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)

In a series of 33 cynomolgus monkeys (Macaca fascicularis) experimentally infected with Simian Immunodeficiency virus (SIV), strain smm3, 13 animals developed malignant Non-Hodgkin lymphomas. These lymphomas presented with unusual primary manifestations like in the orbita, testes, and brain. The morphological features and immunophenotyping identified the tumors as high malignant B-cell lymphomas. In all tumors as well as in tumor-derived cell lines a cynomolgus B-lymphotropic herpes virus (CBLV) with structural homogeneity to the Epstein-Barr virus (EBV) could be demonstrated by Southern blotting with EBV-specific probes. The lymphoma cells also expressed CBLV-associated nuclear antigens involved in B-cell transformation crossreacting with EBNA-specific human sera and monoclonal antibodies. Ig-gene rearrangement studies revealed clonal populations, however, no translocations of the c-myc oncogene could be detected. The lymphomas developing with high frequency in SIV-induced immunodeficiency resemble a major subtype of human EBV-associated AIDS lymphomas. This animal model can therefore be used to further elucidate interactions of HIV and EBV in AIDS-related lymphomagenesis.
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PMID:[Opportunistic malignant lymphomas in SIV infected primates--a model for Epstein-Barr virus associated lymphomas in AIDS]. 128 56

Steady state c-myc mRNA levels determined by Northern blot analysis were examined in non-Hodgkin's lymphomas (NHL) of both high (n = 29) and low malignancy (n = 18), and in non-specific chronic lymphadenitis (n = 6). High grade NHL, classified according to the updated Kiel classification, revealed significantly larger amounts of c-myc mRNA compared with low grade NHL and lymphadenitis. mRNA levels in non-specific lymphadenitis were lower than in low grade NHL, but the differences were not statistically significant. No correlation between c-myc mRNA levels and the immunologic phenotype was discernible. Growth fractions of the NHL were determined by immunostaining with the monoclonal antibody Ki-67. Significant correlations between the percentages of Ki-67-positive cells, as well as the amounts of c-myc mRNA, and classification into high or low grade NHL were found. However, the percentage of Ki-67 positive cells and c-myc mRNA levels in individual cases and in the various histologic entities of NHL did not correlate. Our results indicate the overexpression of the c-myc gene in NHL, and a highly significant correlation of steady state c-myc mRNA levels with the prognosis-related histomorphologic Kiel classification of NHL into different subgroups of low and high grade malignancy.
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PMID:c-myc mRNA expression in non-Hodgkin's lymphomas. 135 77

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

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

The expression of the proto-oncogene c-myc was studied in tumorous skin lesions of (cutaneous) lymphoproliferative diseases (3 cases of pseudolymphoma, 8 cases of non-Hodgkin lymphoma and 1 case of lymph node involvement in mycosis fungoides) in a total of 12 patients. c-myc mRNA levels were quantified by Northern blot analysis followed by densitometric evaluation of the specific bands. Higher levels of c-myc mRNA expression were observed in lymphomas as compared with pseudolymphomas (p greater than 0.05). No significant differences in c-myc mRNA values were detected between B and T cell pseudolymphomas. Our results suggest that c-myc mRNA overexpression is associated with malignant lymphomas of the skin. We conclude that the measurement of c-myc mRNA levels may contribute to further characterize cutaneous lymphoproliferative diseases.
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PMID:Expression of c-myc in cutaneous lymphomas and pseudolymphomas. 176 8

Forty-six fine-needle aspirates of lymphoproliferative lesions from 31 human immunodeficiency virus (HIV)-positive patients were reviewed using cytomorphologic, immunocytochemical, flow cytometric (FCM), cytogenetic, and molecular studies. There were 29 lymphomas (15 small non-cleaved cell [SNCL], 11 large cell [LCL], one small lymphocytic, and two Hodgkin's), 14 reactive hyperplasias, and three "atypical lymphoid proliferations." The reactive hyperplasias were characteristically polymorphic and polyclonal lymphoid populations; six of seven were diploid on FCM, the seventh was hypodiploid. Higher proliferative indices (mean, 11.6%) and higher RNA indices (mean, 1.2) characterized this subgroup compared with published reactive lymphoid hyperplasias from patients without HIV positivity. Aspirates of SNCL showed monotonous populations of intermediate-sized cells except in one patient where a giant cell syncytial variant occurred. Nine of 13 SNCL aspirates showed light chain restriction. JH rearrangement revealed B-cell lineage in one aspirate in which immunocytochemical study was negative for Kappa, lambda, B1, and Leu-4. Nine of 12 SNCL were diploid; the mean proliferative index was 25.6% and the mean RNA index 2.3. Chromosomal translocations involving the c-myc locus were demonstrated in five of seven SNCL aspirates karyotyped. Five of eight LCL showed light chain restriction the remaining three showed null cell phenotype. Large cell lymphomas were diploid on tetraploid with the mean proliferative index of 22.0% and mean RNA index of 2.2. One of two LCL aspirates karyotyped demonstrated c-myc translocation. Despite the multiparameter approach, a definitive diagnosis could not be reached in three aspirates.
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PMID:Fine-needle aspiration evaluation of lymphoproliferative lesions in human immunodeficiency virus-positive patients. A multiparameter approach. 199 Dec 48

We have investigated the frequency of p53 mutations in B- and T-cell human lymphoid malignancies, including acute lymphoblastic leukemia, the major subtypes of non-Hodgkin lymphoma, and chronic lymphocytic leukemia. p53 exons 5-9 were studied by using genomic DNA from 197 primary tumors and 27 cell lines by single-strand conformation polymorphism analysis and by direct sequencing of PCR-amplified fragments. Mutations were found associated with (i) Burkitt lymphoma (9/27 biopsies; 17/27 cell lines) and its leukemic counterpart L3-type B-cell acute lymphoblastic leukemia (5/9), both of which also carry activated c-myc oncogenes, and (ii) B-cell chronic lymphocytic leukemia (6/40) and, in particular, its stage of progression known as Richter's transformation (3/7). Mutations were not found at any significant frequency in other types of non-Hodgkin lymphoma or acute lymphoblastic leukemia. In many cases, only the mutated allele was detectable, implying loss of the normal allele. These results suggest that (i) significant differences in the frequency of p53 mutations are present among subtypes of neoplasms derived from the same tissue; (ii) p53 may play a role in tumor progression in B-cell chronic lymphocytic leukemia; (iii) the presence of both p53 loss/inactivation and c-myc oncogene activation may be important in the pathogenesis of Burkitt lymphoma and its leukemic form L3-type B-cell acute lymphoblastic leukemia.
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PMID:p53 mutations in human lymphoid malignancies: association with Burkitt lymphoma and chronic lymphocytic leukemia. 205 20

Four Epstein-Barr virus-positive lymphoblastoid cell lines (LCL) were successfully infected in vitro with immunodeficiency virus type 1 (HIV-1) as demonstrated by reverse transcriptase activity and p24 HIV antigen in culture supernatants, positive cell staining for gag-encoded HIV proteins, presence of viral HIV genome by Southern blot analysis and ulstrastructural observations. In addition, both HIV-1-infected B cells and their supernatants efficiently transactivated the chloramphenicol acetyl transferase reporter gene which is under the control of the HIV-1 long terminal repeat. The LCL cells displayed long-term HIV-1 infection and production, but no cytopathic effects were observed. Cytofluorimetric analysis did not detect membrane CD4 presence in the LCL cells before and after HIV-1 infection; moreover, a minute amount of CD4 mRNA was observed only in one of the LCL. A monoclonal antibody specific for the viral binding site of the CD4 molecule delayed, but did not block, HIV-1 infection of the LCL cells. Following HIV-1 infection, changes in LCL phenotype were observed, consisting of a decrease in CD23- and CD39-positive cells, and a concomitant increase of cells with surface CD10 and Bac-1. Furthermore, HIV-1-infected LCL cells did not grow in tight clumps, as usually observed in uninfected LCL, but as disperse suspensions, and formed more agar colonies than control LCL. However, despite this apparent acquisition of a malignant-like phenotype, c-myc proto-oncogene rearrangement was not detected. The appearance of cells with new characteristics did not seem due to clone selection by HIV-1 infection, since all the LCL conserved their clonotypic pattern of IgH chain rearrangement. The acquisition of malignant-like features by HIV-infected B cells might be clinically significant in terms of the pathogenesis of non-Hodgkin's B cell lymphomas, which occur frequently in AIDS patients.
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PMID:Infection of Epstein-Barr virus-transformed lymphoblastoid B cells by the human immunodeficiency virus: evidence for a persistent and productive infection leading to B cell phenotypic changes. 217 Jan 47

To study the pathogenesis of malignant lymphomas (ML) in intravenous drug-abuser HIV-infected patients, we analyzed 19 cases of reactive lymphadenopathy (LAS) and 10 cases of ML. Clonality and differences in characteristics of these lymphoproliferative disorders were investigated by immunohistochemical and Ig and TCR gene rearrangement analyses. Rearrangements at the c-myc locus and presence of HIV and EBV viral genomes were also investigated. Four out of the five non-Hodgkin's lymphomas (NHL) analyzed were high-grade extranodal ML and were found to derive from precursor B cells. Monoclonal cell expansions were also detected in 2 cases of LAS. These cell expansions also consisted of precursor B cells. HIV genome was not detected in any of the samples tested and was therefore considered not to be involved as an etiological agent in these lymphoproliferative disorders. EBV genome was present in a clonal episomal form in the five Hodgkin's disease (HD) specimens tested. This finding suggested that a clonal cell population harboring the EBV viral genome must be present in HDs, pointing to a possible etiological relationship between EBV and HD in HIV-infected patients.
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PMID:Pathogenesis of malignant lymphomas in intravenous drug-abuser, HIV-infected patients. 217 49

Congenital and acquired states of immunodeficiency have long been associated with an increased incidence of malignant lymphoma. An increased incidence of non-Hodgkin's lymphomas was recognized early in the epidemic immunodeficiency state associated with the human immunodeficiency virus (HIV) infection AIDS. Although the precise etiologic mechanism of these lymphomas remains speculative, the presence of Epstein-Barr viral proteins or sequences and characteristic chromosomal translocations giving rise to altered expression of the c-myc oncogene have frequently been observed. It has been suggested that HIV infection leading to disordered T-lymphocyte function (possibly in conjunction with Epstein-Barr infection) leads to the emergence of polyclonal populations of stimulated B lymphocytes. These cells, which undergo physiologic immunoglobulin gene rearrangement, may provide the background for the occurrence of characteristic chromosomal translocations that lead to the emergence of malignant lymphomas. These lymphomas tend to present clinically with high-grade histopathologic subtype, advanced stage, and a propensity for the involvement of otherwise unusual extranodal sites, including the central nervous system. The experience with therapy for HIV-associated lymphomas has indicated that highly aggressive, dose-intensive chemotherapy regimens may be associated with inferior results. More recent regimens have stressed less myelosuppressive therapy combined with prophylaxis for central nervous system disease and pneumocystis infection. The dominant prognostic factors in the HIV-associated lymphomas appear to be primarily related to the underlying HIV infection and include total CD4 lymphocyte count, performance status, and prior AIDS diagnosis.
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PMID:Acquired immunodeficiency syndrome-associated lymphomas. 218 76


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