Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monoclonal membrane-bound Ig were found by immunofluorescence on the lymphocytes in the vast majority of cases of chronic lymphocytic leukemia. The distribution of H and L chains among these patients reflected the distribution of surface Ig on normal lymphocytes and IgM was the predominant class. The importance of the study of surface Ig synthesized in vitro is outlined. The simple staining of freshly drawn cells may lead to erroneous conclusions, since an apparently polyclonal staining can result from the anti-IgG antibody activity of a monoclonal surface IgM, from the attachment of immune complexes at the lymphocyte surface or from the binding of serum antibodies to cell membrane determinants. A biclonal proliferation, characterized by distinct surface-Ig markers, was demonstrated in several cases of chronic lymphatic leukemia. Monoclonal surface Ig were also detected on the lymphoblasts in 2 cases of acute transformation of chronic lymphocytic leukemia, in several patients with acute lymphosarcoma cell leukemia and in 1 case of acute lymphatic leukemia. In most cases of acute lymphatic leukemia, the leukemic cells were devoid of detectable B- or T-cell membrane markers. In 2 cases of acute lymphatic leukemia, 1 case of chronic lymphatic leukemia and in all patients with the Sezary syndrome, the leukemic cells appeared to be thymus-derived.
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PMID:The monoclonal nature of lymphatic leukemia. 5 95

The expression of B-cell antigens on various cell populations was studied through the use of human alloantisera and with heteroantisera raised to preparations of the alloantigen bearing molecules isolated from B-cell lines. The allo-and hetero-antisera competed with each other in blocking experiments and gave closely parallel results, reacting with normal and leukemic B lymphocytes, monocytes, E-rosette-negative acute lymphatic leukemias, all acute and certain chronic myelogenous leukemias, and a minor population of cells in fetal spleen and liver. These highly immunogenic surface components appeared to comprise the dominant B- cell specific plasma membrane determinants. Neither type of antiserum reacted with any but a minor population of normal or pokeweed-mitogen-transformed T cells, fetal thymic lymphocytes, E-rosette-positive acute lymphatic leukemias, or Sezary-cell leukemia. Through the use of these antisera evidence was obtained that Fc-receptor-bearing Ig-negative lymphocytes were divisible into two groups according to the presence or absence of the B-cell antigens. Both hetero- and allo-antisera blocked binding of immune complexes or antibody-coated ox erythrocytes to Fc receptors on B cells. F(ab')2 fragments of the heteroantibodies strongly inhibited antibody-dependent cell-mediated killing.
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PMID:Studies with B-cell allo- and hetero-antisera: parallel reactivity and special properties. 6 89

Leucocyte alkaline phosphatase (LAP) was histochemically detected in 7 to 18% of cells in tissue culture lines derived from the peripheral blood or bone marrow of each of 5 patients with untreated acute myelogenous or monomyelogenous leukaemia and in 30% of the cells in a clonal line of a rat promyelocytic leukaemia. Following transfer to diffusion chambers intraperitoneally implanted into total body irradiated rats, LAP levels were detected in up to 92% of human and 80% of rat leucocytes. There was no associated morphologic differentiation. In rat leukaemia cells peroxidase and myeloid specific esterase also increased from tissue culture levels. Return of cells to tissue culture decreased enzymes to pre-implant levels. Addition of plasma or peritoneal fluid from irradiated rats to cells in tissue culture again induced LAP. In contrast, LAP was not increased under these conditions with cell lines derived from patients with acute lymphatic leukaemia, or Sezary cell leukaemia. These studies indicate that a humoral factor in peritoneal fluid and plasma of irradiated rats increases LAP in human as well as rat leucocytes.
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PMID:Leucocyte alkaline phosphatase elevation in human acute leukaemia derived cell lines cultured in diffusion chambers. 26 91

Cytopheresis techniques have proven useful in the provision of platelets and granulocytes for transfusion to the pancytopenic patient. Mechanical cell removal has been applied to the treatment of chronic myelocytic and lymphocytic leukemias and the Sezary syndrome. We have treated a 16-year-old pregnant acute myelomonocytic leukemia (AMML) patient for 12 weeks solely with the use of intensive leukopheresis utilizing batch processing centrifugation and packed red cell transfusions. The patient presented with a white blood cell count of 54,000/mm3 with 64% myelomonoblasts, a platelet count of 45,000/mm3, marked gingival hyperplasia, and splenomegaly. Patient had a normal spontaneous delivery of a 2.5-kg male infant without complications. At the time of delivery, 12 weeks later, the white blood count had fallen to 4,9000/mm3 with 8% blasts and the platelet count had risen to over 100,000/mm3. Gingival hyperplasia decreased and the patient felt well. We have treated an additional small group of patients with acute myelogenous leukemia (AML) with high white counts with short term intensive leukopheresis followed by chemotherapy with promising results.
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PMID:Therapeutic leukopheresis of acute myelo-monocytic leukemia in pregnancy. 27 83

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

Lymphoid cells from 20 patients with lymphoproliferative disorders, including chronic lymphocytic leukemia, hairy cell leukemia, Sezary syndrome, lymphoma, and lymphadenitis, were studied for redistribution of surface membrane immunoglobulins (SmIg) and concanavalin A (Con-A) receptors. Fluorescein-labeled polyvalent goat anti-human immunoglobulin and fluoresceinated concanavalin A were used as ligands. Results were similar with both ligands. The highest percentage of capping of ligand-membrane receptors was noted in mononuclear cells from patients with "hairy" cell leukemia: from 24% to 90%. These cells showed moderate to marked fluorescein activity and were able to cap within 15 min at 4 degrees C. Chronic lymphocytic leukemia cells showed a weak fluorescein stain with a very low percentage of cells (0%--16%) capping. Lymph node cells from patients with lymphoma demonstrated moderate to strong fluorescein activity with only an average of 3% of the cells capping; while lymphoid cells from patients with lymphaedenitis showed an average of 27.5% capping and moderate fluorescein activity. Capping of Con-A receptors in mononuclear cells from patients with Sezary syndrome was poor (0%--14%) with moderate fluorescein intensity. This report demonstrates difference in density and mobility of binding sites for SmIg and Con-A on the surface membrane of lymphoid cells from various subclasses of lymphoproliferative disorders. These differences may assist in the differential diagnosis and classification of these conditions.
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PMID:Membrane receptors and their redistribution in lymphoproliferative disorders. 46 33

Rosette formation with mouse erythrocytes and other cell-surface markers were examined on lymphocytes from patients with a variety of primary immunodeficiency and lymphoproliferative disorders. Mouse erythrocyte rosette-forming cells and lymphocytes with surface immunoglobulins were regularly absent in patients with Bruton type agammaglobulinaemia, immunodeficiency and thymoma syndrome and severe combined immunodeficiency disease. However, they were present in normal or low numbers in patients with common variable immunodeficiency, selective IgA deficiency and ataxis telangiectasia. Lymphocytes from patients with acute lymphoblastic leukaemia Sezary syndrome and mycosis fungoides made no or few rosettes with mouse erythrocytes. Increased numbers of mouse erythrocyte rosette-forming cells were present in patients with chronic lymphocytic leukaemia and Waldenstrom's macroglobulinaemia. The significance of the mouse erythrocyte rosette as a B-cell marker in the analysis of primary immunodeficiency and lymphoproliferative disorders is discussed.
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PMID:Rosette formation with mouse erythrocytes. III. Studies in patients with primary immunodeficiency and lymphoproliferative disorders. 106 59

The nature of the immunological defect in patients with hypogammaglobulinemia associated with a thymoma was investigated using a technique established to study the differentiation of lymphocytes into immunoglobulin synthesizing and secreting cells. Exhaustively washed peripheral blood lymphocytes were cultured for 7 days in RPMI-1640 medium supplemented with fetal calf serum in the presence of the lectin, pokeweed mitogen. The IgG, IgA, and IgM synthesized and secreted into the medium were measured by competitive double antibody radio-immunoassays. Twenty-two normal individuals synthesized 1625 ng of IgG, 1270 ng of IgA, and 4910 ng of IgM per 2 million lymphocytes in culture. In contrast, the three patients with hypogammaglobulinemia and a thymoma synthesized less than 100 ng of each class of immunoglobulin. When lymphocytes from 2 of the 3 patients studied were cocultured with normal lymphocytes and pokeweed mitogen, the synthesis of immunoglobulin by normal lymphocytes was depressed by a factor of 66 to 97%. Co-cultue of purified T cells from the hypogammaglobulinemic patients with normal lymphocytes resulted in an 87% suppression of immunoglobulin synthesis by the normal cells. However, no suppression of immunoglobulin synthesis was observed when preparations of B cells and macrophages depleted of T cells from the hypogammaglobulinemic patients were co-cultured with normal lymphocytes. In addition, in control studies no such suppression of immunoglobulin synthesis was seen when normal cells were co-cultured with lymphocytes from unrelated normals, patients with isolated IgA deficiency, patients with chronic lymphocytic leukemia or patients with the Sezary syndrome, a T cell leukemia nor were they inhibited when incubated with T cells from unrelated normals. These observations suggest that in some patients the hypogammaglobulinemia associated with a thymoma may be caused or perpetuated by an abnormality of regulatory T cells which suppress the maturation of lymphocytes into antibody producing cells.
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PMID:Suppressor T cells in the pathogenesis of hypogammaglobulinemia associated with a thymoma. 108 79

The term ""cutaneous lymphoma'' is used for lymphoreticular proliferative processes which primarily affect the skin. This term includes: mycosis fungoides, Sezary-syndrome and ""pagetoid epidermotropic reticulosis''; ""malignant reticulosis'', ""reticulum cell sarcoma'' and lymphosarcoma; in a wide sense of this term pseudolymphomas (lymphadenosis benigna cutis, benign lymphocytoma), specific skin infiltrates in leukemia and Hodgkin's disease might be included as well.
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PMID:[Progress in the diagnosis of cutaneous lymphomas. Enzyme cytochemical and immunocytological studies]. 108 39

2',5'-oligoadenylate synthetase (2-5OAS) has been studied in peripheral blood mononuclear cells from nine patients with hairy cell leukaemia (HCL) receiving therapy with the adenosine deaminase inhibitor deoxycoformycin (dCF) or alpha interferon (alpha-IFN). 2-5OAS mRNA was assayed by dot-blot hybridization. Increase of 2-5OAS mRNA level was seen in six patients with HCL treated with dCF and in one patient treated with alpha-IFN who responded to therapy. A patient with a variant form of HCL treated with dCF and the second patient treated with alpha-IFN did not show an increase of 2-5OAS mRNA and neither responded to therapy. The 15 other patients with T or B-chronic lymphoblastic leukaemia (CLL), T-acute lymphoblastic leukaemia (ALL), adult T-cell leukaemia lymphoma (ATLL), non-Hodgkins lymphoma (NHL), Sezary and T or B-prolymphocytic leukaemia (PLL) treated with dCF did not show an increase in 2-5OAS, though four patients, all with T-cell tumours, responded clinically. 2-5OAS activity is known to be stimulated by alpha-IFN and recent work suggests that this rise in 2-5OAS may result in increased cleavage of mRNA for tumour necrosis factor (TNF) and other cytokines on which autocrine growth and proliferation of the tumour cells are dependent. By analogy, we suggest that one mechanism of action of dCF in hairy cell leukaemia may be to break down an autocrine growth loop for TNF or other cytokines. An alternative explanation for these observations is that cytokines released from hairy cells in the bone marrow killed by dCF induce a rise in 2-5OAS in circulating leucocytes.
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PMID:Increase in 2',5'-oligoadenylate synthetase caused by deoxycoformycin in hairy cell leukaemia. 155 Jul 76


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