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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The incidence of second tumours occurring in the course of Hodgkin's disease has been investigated in a series of 452 patients treated with standard chemotherapy or radiotherapy, combination chemotherapy alone, intensive radiotherapy alone, or both intensive radiotherapy and combination chemotherapy administered in sequence. 16 tumours were noted. When analysed according to mode of treatment, 6 cases occurred in a group of 62 patients who received both modalities. When analysed for age, sex, and man-years of follow-up, this group appears to have 14-5 times the risk of developing a second tumour. However, that subgroup which had a complete remission after intensive radiotherapy followed by a relapse of disease, prior to receiving combination chemotherapy, had the highest risk with 18-5 times greater incidence of second tumour than expected. It is noteworthy that, of the 16 second tumours, 2 were acute myeloid leukaemia; in both cases a similar chromosomal abnormality (45 chromosomes, C-group deletion) was noted. The mechanism of oncogenesis may represent a combination of the immunosuppressive effects and cellular effects of those forms of treatment.
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PMID:Second malignancies complicating Hodgkin's disease in remission. 4 22

We inoculated common marmosets (Callithrix Jacchus) with Herpesvirus ateles (HVA), Herpesvirus saimiri (HVS), and Epstein-Barr virus (EBV). HVA-induced tumors contained several cell types, including giant cells reminiscent of the Sternberg-Reed cells observed in human Hodgkin's disease. HVS and EBV did not induce tumors, although HVS was present in lymphocytes and elicited a strong antibody response. EBV elicited only a variable antibody response. We feel that more common marmosets should be used to determine if the pathologic and immunologic lesions caused by HVA would be a suitable animal model for Hodgkin's disease and/or other malignant lymphomas of man. Inconsistency in the induction of tumors by EBV and HVS in common marmosets suggets that this species may be a different type of model for human cancer research than the cottontop marmoset, which is the most susceptible animal host for EBV and HVS oncogenesis.
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PMID:Experimental infection of Callithrix Jacchus marmosets with Herpesvirus ateles, Herpesvirus saimiri, and Epstein Barr virus. 20 78

19 months after the clinical manifestation of acute lymphoblastic leukaemia, Hodgkin's disease, stage Ia, of the cervical lymphnodes developed in a 10 year old girl during continuous complete remission of leukaemia under chemotherapy. After a regional irradiation and after completing the antileukamic therapy the patient is at present off therapy, healthy and without signs of relapse of both malignant systemic diseases. The coincidence of acute lymphoblastic leukaemia in children with other malignant neoplasias is rare. The expected frequency of second malignancies and the theories concerning oncogenesis are shortly reviewed.
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PMID:[Morbus Hodgkin as a second malignancy in acute lymphoblastic leukaemia (author's transl)]. 28 52

Cytokines are potent modulators of the physiological immune response. A number of reactive processes are associated with a deregulation of this cytokine expression. Animal models with transgenic mice or transfection experiments have shown that an autocrine or paracrine pathway might be involved in tumor progression and/or tumorigenesis. The study of cytokine expression in malignant lymphomas showed a heterogeneous expression pattern with a number of cases which quantitatively show indications for a marked deregulation of the cytokine expression. The expression od IL-7 and IL-9 seem to be special features of Hodgkin's disease and large cell anaplastic lymphomas. Transfection experiment with IL-9 into mouse T cells results in an autocrine loop and tumorigenesis of the transfected cells. These tumors share a number of similarities to Hodgkin's disease and large cell anaplastic lymphomas in human.
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PMID:[Cytokines and malignant lymphomas]. 128 79

Sinonasal non-Hodgkin's lymphomas (SNHL) of B- or T-cell immunophenotype have been associated with the Epstein-Barr virus (EBV) in Asian patients. We investigated eight sinonasal and 10 Waldeyer's ring NHL from Western patients for evidence of EBV genomes using a sensitive in situ hybridization technique. EBV DNA was detected in each of three sinonasal NHL with a T-cell immunophenotype and two of five cases with a B-cell immunophenotype. Two of 10 B-cell Waldeyer's ring NHL were positive for EBV genomes. In each positive case, EBV genomes were evenly distributed among the neoplastic cells, whereas no evidence of EBV in associated nonneoplastic lymphocytes or epithelium was seen. The results indicate that B-cell and T-cell sinonasal NHL are associated with EBV in Western as well as in Asian patients, and that EBV may have a role in oncogenesis in NHL of the upper aerodigestive tract. The strong association of EBV with nasopharyngeal carcinoma suggests that the anatomic site is important in the development of EBV-related neoplasms.
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PMID:Frequency of Epstein-Barr viral DNA in "Western" sinonasal and Waldeyer's ring non-Hodgkin's lymphomas. 131 Feb 41

The recurrent loss of genetic material from a specific chromosomal region in a given tumor type suggests the presence of a tumor-suppressor gene, the loss or inactivation of which may be relevant for tumorigenesis. In this study, we provide molecular evidence for the recurrent association between deletions on the long arm of chromosome 6 and B-cell non-Hodgkin lymphoma (B-NHL). Normal and tumor DNAs from 71 cases of B-NHL were studied for loss of constitutional heterozygosity (LOH) at 19 loci on chromosome 6 using a panel of restriction fragment length polymorphism (RFLP) probes. LOH, indicating deletion of all or part of 6q, was detected in 16 of 71 cases (22.5%), ranging from low-grade to high-grade B-NHL. The isolated loss of 6p or the loss of other chromosomes (8, 17, 22) tested as controls for specificity was not observed in any case. Comparison of the extent of the deletions among different cases allowed the identification of two distinct regions of minimal deletion (RMD) at 6q25 to 6q27 (RMD-1) and at 6q21 to 6q23 (RMD-2), respectively, suggesting the existence of two tumor-suppressor genes. These data support a role for 6q deletions in B-NHL pathogenesis and provide a basis for identifying the corresponding tumor-suppressor genes.
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PMID:Deletions involving two distinct regions of 6q in B-cell non-Hodgkin lymphoma. 135 11

Mutation of the p53 protein may represent the commonest genetic event in human malignancy. Abnormal p53 expression has been reported in a variety of carcinomas, sarcomas and lymphoid neoplasms; however there is little information in relation to Hodgkin's disease. The expression of the nuclear phosphoprotein was investigated in paraffin-embedded biopsies from fifty patients with Hodgkin's disease using a polyclonal antibody, CM-1 and in snap-frozen material with monoclonal antibodies, PAb 1801 and PAb 240. Specifically, immunoreactivity was localised to the Reed-Sternberg cells or mononuclear variants in both nodular sclerosing (86% cases) and mixed cellularity (57% cases) subtypes of Hodgkin's disease. However, no positive staining was found in our cases of nodular lymphocyte predominant type Hodgkin's disease. Serial biopsies following recurrence of disease demonstrated consistent results. It is suggested that overexpression of p53, probably mutant, may have a role in the tumorigenesis of Hodgkin's disease.
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PMID:p53 expression in Reed-Sternberg cells of Hodgkin's disease. 141 1

Non-Hodgkin's lymphomas (NHL) are part of an overlapping spectrum of lympho-proliferative diseases in childhood. In the first of this 2 part series, the clinicopathological aspects of NHL in childhood are discussed. The rapid progression of disease, the high incidence of micrometastases (over 80%) at diagnosis, and the propensity of hematogenous spread to the bone marrow and the central nervous system (CNS) as well as the clinico-pathologic 'clusters' associated with particular presenting sites distinguish the pediatric forms of disease. Abdominal primary sites most frequently manifest diffuse undifferentiated (Burkitt's or non-Burkitt's) histopathology, B-cell immunophenotype, FAB-L3 cytomorphology and specific karyotypic and/or genotypic alterations of the immuno-globulin genes and the c-myc oncogene. Mediastinal presentation is associated with lymphoblastic histopathology, T-cell immunophenotype and a variety of less consistent karyotypic and genotypic aberrations. Ki-1 lymphoma, a rare subtype of large cell NHL with specific features is often of T cell origin. The requirements for diagnosis, staging and monitoring are presented in the context of the associations between clinico-pathological presentation and subsequent behavior. The most frequent sites of disease progression and relapse are involvement of the bone marrow and the CNS. For Burkitt's lymphoma there is a historic perspective and a description of particular epidemiologic, clinical, virologic, immunophenotypic and genotypic features. Cytogenetic and molecular biologic studies of genomic rearrangements are advancing the understanding of oncogenesis, clonality, lineage, and clinical behavior. The capacity to detect and amplify DNA from submicroscopic disease may contribute to prognostic stratification both at diagnosis and during subsequent monitoring.
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PMID:Non-Hodgkin's lymphomas in children. I. Patterns of disease and classification. 144 19

People with deficient cell-mediated immunity have an increased susceptibility to viral infections and certain cancers, particularly non-Hodgkin's lymphomas and cancers of the skin and anogenital region. These are linked to viral origins. Anogenital neoplasms in immunodeficient patients show a strong association with HPV infection; often occur at relatively young ages; involve multifocal locations; and tend to persist, recur, and progress rapidly, despite standard therapy. Because standard therapy of anogenital HPV lesions and neoplasia is often not effective in immunodeficient patients (and others with an anogenital neoplastic syndrome), special treatment is required. 5-Fluorouracil chemosurgery, followed by maintenance 5-fluorouracil therapy, is often effective and provides field suppression against recurrent HPV infection and neoplasia, with minimal damage to affected organs. After removal of all detectable HPV and neoplastic lesions, immunodeficient patients require close surveillance of the entire anogenital tract. Immunodeficient patients are an in vivo human laboratory in which to study the natural history of HPV and its oncogenic effects on the anogenital tract. The theory of HPV oncogenesis is supported by the evidence gathered from these patients.
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PMID:Anogenital papillomavirus infection and neoplasia in immunodeficient women: an update. 164 9

Correlations between cytogenetics, histology, and clinical course continue to emerge in studies of non-Hodgkin's lymphomas. The previously recognized association between the t(14;18) chromosomal translocation and follicular lymphoma has been confirmed; abnormalities of chromosome 3 have correlated specifically with diffuse large cell lymphoma and abnormalities of chromosome 1 have been frequently present in T-cell lymphomas. Rearrangements involving 11q13 (bcl-1) occur most commonly in diffuse lymphocytic lymphoma of intermediate differentiation. Several new recurrent chromosomal abnormalities have also been described. The molecular fine structure of the t(8-14) chromosomal translocation in Burkitt's lymphoma appears to differ between endemic (Epstein-Barr virus-associated) and sporadic cases. In endemic Burkitt's lymphomas, the chromosomal breakpoint is usually far upstream of c-myc oncogene, leaving the regulatory region of the gene intact. In sporadic tumors, a large part of the regulatory region is separated from the gene and transcription is initiated at sites within the first intron. These data raise the possibility that Epstein-Barr virus may contribute to the deregulation of the c-myc gene and that this interaction may be required for tumorigenesis in the presence of some, but not all, types of c-myc damage arising from chromosomal translocations. Partner proteins that oligomerize with c-Myc have been identified in humans and mice (Max and Myn). The partners share with c-Myc the DNA-binding and coiled-coil motifs that are recognized in many other proteins and that function as transcriptional regulators. The Bcl-2 protein has been shown to be a mitochondrial inner membrane protein that blocks programmed cell death (apoptosis). Viral expression has been demonstrated in Epstein-Barr virus-associated Hodgkin's disease, and the spectrum of Epstein-Barr virus-associated lymphoproliferative disease has been expanded to include some T-cell malignancies. A new human herpesvirus has been associated with some cases of Hodgkin's disease.
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PMID:Biology of the lymphomas: cytogenetics, molecular biology, and virology. 166 Nov 67


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