disease, Burkitt's lymphoma, and adult T-cell leukemia. Here we report familial B-cell lymphomas occurring in a mother and her daughter at the same time. The daughter (43 years old) was admitted because of fever. She died of a rapidly progressive neurological disturbance. The mother (75 years old) was admitted because of fever and pleural effusion, and then died with a complication of cryoglobulinemia. The histological findings of their lymph nodes revealed diffuse lymphoma, medium-sized cell type, with B-cell phenotype and mixture of cleaved and non-cleaved nuclei. They had no common chromosome abnormalities, while they shared HLA-A 2, B 35, and Cw 3 antigen. Viral infection was not identified, by routine serological test and electronmicroscopic study.
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PMID:[Two cases of B-cell lymphoma occurring in a mother and her daughter at the same time]. 278 18

The proliferative response of T lymphocytes cultured with autologous non-T lymphocytes is known as the autologous mixed lymphocyte reaction (MLR). This reaction can be demonstrated reproducibly in healthy individuals and has been shown to generate specific cytotoxic T cells, as well as T cells that regulate antibody synthesis and cell-mediated immunity. In this study, we demonstrate that the autologous MLR is impaired or absent in most patients with Hodgkin's disease regardless of age, sex, pathologic stage, or histologic classification. In 64 patients, the mean autologous MLR was 3,084+/-1,878 cpm compared to 16,552+/-6,532 in 29 healthy donors. A defect in autologous MLR was observed in newly diagnosed patients before the initiation of therapy, but was also found in patients without evidence of recurrent disease up to 15 yr after treatment. These findings could not be explained by abnormal kinetics or poor viability of stimulator or responder cells. The possibility that suppressor cells are responsible for the reduction of T cell autoreactivity was examined by comparing the autologous MLR of a healthy HLA-identical sibling in the presence and absence of T or non-T cells of an affected sibling. No inhibitory effects were observed. Similarly, substitution of patient plasma for pooled AB serum failed to inhibit the autologous responses of normal donors. Increasing the number of responder T cells in the culture or removing adherent cells from the stimulator population enhanced autoreactivity in some patients, indicating that the defect is not absolute. In two families, T cells of healthy HLA-A, B, and DR-identical siblings of patients responded normally to the non-T cells of their affected siblings, whereas patients' T cells failed to respond both to their own stimulator cells and those of their healthy HLA-identical siblings. These data indicate that the impairment of autologous MLR in some patients is due to a reduction or dysfunction of responder T cell activity and not to a defect of autologous stimulator cells.
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PMID:Autologous mixed lymphocyte reaction in patients with Hodgkin's disease. Evidence for a T cell defect. 644 64

Over 200 cases of non-Hodgkin's lymphoma were typed for HLA-A, B, C and DR antigens, and typing was correlated with the morphologic diagnosis according to the Lukes-Collins classification system of non-Hodgkin's lymphomas. Three major racial groups were represented: Caucasoids, Mexican-Americans and Negroids. Significant associations were observed between HLA-AW33 and Caucasoid B-cell lymphomas, and for HLA AW24, HLA-B37 and HLA-B40 and B cell lymphomas in Negroids. No significant correlations were found within the Mexican-American patient population. The number of T cell lymphomas was insufficient to draw any conclusions. The DR antigens were not significantly associated with any of the diagnostic subgroups.
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PMID:HLA typing in non-Hodgkin's lymphomas. Comparative study in Caucasoids, Mexican-Americans and Negroids. 676 Apr 59

HLA-A, -B, -C, and -DR antigens were determined in order to study the association of HLA in Japanese patients with several autoimmune diseases, hypertrophic cardiomyopathy, and Hodgkin's disease. The frequency of HLA-DR4 was significantly increased in the patients with rheumatoid arthritis, juvenile-onset insulin-dependent diabetes mellitus (IDDM) and hypertrophic obstructive cardiomyopathy. In this study, no significant associations with A, B, or C specificities were observed except BW22 in IDDM. In contrast, the negative association with HLA-DR2 was observed in Hashimoto's thyroiditis, pemphigus vulgaris and hypertrophic non-obstructive cardiomyopathy.
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PMID:HLA-DR specificities among Japanese with several autoimmune diseases. 695 29

We studied 23 consecutive patients, median age 34 years, with relapsed or resistant aggressive lymphoma who underwent allogeneic BMT at the UCLA Medical Center Bone Marrow Transplantation Unit from 1 November 1984 to 30 March 1993. All patients were < 50 years of age and had sibling donors who were matched at the HLA-A, B and DR loci. Nine patients had Hodgkin's disease (HD) and 14 had non-Hodgkin's lymphoma (NHL); three of these had low grade histology and 11 had intermediate or high grade lymphoma histology. After a median follow-up of 34 months, eight patients are alive, seven without recurrent lymphoma. Five patients had early deaths. The disease-free survival for the entire group is 26% with an overall survival of 29%. There was no difference in survival rate on the basis of disease or histology. Comparing preparative regimens containing TBI to those without there was no difference in survival rate (P = 0.35). Neither age nor sex was a significant determinant of outcome (P = 0.63 and 0.36, respectively). Disease status at the time of transplantation proved to be the important determinant of outcome. Patients transplanted with chemotherapy sensitive disease (n = 9), defined as a partial or complete response to salvage chemotherapy, had a survival rate of 42%, which was significantly better than those who had refractory disease at transplantation (n = 14), who had a survival rate of 21% (P = 0.006). However, this small, but significant fraction of patients with refractory disease was curable. Thus, our data demonstrate that allogeneic bone marrow transplantation is an effective means of treatment for relapsed or aggressive Hodgkin's and non-Hodgkin's lymphoma.
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PMID:Allogeneic bone marrow transplantation for Hodgkin's and non-Hodgkin's lymphoma. 777 22

A study of 11 immunogenetical blood systems (HLA-A, B C, DR; ABO; Rh-Hr; MNSs; Kidd; Kell-Chellano; Duffy; Lewis; Diego; Gm; Inv) involving 59 antigens was performed in patients of Armenian nationality with lymphogranulomatosis (LGM). Pathogenic associations of HLA, MNSs and Duffy systems with LGM were established. Positive correlations were found (p < 0.001) with HLA phenotypes DR-8, B-14, B-21, SS, Fy(a+b-). These phenotypes have significant correlation with LGM (RR = 4.7-2.1) and can be considered as genetic markers of LGM in the Armenian population.
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PMID:[An analysis of the associational connections of immunogenetic blood markers with lymphogranulomatosis in Armenians]. 866 95

A 32-year-old male received an allogeneic peripheral blood stem cell transplant (alloPBSCT) for myelodysplasia from his one HLA-A antigen mismatched brother. He is alive with trilineage engraftment and without active GVHD 200 days after transplant. In July 1986 he underwent orthotopic cardiac transplantation for viral cardiomyopathy and has received continuous immunosuppressive therapy. A post-transplant lymphoproliferative disorder with Hodgkin-like histopathology was diagnosed in August 1993 and was successfully treated with four cycles of MOPP chemotherapy. Due to persistent pancytopenia he underwent a bone marrow aspiration and biopsy in May 1996 which revealed monosomy 7 and morphologic changes compatible with myelodysplasia. This is the first report of a cardiac transplant recipient receiving an allogeneic hematopoietic stem cell transplant.
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PMID:Allogeneic peripheral blood stem cell transplant for myelodysplasia after chemotherapy for post-transplant lymphoma in a cardiac transplant recipient at 10 years. 915 71

Thirty-four primary (untreated) patients with non-Hodgkin's lymphomas (NHL) infected with Epstein-Barr virus (EBV) were examined. Their HLA phenotype and the production of interleukin-1 beta and tumor necrosis factor alpha were assessed. Serological profiles characteristic of the late stages and reactivation of EBV infection were detected in 16 (47.1%) patients. NHL of low malignancy predominated in EBV-infected patients. A greater number of blank HLA-A antigens and a higher incidence of HLA-DR7 antigen was observed in infected patients. Serum concentration of tumor necrosis factor alpha was reliably higher in them, whereas the production of this cytokine by the peripheral blood mononuclears decreased. Hence, serum tumor necrosis factor is a product of transformed B lymphocytes. Spontaneous and stimulated production of interleukin-1 beta by peripheral blood mononuclears was significantly decreased in EBV-infected patients, and the serum concentration of this cytokine similarly had a trend to decrease, which indicates an inhibition of interleukin-1 beta production in EBV-infected patients with NHL.
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PMID:[Connection between Epstein-Barr virus infection and HLA phenotype and features of cytokine status in patients with non-Hodgkin's lymphomas]. 960 76

The gene causing hereditary hemochromatosis (HH), HFE is an HLA class I-like gene with no known immunological function but indirectly related to the immune functions because of its role in iron transport. It is located 6.5 Mb telomeric to HLA-A. The most common mutation of HFE, C282Y, has a Celtic origin and most patients with HH are homozygous for it in Northern European populations. While there is an enormously increased risk for hepatocellular cancer in hemochromatosis that is attributed to the toxic effects of iron, the risk for extra-hepatic cancers is also increased slightly. Recent studies have found genetic associations between several cancers and C282Y but only in the presence of a particular allele of the transferrin receptor gene. This suggests that the increased cancer risk is more likely due to the effects of iron. In childhood acute lymphoblastic leukemia (ALL), however, there is a strong association of C282Y with a gender effect in two different Celtic populations. This association does not require homozygosity for C282Y or an interaction with the transferrin receptor gene, and is male-specific. The other HFE mutation H63D does not confer increased risk to childhood ALL. Acute myeloblastic leukemia and Hodgkin's disease in adults do not have an association with HFE. Its male-specificity, occurrence in childhood and the lack of a gene-dosage effect suggest that the C282Y association in childhood ALL may reflect the involvement of another HLA-linked gene in leukemia susceptibility.
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PMID:Hemochromatosis gene in leukemia and lymphoma. 1200 48


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