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)

Tumorigenicity of lymphoid cell lines of different origin upon xenotransplantation (s.c. and i.m.) in cell concentrations of 1 X 10(6) cell/inoculum into nude mice was correlated to karyotype, presence of the 14 q + marker, EBV reactivity and immunological markers. Lymphoblastoid cell lines (LCL), lacking the 14 q + marker failed to produce tumors independent upon diploidy or aneuploidy. Lymphoma-type lines of Burkitt lymphoma, lymphosarcoma and Hodgkins disease-origin, genotypically aneuploid, and expressing the 14 q + marker were tumorogenic in nude mice, when inoculated in the same cell quantities where LCL failed to form tumors. Tumorgrowth in nude mice was independent upon the presence of EBV in the inoculated cells.
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PMID:Lymphoid cell lines: in vitro cell markers in correlation to tumorigenicity in nude mice. 20 50

The karyotypes of cells from 10 Burkitt lymphoma (BL) biopsies, eight cell lines established from BL and nine cell lines from non-BL sources were studied by chromosome banding techniques. With the exception of the BL-derived cell lines BJAB, GC-BJAB, Maku and U-8691 all biopsies and lines of Burkitt origin contained an extra band at the distal region of the long arm of one chromosome 14. An extra band on chromosome 14 was also found in cells of one non-BL biopsy, in cells from a lymphosarcoma-derived cell line and in a long-established cell line derived from the pleural exudate of a patient with Hodgkin's disease. A distal region at the long arm of one chromosome 8 was missing in all metaphase figures of good technical quality in the same material. The size, morphology and stain-ability of the missing region corresponded fairly well to the extra region at chromosome 14. We therefore suggest that the chromosome 14 marker represents a translocation between chromosomes 8 and 14,t (8q-; 14q+). The translocation was present neither in lymphocytes of the peripheral blood of five Burkitt patients nor in five lymphoblastoid cell lines of non-BL origin. Trisomy 7 was found in two of the 10 BL biopsies, in two BL-derived cell lines, in one non-BL biopsy, in two lymphosarcoma-derived cell lines and in one cell line derived from a patient with Hodgkin's disease.
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PMID:Characteristic chromosomal abnormalities in biopsies and lymphoid-cell lines from patients with Burkitt and non-Burkitt lymphomas. 94 70

The clinical and pathological features of 64 children with non-Hodgkin's malignant lymphoma seen between April 1962 and June 1973 are described. Forty-one children had diffuse, undifferentiated, non-Burkitt lymphoma (lymphoblastic lymphoma). They tended to be boys under 10 years of age and their median survival was 1 year. Almost one-third are surviving for 1-11 years, most in initial complete remission. Nineteen children had diffuse, poorly differentiated, histiocytic lymphoma. They tended to be boys more than 10 years of age, their median survival was only 6 months, and only the 3 patients with Stage I peripheral node tumour survived. Two children had nodular, lymphocytic, poorly differentiated lymphoma and 2 had lymphoma resembling the Burkitt type. From our clinical and pathological observations, we conclude that non-Hodgkin's malignant lymphomata in children cannot be separated from the acute lymphocytic, histiocytic and unclassified leukaemias by cytological or histological methods. What is called diffuse, undifferentiated, non-Burkitt type, or lymphoblastic lymphoma is actually acute lymphocytic leukaemia without apparent invasion of marrow and peripheral blood by neoplastic lymphocytes at time of diagnosis. What is termed diffuse, histiocytic lymphoma is acute histiocytic leukaemia without apparent infiltration of marrow and peripheral blood at initial presentation. One could say just as well that acute lymphocytic leukaemia is Stage IV lymphoblastic lymphoma and that acute histiocytic leukaemia is Stage IV histiocytic lymphoma. Further classification of lymphocytic and histiocytic cancers by newer functional, chemical and morphological methods should include both what is called lymphocytic or histiocytic leukaemia and what is called non-Hodgkin's lymphoma as one group of diseases, susceptible to subclassification by the new methods. We recommend that Stage I lymphocytic and histiocytic cancers be treated with local irradiation. Patients with Stages II-IV tumours should receive anti-leukaemic forms of therapy including prolonged multiple agent chemotherapy and preventive central nervous system irradiation. Staging laparotomy should be considered in patients with Stage I tumour in low cervical, axillary and inguinal nodes.
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PMID:Non-Hodgkin's lymphoma in children. 110 24

Epstein-Barr virus (EBV), an ubiquitous human B lymphotropic virus, is the cause of infectious mononucleosis. Moreover, EBV infection can be followed by lymphoproliferative diseases in patients with inherited and acquired immunodeficiencies. Primary EBV infection may be a threat to all children after marrow or organ transplantation or those receiving chronic immunosuppressive treatment for various other reasons. The virus has been also implicated in the pathogenesis of different malignant tumours such as Burkitt lymphoma, nasopharyngeal carcinoma, Hodgkin disease and some T-cell lymphomas. This review focuses on various aspects of virus-host interactions, immune mechanisms of the host, and the still experimental therapeutic approaches in EBV-associated diseases.
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PMID:Epstein-Barr virus infection and associated diseases in children. I. Pathogenesis, epidemiology and clinical aspects. 133 May 72

Epstein-Barr virus (EBV), an ubiquitous human B lymphotropic virus, is the cause of infectious mononucleosis. Moreover, EBV infection can be followed by lymphoproliferative diseases in patients with inherited and acquired immunodeficiencies. Primary EBV infection may be a threat to all children after marrow or organ transplantation or those receiving chronic immunosuppressive treatment for various other reasons. The virus has been also implicated in the pathogenesis of different malignant tumours such as Burkitt lymphoma, nasopharyngeal carcinoma, Hodgkin disease and also some T-cell lymphomas. This review focuses on various aspects of virus-host interactions, immune mechanisms of the host, and the still experimental therapeutic approaches in EBV-associated diseases.
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PMID:Epstein-Barr virus infection and associated diseases in children. II. Diagnostic and therapeutic strategies. 133 34

Malignant tumors registered with the Tumour Registry of Papua New Guinea (PNG) from 1958-1988 were analyzed with emphasis on the variation of incidence with time and different regions. Cancer incidence was generally low in PNG. During this period, carcinoma of oral cavity, cervix, breast, and skin, hepatoma, and lymphoma were the most common types of malignant lesions detected. The incidence of carcinoma of the oral cavity has increased. Currently, it is more common in the Highlands region and is associated with the spread of betel nut chewing. A threefold increase in cervical carcinoma registration was observed nationally, with a sixfold increase in the Highlands region; this was attributed both to social changes and improved registration. The incidence of breast cancer has doubled, in keeping with better registration, but there is little interregional variation. The decline in registrations of hepatocellular carcinoma is artifactual. PNG is a high-incidence area for Burkitt lymphoma, but Hodgkin disease is rare. Both Burkitt and other non-Hodgkin lymphomas are uncommon in the Highlands. A decline in the incidence of squamous carcinoma of skin was observed that was associated with improved control of tropical ulcers. The incidence of stomach cancer is falling. The registered cancer incidence in PNG is low, even when compared with that in native people from other Pacific nations, such as Fijians and New Caledonian Melanesians. Preventive measures have been hitherto ineffective, with the exception of squamous carcinoma of skin.
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PMID:The spectrum of cancer in Papua New Guinea. An analysis based on the Cancer Registry 1979-1988. 145 Oct 78

Cryostat sections from lymph nodes of 47 Hodgkin disease patients were examined by immunohistology for the Epstein-Barr virus (EBV)-encoded latent membrane protein (LMP), nuclear antigen 2, and late viral glycoprotein gp350/250. A distinct LMP-specific membrane and cytoplasmic staining was detected exclusively in Hodgkin and Reed-Sternberg cells in 18 patients (38%); EBV nuclear antigen 2 and gp350/250 immunoreactivity was absent in all instances. Thirty-two of 47 (68%) cases contained EBV-specific DNA sequences as detected by PCR, all LMP-positive cases being in this category. Our results confirm previous studies establishing the presence of EBV genomes in Hodgkin and Reed-Sternberg cells by demonstrating expression of an EBV-encoded protein in the tumor-cell population. The finding of LMP expression in the absence of EBV nuclear antigen 2 suggests a pattern of EBV gene expression different from that of B-lymphoblastoid cell lines and Burkitt lymphoma, whereas this finding shows similarities with that seen in undifferentiated nasopharyngeal carcinoma. Because the LMP gene has transforming potential, our findings support the concept of a pathoetiological role of EBV in many cases of Hodgkin disease.
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PMID:Epstein-Barr virus latent membrane protein expression in Hodgkin and Reed-Sternberg cells. 164 16

Cytogenetic examinations were carried out in 24 untreated patients with non-Hodgkin, non-Burkitt lymphoma. 10-20 G-banded metaphases, obtained from short-term cultures of unstimulated lymph++ node, bone marrow and blood cells were analyzed in each case. In 18 patients only, the obtained metaphases were suitable for cytogenetic analysis. In 11 patients (group A) karyotype was normal or only single, +non-clonal aberrations were observed. In 7 patients (group B) clonal aberrations were found, among them, in 3-structural changes of chromosome 1, but with different breakpoints: 1p31, 1p31, 1p36. The group of patients with chromosomal aberrations showed statistically significantly shorter survival time than the group without aberrations (p = 0.04). In the former group more patients had low grade malignancy lymphoma. Our observations confirm those data from the literature which indicate that the presence of chromosomal aberrations is a factor of poor prognosis, independent of other clinical and histopathological prognostic factors in non-Hodgkin Lymphoma.
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PMID:[Cytogenetic studies in patients with non-Hodgkin's lymphoma (nHL)]. 180 98

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

The histopathologic changes of bone marrow during infection with the human immunodeficiency virus type 1 (HIV-1) are described. Bone marrow biopsies from 73 patients at different stages of HIV-1 infection were studied. Indications for biopsy included peripheral blood abnormalities, suspicion of lymphoma, or search for specific pathogens. Common histopathological features, suggestive of HIV-1 infection but nonpathognomonic were hypercellularity (67%), myelodysplasia (86.1%), plasmacytosis (98.6%), lymphocytic infiltration (31.1%) and histiocytic infiltration with or without granulomata (13.7%). Increases in reticulin fibers (54.7%), and stainable iron deposits, vascular congestion and serous atrophy of fat were frequent features. Opportunistic infections and neoplastic complications were detected in 7 cases: pathogens were demonstrated in 4 cases (Mycobacterium avium intracellulare (MAI), Cryptococcus neoformans, Toxoplasma gondii and Leishmania) and lymphoma in 3 cases (1 Burkitt lymphoma and 2 Hodgkin's disease). Bone marrow hypoplasia is usually a terminal event in AIDS and may be iatrogenic.
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PMID:Bone marrow findings in HIV infection: a pathological study. 210 65


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