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)

Activities of dipeptidyl-aminopeptidase IV, urokinase-like plasminogen activator, cathepsins B and L were studied in lymphoid cells of patients with various forms of lymphoproliferative disorders. Activity of the enzymes studied was found in all the T- and B-cell, although rate and ratio of the enzymatic activity were dissimilar in various cell types. The highest rate of activity exhibited cells at early stages of maturation obtained from patients with acute lymphoblastic leukemia, while low level of the proteinase activity was detected in cells of patients with chronic lymphoid leukemia, non-Hodgkin lymphoma, hairy cell leukemia and Sezary disease, corresponding to mature T- and B-subpopulations. As shown by analysis of the cells immunological phenotype and their proteolytic activity, the rate of lymphoid cells differentiation correlated with level of proteinases activity. Series of proteinases were firstly studied in human malignant lymphoid cells with known phenotype. The enzyme assay may be used in diagnosis and treatment of patients with lymphoproliferative disorders.
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PMID:[Protein kinase activity in lymphoid cells in various forms of lymphoproliferative disorders]. 168 94

We have studied the effects of recombinant human granulocyte colony-stimulating factor (rhG-CSF), hG macrophage-CSF (hGM-CSF), and gibbon interleukin-3 (gIL-3) on cell proliferation and differentiation in human long-term bone marrow culture (LTBMC). hG-CSF induced a maximal increase of 2.3-fold in both total nonadherent cells and GM cluster-forming cells, but only an increase of 1.7-fold in GM-colony-forming cell (GM-CFC) numbers, influencing mainly neutrophil differentiation. Cultures treated with hGM-CSF demonstrated a peak of 12.8-, 21- and 3.2-fold elevations in total nonadherent cells, cluster, and GM-CFC, respectively, and influenced differentiation of neutrophils, monocytes, eosinophils, and lymphocytes. Cultures treated with gIL-3 demonstrated the largest expansion in the GM-CFC population, reaching a maximum of 5.3-fold in relation to that of unstimulated controls. IL-3 treatment also increased the numbers of GM clusters and mature cells (including all myeloid cells and lymphocytes) 7.8- and 4.8-fold, respectively. Similar quantitative and qualitative changes were induced by G-CSF, GM-CSF, and IL-3 in LTBMCs of patients in remission after treatment for acute lymphoblastic leukemia or Hodgkin's lymphoma. Overall, the expansion of GM progenitor cells in cultures treated with growth factors was larger in the adherent cell layer than in the nonadherent cell fraction. In addition, hGM-CSF, gIL-3, and hG-CSF to a less extent, increased the cycling rates of GM-CFC progenitors located in the adherent layer. These results indicate that hG-CSF is a much less potent stimulus of hematopoiesis in LTBMC than the other CSFs assayed, and that the increases in cell production after treatment with G-CSF, GM-CSF, or IL-3 may be achieved by primary expansion of different cell populations within the hierarchy of the hematopoietic system. The effects of the growth factors were transient and the longevity of hematopoiesis in the cultures was not altered, suggesting that treatment with IL-3, GM-CSF, or G-CSF had not compromised the ability of primitive cells to give rise to mature cells. This indicates that the stromal microenvironment in LTBMC can override potential differentiation-inducing activities of the CSFs.
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PMID:Effects of recombinant human granulocyte colony-stimulating factor (CSF), human granulocyte macrophage-CSF, and gibbon interleukin-3 on hematopoiesis in human long-term bone marrow culture. 169 95

Detailed immunophenotypic analyses of immunologically classified leukemias and lymphomas showed that CD40 displays an exquisite B-lineage specificity within the human lymphopoietic system. Notably, 82% of B-lineage chronic lymphocytic leukemias (CLLs), 82% of B-lineage hairy cell leukemias (HCLs), 86% of B-lineage non-Hodgkin's lymphomas (NHLs), and 29% of B-lineage acute lymphoblastic leukemias (ALLs) were CD40+. Quantitative analyses of the correlated expression of CD40 and other B-lineage differentiation antigens on fetal lymphoid precursor cells by multiparameter two-color/three-color flow cytometry, combined with analyses of sequential antigen expression on fluorescence-activated cell fluorescence activated cell sorter (FACS) isolated immunologically distinct fetal B-cell precursor subpopulations during in vitro proliferation and differentiation, provided evidence that the acquisition of CD40 antigen in human B-cell ontogeny occurs subsequent to the expression of CD10 and CD19 antigens but before the surface expression of CD20, CD21, CD22, CD24, and surface immunoglobulin M (sIgM). Some leukemic pro-B cells from ALL patients as well as normal pro-B cell clones from fetal livers displaying germline Ig heavy chain genes were CD40+, indicating that the acquisition of CD40 antigen likely precedes the rearrangement of Ig heavy chain genes. CD40+ FACS-sorted malignant cells from B-lineage ALL as well as B-lineage NHL patients were capable of in vitro clonogenic growth, indicating the CD40 antigen is expressed on clonogenic leukemia and lymphoma cells. This hypothesis was confirmed by the ability of an anti-CD40 immunotoxin that we used as an antigen-specific cytotoxic probe to effectively kill clonogenic B-lineage ALL and NHL cells.
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PMID:Temporal association of CD40 antigen expression with discrete stages of human B-cell ontogeny and the efficacy of anti-CD40 immunotoxins against clonogenic B-lineage acute lymphoblastic leukemia as well as B-lineage non-Hodgkin's lymphoma cells. 170 26

Recent immunopathologic studies have demonstrated that primary follicles and the mantle zones of secondary follicles are composed largely of virgin B lymphocytes which migrate from the bone marrow to these areas, and are the precursor cells of germinal centers. Non-Hodgkin's lymphomas corresponding to these immature B cells include mantle zone lymphoma (MZL), a primary follicle variant of MZL without reactive germinal centers, and diffuse intermediate lymphocytic (centrocytic) lymphoma. Diffuse intermediate lymphocytic lymphoma (DILL) is considered a late stage in the progression of MZL. Cytologically, these lymphomas usually resemble their normal cellular counterparts and consist predominantly of atypical small lymphoid cells with slightly-irregular and indented nuclei, moderately-coarse chromatin, inconspicuous nucleoli, and scant cytoplasm. Small lymphocytic, cerebriform and blastic variants have also been described. In smears and touch preparations, the neoplastic cells are usually prolymphocytes. Immunologically, the cells have features of virgin B cells, bearing pan-B cell antigens along with monoclonal surface IgM, with or without surface IgD, and CD5 (Leu 1) antigen, and lacking common acute lymphocytic leukemia associated (CALLA) antigen. Cytogenetically, the t(11;14)(q13;q32) has been associated with this group of lymphomas, and expression of the putative cellular oncogene bcl-1 (11q13) has been demonstrated in 30-50% of cases. Clinically, the patients have a median age of 60 years and usually present with advanced stage disease. Splenomegaly, often massive, is present in 80% of those with MZL. Patients with MZL have a significantly longer median survival (74-77 months) than those with DILL (30-33 months), and survival in both groups is significantly prolonged if a complete clinical remission is attained. Based on clinical studies, MZL should be considered a low grade lymphoma and DILL should be considered an intermediate grade lymphoma by Working Formulation criteria. The lymphomas of primary follicle/mantle zone origin are a distinct clinicopathologic entity biologically analogous to the follicular and diffuse lymphomas of germinal center origin, from which they should be distinguished in current and future classifications of non-Hodgkin's lymphoma.
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PMID:Non-Hodgkin's lymphomas of primary follicle/mantle zone origin. 171 36

ICO, IPO and LT series monoclonal antibodies, lectins, PAP and APAAP methods were used to study blood, bone marrow and lymph node cells in children with acute lymphoblastic leukemia (ALL), non-Hodgkin's malignant lymphomas and Hodgkin's disease. The immunological phenotype of malignant lymphoid cells has been characterized and cytological variants of ALL and lymphomas of T and B cell origin have been distinguished.
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PMID:[Immunoenzyme cytochemical methods, monoclonal antibodies and lectins in the diagnosis of tumors of the lymphoid tissue in children]. 176 34

We analyzed the T-cell receptors and immunoglobulin genes in 140 cases of hematopoietic malignancies, including ALL/LBL, malignant lymphomas, AILDs, Hodgkin's disease, ATL and CLL. In many cases, the findings obtained by immunoassociated gene analysis were in parallel to the phenotypic findings. Gene analysis is useful to determine the clonality and the lineage of malignant cells. However, 10-30% cases appeared bigenotype. In some cases, oligoclonalities were recognized. The relationship to the prognosis in these cases was discussed. The development of gamma delta- and alpha beta-cells on T-cell ontogeny was elucidated. Some T-cell leukemic lines were found to be pre-alpha beta T-cells with some consensus characteristics. We also analyzed the V beta family of 15 alpha beta T-cell leukemia cell lines using six V beta cDNA probes. This approach may be useful to determine the clonality of T-cell malignancies. The method of using a PCR system on immunoassociated genes has been described. The PCR method, using the super variable region as a tumor specific fragment, is valuable in the detection of the residual cells of lymphoma and leukemia at a concentration of 1/10(5) cells.
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PMID:[Gene analysis in human hematopoietic malignancies]. 177 63

Hodgkin's disease, manifested as a second malignant neoplasm in acute lymphoblastic leukemia, rarely occurs, with seventeen cases reported including this cases. We presented the clinical and pathological features of a nine-year-old male child with acute lymphoblastic leukemia in remission. He had cervical lymph node involvement 22 months after the diagnosis of leukemia as an initial presentation of Hodgkin's disease of mixed cellularity. A brief review of related literatures was also done.
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PMID:Hodgkin's disease in a child with acute lymphoblastic leukemia. 178 Nov 87

Among a cohort of 981 children who were followed up 4.3-26.5 years after cessation of antileukemic therapy, eight patients in remission of acute lymphoblastic leukemia (ALL) developed a distinctively new malignant disease. The second malignant neoplasms (SMN) included brain tumors, basal cell carcinomas, thyroid cancer, leiomyosarcoma and finally rhabdomyosarcoma in a patient who also had suffered from Hodgkin's disease while still on antileukemic treatment. Cranial radiation had been given to 58.4% of the patients in the study group, which consisted of 895 ALL patients who had completed various chemotherapy protocols. With one exception, the SMN appeared after 7.5-16.5 years at a location previously exposed to radiotherapy (RT). The estimated cumulative risk of SMN appearing within 20 years after diagnosis was 2.9%, and the corresponding risk for cases with RT was 8.1% compared to 0.3% for those without (p = 0.05). In a Cox regression analysis, the incidence rate ratio of SMN between patients with and without RT was 6.7 (95% CI = 0.8, 57.7). Based on age-, year- and sex-specific cancer incidence figures for Norway, the overall standardized incidence rate ratio (SIR) of SMN after treatment for ALL was 5.9 (95% CI = 2.2, 12.9). The number of brain tumors among patients who had received cranial radiation was nearly 27 times greater than expected, whereas no such tumors were seen after chemotherapy. Individuals treated for childhood ALL are at increased risk of a new malignancy, and this seems mainly to be associated with previous irradiation.
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PMID:Second malignant neoplasms in patients treated for childhood leukemia. A population-based cohort study from the Nordic countries. The Nordic Society of Pediatric Oncology and Hematology (NOPHO). 178 95

We present results concerning the reactivity of two moAbs (BR3, BR31) with human B cell lines and malignant B cells from patients. The first antibody BR3 shows a broad reactivity with B cell malignancies and B cell lines. It also weakly stains some non-T ALL cells and is negative on plasma cell tumors. The second moAb BR31 shows a restricted reactivity. It stains only HCL and PLL cells as well as Burkitt's lymphoma lines. Some moderate staining was also observed on 4 out of 12 cases of CLL and some non-Hodgkin lymphomas. PLL cells, cultured with polyclonal activators, lose BR31 Ag by day 4 of culture. These results suggest that BR3 Ag is present on the cell surface throughout B cell ontogeny while BR31 Ag expression is related to a particular stage of B cell maturation.
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PMID:Further studies on the specificity of anti-human B cell monoclonal antibodies (BR3, BR31)--reactivity with hematopoietic malignant cells. 181 Feb 15

Activity of 8 glycosidases (6 acid lysosomal and 2 neutral cytosolic enzymes) was estimated in lymphoid cells of 28 patients with different forms of lymphoproliferative disorders: B- and T-chronic lymphocytic leukemia (CLL), non-Hodgkins lymphoma (NHL), Sezary syndrome, hairy cell leukemia (HCL) and B- and T-acute lymphoblastic leukemia (ALL). Activity of these glycosidases was also studied in mononuclear cells and granulocytes of healthy volunteers and in immature myeloid cells of 16 patients with chronic myeloid leukemia (CML). In lymphoid cells of all the patients studied (except of ALL) the glycosidases activity was decreased as compared with that of normal mononuclear cells and immature myeloid cells. Activity of the majority enzymes studied was higher in T-lymphoid cells of patients with lymphoproliferative disorders as compared with B-cells. The highest glycosidases activity was found in ALL cells and the lowest--in CLL cells of the patients with B-lymphoid cells forms of the disease. Activities of N-acetyl-beta-D-hexosaminidase, alpha-D-mannosidase and beta-D-glucuronidase were distinctly dissimilar in cells of the patients with B-CLL, B-NHL and HCL. Estimation of these glycosidases activity in lymphoid cells may be of importance in differential diagnosis of lymphoproliferative disorders.
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PMID:[Lymphoid cell glycosidases in various forms of lymphoproliferative disorders]. 181 21


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