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)

It is well known that there are many independent and inter-related clinical and pathologic factors which influence the prognosis of patients with benign and malignant conditions. Lymphocyte level is an index of cell-mediated immunity which is important in host defense against cancer. But it is surprising that a simple test such as peripheral lymphocyte count could be correlated with clinical stages and survival results in patients with Hodgkin's disease, non-Hodgkin's lymphoma and non-lymphomatous solid tumors. Regarding the latter, lymphocyte count had prognostic values in patients with cancer of the bone, Ewing's sarcoma; breast; colon; kidney, neuroblastoma; uterine cervix, and other sites. In general, higher lymphocyte counts before therapy correlated with longer survival. Using newer immunologic techniques, T and B lymphocytes can be identified and the different subtypes of leukemia, immunodeficiency and lymphoproliferative diseases have been studied intensively. Chronic lymphocytic leukemia represents a proliferation of B cells, while the Sezary syndrome represents that of T lymphocytes. There is a qualitative and quantitative disturbance of Blymphocytes in patients with multiple myeloma. In Hodgkin's disease, there is hyperactivity of the B cells and functional defect of the T cells. Finally, the nodular non-Hodgkin's lymphoma resulted from neoplastic transformation of the B lymphocytes. In several nonmalignant autoimmune conditions, abnormality of T-cell or B-cell counts has been reported. For example, T cells were reported to be decreased in patients with ulcerative or granulomatous colitis and in patients with rheumatoid arthritis, However, it needs to be pointed out that, in 1973, Farid and associates (44) reported a significant increase in T and a proportionate reduction of B rosette in 17 patients with untreated Grave's disease and 16 with Hashimoto's thyroiditis as compared with 24 normal and eight goiter controls. In 1975, six publications later, they (143) had to announce a retraction because further studies by them and by other investigators could not repeat the earlier results. Despite variations and lack of standardization of the test systems, some consistent deviations of T-lymphocyte and B-lymphocyte counts have been reported. T lymphocytes were quantitatively decreased in patients with carcinoma of the brain, breast, head and neck, liver, lung and urologic organs and with malignant melanoma. In general, there is a marked decrease of T cells with increasing stage of disease and a return of T cells to normal level after successful therapy. Cellular immunity is depressed, often lasting for years after localized radiation therapy, whether or not the thymus is included in the treatment field...
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PMID:Peripheral lymphocyte count and suppopulations of T and B lymphocytes in benign and malignant diseases. 30 Jan 79

Expression of glutathione-S-transferase-pi (GST-pi) gene was quantitatively analysed on various human tumours (renal cell, colorectal, head and neck, ovarian carcinomas, soft tissue sarcomas; non-Hodgkin lymphomas) and on the corresponding normal tissues when available (kidney, colorectum and head and neck). GST-pi mRNA expression level was found to be significantly higher in tumours (P less than 0.01) than in the normal counterparts (mainly 7.3, 3.5- and 3.0-fold in colorectal, head and neck, and renal carcinomas, respectively). Most tumours displayed a significant relationship between higher GST-pi expression level and poor differentiation grade of tumour cells, thus suggesting a relationship between GST-pi activity, neoplastic transformation and cellular differentiation grade. The high requirement of GST-pi activity neoplastic cells displayed was not singularly related to cellular replication rate. Finally, GST-pi gene expression levels were not affected by chemotherapeutic treatments.
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PMID:Expression of glutathione-S-transferase-pi in human tumours. 151 67

Circulating immune complexes (CIC) were estimated in 28 cases of Non-Hodgkin's lymphomas, Hodgkin's disease, bone and soft tissue sarcomas in the pediatric age group by polyethylene glycol (PEG) precipitation and latex agglutination inhibition (LAI) techniques. Results were compared with 25 age-matched controls. Highly significant CIC values were obtained by LAI technique (P less than 0.01) as compared to PEG pptn technique (P less than 0.05) in malignancy. However, seropositivity for CIC in lymphomas and Hodgkin's disease was 85.71 per cent by LAI test as compared to 57.14 per cent by PEG pptn test. In sarcoma group, seropositivity for CIC was 57.11 per cent by LAI test and 28.57 per cent by PEG pptn test. Combination of both these tests increases the sensitivity of immune complex detection in serum of cancer patients. CIC begin to rise in serum in early stages of neoplastic transformation, and the level of CIC is directly proportional to proliferating tumour mass in vivo.
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PMID:Role of circulating immune-complexes as prognostic indicators of lympho-reticular and mesenchymal malignancies in children. 152 15

Recent advances in immunology, cytogenetics and molecular genetics has allowed for a better understanding of the origin and evolution of non Hodgkin lymphoma (NHL). Over the last decade a number of recurrent chromosome aberrations has been disclosed and some correlations with well defined histologic subsets of B-cell NHL has been established. Five important cytogenetic-histologic associations has been documented, well defined by combined cytologic, immunologic and genetic investigations: t(14;18) (q32;q21) and NHL of follicle centre cell origin, frequently with follicular histologic pattern; t(8;14) (q24;q32) and Burkitt's lymphoma, Burkitt-like lymphoma or the equivalent small non-cleaved cell category of the "working formulation system"; t(3;22) (q27;q11) and diffuse large cell lymphoma; t(11;14) (q13;q32) and mantle zone lymphoma; trisomy 12 and chronic lymphocytic leukemia and well-differentiated small lymphocytic lymphoma. Molecular genetic studies elucidated some mechanisms operating during the normal lymphocyte differentiation which may be held responsible for the illegitimate recombination between the immunoglobulin genes and some oncogenes normally located on other chromosome regions. It has thus been demonstrated that the early events leading to neoplastic transformation in B-cell neoplasias occur in immature lymphocyte precursors in the bone marrow during the assembly of the immunoglobulin heavy chain gene. According to some recent studies chromosome changes may have prognostic value in B-cell NHL and chronic lymphocytic leukemia and may be employed in clinical practice in the construction of proportional hazard models in several histologic subsets of NHL.
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PMID:[Current view on non-Hodgkin lymphomas. Origin and evolution in relation to cytogenetic-histologic correlations]. 158 38

Attempts to understand the malignant lymphomas have followed two major lines of investigation: attempts to define the relationship of neoplastic lymphoid cells to stages of normal T- and B-lymphocyte differentiation, and attempts to understand the genetic abnormalities associated with malignant transformation. It is hoped that these two lines of investigation will make it possible to define clinically important entities, so that specific treatment strategies can be developed and tested, and will also point the way to new options for treatment and prevention. Despite the advances in immunology of the last two decades, our understanding of the relationships of lymphoma cells to the normal immune system remains incomplete. Techniques of molecular genetics, which initially promised to resolve questions of clonality and lineage, have proven less definitive than had been hoped. Studies in the field of molecular cytogenetics--the study of chromosomal translocations by molecular techniques--have just begun to unravel some of the mysteries surrounding neoplastic transformation and differentiation. As we enter the last decade of the century, small advances continue to chip away at the uncertainties shrouding the malignant lymphomas. Advances in the past year include the subclassification of low-grade B-cell lymphomas, including so-called intermediate lymphocytic lymphoma and extranodal lymphomas of mucosa-associated lymphoid tissue, the classification of T-cell lymphomas, the definition of Hodgkin's disease and its relationship to anaplastic large cell lymphoma, and new techniques for characterizing lymphoid cells in paraffin-embedded tissue sections.
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PMID:Pathology of malignant lymphomas. 166 Nov 68

The neoplastic Hodgkin's Reed-Sternberg (H-RS) cells in Hodgkin's disease are surrounded in vivo by abundant reactive cells, the function of which may be attributed in part to their elaboration of various cytokines. Thus, a study of the interaction of H-RS cells with exogenous cytokines may provide information as to the mechanism of the clinical and histopathologic changes observed in Hodgkin's disease. This study examined the effect of various cytokines, and of phorbol ester (TPA) and retinoic acid, on the differentiation and proliferation of cultured H-RS cells (cell lines HDLM-1 and KM-H2). In addition, it was determined whether these cells were able to secrete cytokines after being treated with exogenous cytokines. The cytokines used included various types of interleukins (1, 2, and 3), colony-stimulating factors (GM, G, and M), interferons (alpha, beta, and gamma), and tumor necrosis factor (alpha). It was found that these cytokines, used alone or in combination, were not effective in modulating the proliferation and differentiation of cells, or the production of cytokines, in cultured H-RS cells. In contrast, this study revealed that retinoic acid can potentiate TPA-induced growth inhibition in cultured H-RS cells. Retinoic acid, when used alone, exhibited a minimal effect on cell differentiation. No synergistic effects of cytokines and retinoic acid on H-RS cells were observed. The failure of cultured H-RS cells to respond to exogenous cytokines suggests that, during the course of neoplastic transformation, of progression of disease, or of establishment of the cells in culture, H-RS cells lose their dependence on cytokines, although they retain the capacity to produce various cytokines.
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PMID:Lack of effect of colony-stimulating factors, interleukins, interferons, and tumor necrosis factor on the growth and differentiation of cultured Reed-Sternberg cells. Comparison with effects of phorbol ester and retinoic acid. 168 89

Primary central nervous system lymphoma (PCNSL) is a rare neoplasm, but it is occurring with increased frequency even among apparently immunocompetent patients. Although secondary malignancies frequently involve the lymphoreticular system, PCNSL has been reported as a second neoplasm only once previously. Seven patients are discussed who developed PCNSL after successful treatment for a prior neoplasm. The original cancer was colon (one), breast (one), thyroid (one), Hodgkin's disease (two), and non-Hodgkin's lymphoma (two). Patients with systemic non-Hodgkin's lymphoma were thought to have a separate cerebral lymphoma on the basis of a prolonged disease-free interval from their systemic lymphoma, and the absence of systemic disease, when PCNSL was diagnosed and through subsequent follow-up. The PCNSL developed a median of 10 years after the diagnosis of the first tumor and 6 years after the last evidence of systemic disease. The diagnosis of PCNSL was often delayed because of confusion with brain metastases, and initial shrinkage or disappearance of the lesion after corticosteroids. Formation of PCNSL may be a consequence of treatment for the first malignancy, reflect an unidentified inherent predisposition to neoplastic transformation, or result from the changing epidemiology of PCNSL in the general population. These mechanisms are not mutually exclusive, and a single hypothesis cannot account for all these cases.
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PMID:Primary central nervous system lymphoma as a secondary malignancy. 199 9

Pre-stages and early stages of malignant Non-Hodgkin's-lymphomas mark the border area between benign, reactive lymphoproliferation and neoplastic transformation. The advances of immunological classification of lymphoid cells with monoclonal antibodies and molecular genetic analysis have contributed to our present knowledge of pathomorphology, pathophysiology and nosology of malignant lymphomas. The stepwise evolution between polyclonal reactive lymphoproliferation and clonal autonomous growth in malignant lymphomas are presented by discussion of the mucosa-associated lymphomas (MALT-lymphomas) and typical lymphoproliferative diseases.
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PMID:[Benign (reactive) lymphoproliferation or malignant lymphoma?]. 203 77

The past several years have seen major advances in the immunopathology of Hodgkin's disease, although the cell of origin remains unproven. Reed-Sternberg cells have been characterized with monoclonal antibodies and are found to consistently express panleukocytic antigen (T-200), HLA-DR antigens, and several activation-proliferation antigens (Tac, OKT-9, Ki-1). Reed-Sternberg cells also express a nonlineage-specific antigen defined by the antigranulocyte antibody Leu M-1. Lineage-specific B, T or monocyte-macrophage antigens are generally lacking. With the possible exception of the lymphocyte predominant form of the disease, Hodgkin's disease appears immunologically homogeneous. The possible origin of Reed-Sternberg cells by neoplastic transformation of antigen-presenting dendritic cells (interdigitating reticulum cells) appears to be an attractive albeit unproven hypothesis. Application of molecular biologic techniques in the future may yield definitive evidence as to the origin and nature of these enigmatic cells, and to the pathophysiology of the disease which they define.
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PMID:Immunopathology of Hodgkin's disease. 311 Jul 53

Chromosome translocations are consistently present in leukemias and lymphomas and are likely to represent primary events in the development of these neoplasias. A study of conditions that predispose to leukemia could shed some light on the origin of these translocations and therefore help in clarifying their exact role in the process of neoplastic transformation. Based on this assumption, we studied a group of individuals treated with radiochemotherapy for previous lymphoma and who were at increased risk of developing a secondary leukemia. The group comprised 14 Hodgkin's disease patients, 11 non-Hodgkin's lymphoma patients, and 13 controls. The patients were in remission and had been off therapy for at least 6 months. Chromosomes were studied from phytohemagglutinin (PHA)-stimulated peripheral lymphocytes and from bone marrow cells by the direct method and after short-term cultures (72 hours). The latter were also exposed to 5-bromodeoxyuridine (BrdU). Metaphases were scored for chromosome breaks, gaps, and other rearrangements. The percentage of gaps and breaks was significantly higher in patients than in controls. The difference was induced by BrdU and was apparent in bone marrow cells, but not in peripheral lymphocytes. We conclude that individuals exposed to the action of mutagenic agents (radiochemotherapy) have an increased chromosome instability that could be related to their increased risk of developing a secondary leukemia.
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PMID:Long-term cytogenetic effects of antineoplastic treatment in relation to secondary leukemia. 338 68


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