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At least 19 recordsLinked to original sources
PubMed1979

Membrane receptors and their redistribution in lymphoproliferative disorders.

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.

Cell Membrane↗
PubMed1978

Bone-marrow mast cells in lymphoproliferative disorders.

Increased bone-marrow mast-cell content and lymphoproliferative disorders have been previously linked. Using a semiquantitative method we examined bone-marrow mast-cell content in 120 marrow specimens from patients with multiple myeloma, chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and reactive lymphocytosis. Results indicated a statistically significant increase of marrow mast-cell content in patients with chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and reactive lymphocytosis when compared with iron-deficient control subjects (p less than or equal to 0.0005). Patients with multiple myeloma had decreased marrow mast-cell content, clearly separating them from patients with lymphoproliferative disorders and reactive lymphocytosis. Linear regression plot of marrow mast-cell content against percentage of marrow lymphocytes showed a direct relation, indicating that marrow mast-cell density may be related more to the degree of lymphoid proliferation than to the specific lymphoproliferative process. Marrow mast-cell content may therefore be reproducibly determined and used to support the morphologic diagnosis of lymphoproliferative disorders and differentiate them from atypical myelomas.

Adolescent↗
PubMed1979

T-lymphocyte colonies in normal blood, bone marrow and lymphoproliferative disorders.

The formation of T-lymphocyte colonies was studied in normal individuals and in different lymphoproliferative disorders, using the double layer technique of Lowenberg & de Zeeuw (1977). All normal peripheral blood and bone marrow samples formed colonies: range 102-270 (mean 177) and 55-245 (mean 138) per 1 X 10(5) cells, respectively. Bone marrows from acute leukaemias in complete remission showed normal or increased colony formation. The T cell nature of the colonies was shown by rosette formation with sheep and human red blood cells (RBC). Most lymphoproliferative disorders of T and B cell either failed to grow colonies or showed reduced colony numbers. This was of particular interest in the chronic T cell disorders in which a high proportion of T cells was plated. This technique may help in the further characterization of leukaemic cell populations and may also provide clues on the distribution of particular subsets of T-lymphocytes in peripheral blood and bone marrow.

Adult↗
PubMed1977

HBsAg, chronic lymphoproliferative disorders, and cirrhosis of liver.

This study reports the incidence of HBsAg in a series of chronic lymphoproliferative disorders in which a high incidence of cirrhoses had been previously observed. Twenty-three cases were collected from the necropsy records. The type of lymphoma was reviewed in the light of the new functional classifications of non-Hodgkin malignant lymphomas introduced by Lennert and Lukes. The presence of HBsAg in the liver was investigated by the indirect immunofluorescence technique. Eleven cases showed plasmocytoid features and were considered as immunocytomas. Seven cases showed cirrhosis of the liver; six of them belonged to the immunocytoma group. Four cases were positive for HBsAg. Three of them were found among the group combining cirrhosis and immunocytoma. They presented the abundant nodular distribution of HBsAg typical of inactive cirrhosis.A parallel is drawn between the often reported association of Waldenström's syndrome and cirrhosis and the association of immunocytoma and cirrhosis observed in this study. The analogy is all the more justified since most of the lymphomas associated with Waldenström's syndrome happen to be immunocytomas. Therefore the association between HB virus infection and cirrhosis on the one hand and chronic lymphoproliferative disorders on the other may not be purely coincidental. A chronic antigenic stimulus such as persisting HBsAg could trigger the proliferation of a malignant lymphoid clone.

Aged↗
PubMed1979

A new characteristic karyotypic anomaly in lymphoproliferative disorders.

A new characteristic chromosome anomaly t(11;14)(q14;q32?) in lymphoproliferative disorders (LPD) is described in 4 cases. The extra material was found on a "14 chromosome (14q+) and belonged to the long arm of one "11 chromosome in 3 cases and to the long arm of a "14 in the other case. These cases confirm that the distal end of chromosome 14q may function as a "receptor site," according to the hypothesis of Kaiser-McCaw et al. and also tend to indicate that chromosome "14 may not be unique in showing so-called "donor" and "receptor sites," and that other chromosomes, in casu chromosome "11, may behave similarly.

Adult↗
PubMed1976

Rosette formation with mouse erythrocytes. III. Studies in patients with primary immunodeficiency and lymphoproliferative disorders.

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.

Agammaglobulinemia↗
PubMed1976

Mouse red-cell rosettes in B-lymphoproliferative disorders.

A high proportion of peripheral-blood lymphocytes formed spontaneous rosettes with mouse red cells in 22 out of 23 cases of chronic lymphocytic leukaemia (CLL); the proportion was significantly higher than in 19 cases of other B-lymphoproliferative disorders (non-CLL group) and in 19 normal controls. Intermediate findings were obtained in 10 cases of "hairy" cell leukaemia. Blast cells from various types of acute leukaemia did not bind mouse red cells. Pre-treatment of the lymphocytes with neuraminidase led to a significant increase in the proportion of rosettes in CLL only. This test may prove useful in distinguishing CLL from other B-lymphoproliferative disorders, particularly prolymphocytic leukaemia.

Animals↗
PubMedDate not supplied

Red cell hypoplasia and monoclonal gammopathy in a patient with lymphoproliferative disorder.

A 69-year-old male was observed to have red cell hypoplasia. Two years later monoclonal gammopathy IgG-I, K, Gma+ and InV (1-) was documented in this patient. Persistent lymphocytosis, abnormal response to phytohemagglutinin, and at autopsy multiple lymphoid nodules occurring in the bone marrow, suggestive of lymphoproliferative disorder, were observed. A review of the literature indicates that this clinical presentation is rare. The possibility that red cell aplasia may be associated with lymphoproliferative disorder in some instances must be considered inasmuch as this may have an important bearing in the management of such patients.

Aged↗
PubMed1976

Acquired angioedema with lymphoproliferative disorder: association of C1 inhibitor deficiency with cellular abnormality.

A patient with a lymphoproliferative disorder, angioedema, and an acquired deficiency of the inhibitor of the activated first component of complement was studied. The patient's complement profile revealed depletion of the first component of complement, which has not been seen in angioedema of the hereditary type. There was no evidence for C1-depleting activity in the patient's plasma. The majority of the patient's peripheral blood mononuclear cells resembled B cells in their memebrane receptor properties and in that they carried easily detectable immunoglobulin, predominantly IgM. However, these cells were unusual in that they phagocytosed both latex particles and C3-coated erythrocytes. Morphological study of the cells infiltrating the patient's lung revealed immature, atypical, and plasmacytoid lymphocytes and immunoblasts. Both the patient's peripheral blood mononuclear cells and a suspension of cells from the pulmonary infiltrate were capable of depleting the first component of complement and its inhibitor from homologous plasma. Normal ABO-compatible cells did not possess this property. The data suggested that the patient's abnormal lymphoid cells may have interacted with the complement system to produce a biochemical defect and a clinical syndrome closely resembling angioedema of the hereditary type.

Aged↗
PubMed1975

A scanning electron microscopy and immunological study of 84 cases of lymphocytic leukaemia and related lymphoproliferative disorders.

The surface features of cells from 84 cases of lymphocytic leukaemia, and related lymphoproliferative disorders are described as seen by scanning electron microscopy (SEM). Most of the 46 cases of CLL were shown to be B-derived, but rare cases of mixed B and T cell leukaemia and leukaemia with cells bearing both B and T markers were also encountered. Despite the existence of a spectrum of cell surface morphology, it was possible in many cases to identify a dominant cell type. Cells from cases of B derived malignancies were most frequently of the 'predominantly villous' type while a smaller proportion of cases were of the predominantly 'smoother' or 'mixed villous and smooth' type. Variations in surface morphology also occurred with progression of the disease. In most cases of acute lymphoblastic leukaemia (ALL) 'smoother' cells predominated. However, more cases of ALL and T derived leukaemia need to be examined before definite conclusions can be drawn concerning the surface of these cell types. This study also illustrates the importance of examining large numbers of cases of leukaemia, before conclusions are drawn concerning their surface features and indicates that SEM cannot consistently distinguish between leukaemic B and T cells. It will be of interest to determine whether the surface architecture of the leukaemic cell is related to the degree of cell differentiation and eventual prognosis in these cases.

B-Lymphocytes↗
PubMed1979

alpha-Naphthyl acetate esterase activity--a cytochemical marker for T lymphocytees. Correlation with immunologic studies of normal tissues, lymphocytic leukemias, non-Hodgkin's lymphomas, Hodgkin's disease, and other lymphoproliferative disorders.

Cytochemical identification of T lymphocytes on the basis of alpha-naphthyl acetate esterase (NAE) activity was compared with immunologic markers for cell suspensions and/or cryostat sections of 113 specimens. Nonneoplastic tissues (peripheral blood, lymph nodes, spleens, tonsils, thymus, and pleural fluid) and specimens from various lymphoproliferative disorders, including acute and chronic lymphocytic leukemia, lymphosarcoma cell leukemia, hairy cell leukemia, non-Hodgkin's lymphomas of B-and T-cell types, and Hodgkin's disease, were evaluated. T (E-rosetting) cells demonstrated several patterns of NAE reactivity: 1) a strong globular reaction product, the most specific pattern for T-cell identification, 2) granular cytoplasmic staining, or 3) no reactivity. B lymphocytes revealed a granular pattern of NAE staining, were devoid of enzyme, or, in rare instances, exhibited strong NAE activity. Percentages of lymphoid cells with strong (globular) NAE activity closely paralleled T-cell (E-rosette) values in the majority of cases, with the best correlations observed for peripheral blood studies. However, discordant results were noted for some neoplastic and nonneoplastic tissues, including cases of T-cell lymphoma or leukemia. Markedly discrepant results were noted for thymic lymphocytes, most of which revealed E-rosette formation and weak or absent NAE activity. Lymph nodes involved by Hodgkin's disease demonstrated a heterogeneous pattern of staining in E-rosetting cells and in Reed-Sternberg variants. Cryostat section studies of reactive lymph nodes and nodular lymphomas demonstrated strong NAE staining in lymphoid cells of T-cell (interfollicular, internodular) areas, with little or no positivity in follicles or nodules (B-cell areas). NAE staining patterns further suggested that T cells comprise part of the follicular cuff and possibly represent a minor population of some neoplastic nodules. Although NAE determinations do not represent a consistently reliable alternative to immunologic methods for T-cell identification, this easily applicable cytochemical marker is complementary to other techniques in assessing neoplastic or nonneoplastic tissues, particularly cryostat sections. (Am J Pathol 97:17--42, 1979).

Adult↗
PubMed2026

The role of Epstein-Barr virus in NK/T cell lymphoproliferative disorders: molecular mechanisms and potential therapeutic strategies.

Epstein-Barr virus (EBV) is a widely prevalent lymphotropic γ-herpesvirus, with approximately 95% of the population showing evidence of infection at some point during their lifetime. While most infections are asymptomatic or follow a self-limiting clinical course, in certain populations, EBV can lead to a range of lymphoproliferative disorders (LPDs), particularly subtypes originating from T cells and natural killer (NK) cells, which are often characterized by highly aggressive disease progression. This review aims to systematically discuss the molecular basis of EBV infection, covering its viral biological properties, regulation of the latent and lytic cycles, key viral protein functions (e.g., LMP1, LMP2A, EBNA1), miRNA regulatory mechanisms, and the activation of various host signaling pathways (such as NF-κB, PI3K-AKT, JAK-STAT) that contribute to the maintenance of latent infection, cell transformation, and immune evasion. Additionally, the review focuses on the pathogenic contributions of these mechanisms in EBV-related T/NK cell lymphoproliferative diseases. Research highlights include the in-depth analysis of virus-host genome interaction mechanisms, the identification of novel molecular biomarkers, and the development of targeted therapeutic strategies (e.g., PD-1/PD-L1 immune checkpoint inhibitors, EBV-specific T cell therapy). Through this comprehensive review, it is hoped that personalized medicine and artificial intelligence-assisted multimodal decision-making will be applied to the precise prevention and treatment of EBV-related diseases.

Humans↗
PubMed1978

T-lymphocyte colonies in the lymphoproliferative disorders.

Human lymphocytes from peripheral blood, bone marrow spleen and lymph nodes were cultured. Continuous phytoheamagglutinin (PHA) stimulation was used, first during a 24 h liquid preincubation, then during a 5 day culture in methylcellulose. In normal donors a rapid colony formation took place, with a mean of 124+/-82 colonies per 1 times 10(5) preincubated lymphocytes. Cells from such colonies were studied by cytology, scanning electron microscopy and rosette formation techniques; arguments favour the hypothesis that these could be T lymphocytes. Neither granulocytes nor macrophages could be grown, and no lymphoid colony formation occurred without PHA stimulation. The same technique was applied to patients with various lymphoproliferative disorders. Significant colony suppression was observed in nearly every case of chronic lymphatic leukaemia; the number of colonies was reduced in some patients with acute lymphatic leukaemia, lymphosarcoma, dysglobulinaemia and Hodgkin's disease. This lymphoid culture method should be applied to a larger number of patients to determine whether it has a classification value and/or prognostic significance. When colonies were grown in pathological states, rosette formation was identical to that of normal donors; colony formation could be due to persisting normal lymphocytes.

Adolescent↗
PubMed1976

Immunological characterization of lymphoproliferative disorders by membrane markers.

The characterization of lymphocyte subpopulations by means of surface markers improved our understanding of the immunopathology of lymphoproliferative disorders. In chronic lymphocytic leukemia an accumulation of B-lymphocytes have been documented. The antibody deficiency syndrome in these patients might well reflect a maturation defect of the leukemic B-lymphocytes. In patients with Hodgkin's disease the relative number of B- and T-lymphocytes in the blood was not markedly altered in comparison to normal controls. An increased proliferation primarily of T-lymphocytes however, might suggest their accelerated turnover as an indication of the host response. In most patients with "Non-Hodgkin" lymphomas high numbers of B-lymphocytes were found in affected lymph nodes, and these appear occasionally in the peripheral blood. Differences in immunopathological manifestations of the various subgroups of the "Non-Hodgkin" lymphomas are emphasized and the rare occurrence of lymphomas of T-lymphocytes (mainly observed in lymphoblastic lymphomas and in Sézary syndrome) is discussed. Immunopathological alterations in immunocytomas and the myelomas are considered in respect to the involvement of B-lymphocytes at different stages of maturation.

B-Lymphocytes↗
PubMed1978

Oropharyngeal excretion of Epstein-Barr virus by patients with lymphoproliferative disorders and by recipients of renal homografts.

In an attempt to associate oropharyngeal excretion of Epstein-Barr (EB) virus with lymphoproliferative disorders other than infectious mononucleosis, we tested throat gargles collected from adult subjects for the EB virus. Nine (16%) of 55 healthy persons were positive. High EB virus-excretion rates were found among patients with active acute lymphocytic leukemia (6/6, 100%), among renal homograft recipients during the third to 12th month after transplantation (26/30, 87%), and among critically ill patients with leukemia-lymphoma (14/19, 74%). Moderately high excretion rates were found among patients with myeloma (7/16, 44%), patients with poorly differentiated lymphocytic lymphoma (5/11, 44%), critically ill patients with solid cancers (15/37, 41%), and patients with chronic myelogenous leukemia (8/21, 38%). Our data suggested that the higher than normal excretion rate is realted to the basic disease process and to the general health status but not to the duration of cancer chemotherapy.

Antineoplastic Agents↗
PubMed1975

Serial studies of hepatitis-associated antigen and antibody in patients receiving antitumor chemotherapy for myeloproliferative and lymphoproliferative disorders.

The effects of antitumor chemotherapeutic agents on hepatitis B antigen (HBAg) and antibody (HBAb) were studied serially in 25 patients with myeloproliferative and in 60 patients with lymphoproliferative disorders. HBAg was detected at some time in 17 patients, and HBAb in 40 patients. Seventeen patients who had HBAb detected immediately pretreatment had a decrease in HBAb titer which paralleled the fall in white blood cell count. In 5 of these patients, HBAg appeared when HBAb titers fell. In 3 of the 5 patients, a reappearance of HBAb was observed with disappearance of HBAg from the serum, and in the 2 other patients HBAg persisted once it appeared. In all 3 patients who had HBAg at the time of initiation of chemotherapy, bone marrow suppression was associated with a marked increase in HBAg titer. The increase in HBAg titer was associated with hepatocellular damage, as manifested by an elevation in serum transaminase enzymes. These observations suggest that antitumor chemotherapeutic agents reduce HBAb titers. In some patients, HBAg appears after a decrease in HBAb titers. In patients with preexisting HBAg, such therapy leads to large increases in HBAg titer. Whether this appearance or increase of HBAg is related to an inhibition of antibody formation, allowing expression of preexisting antigen, or to an inhibition of cellular immunity, allowing viral proliferation, is uncertain.

Adolescent↗
PubMed1978

Behçet's disease associated with a lymphoproliferative disorder, mixed cryoglobulinemia, and an immune complex mediated vasculitis.

A woman, now 59 has been followed for 13 years with several manifestations of Behçet's disease. These were aphthous stomatitis, genital ulcers, uveitis causing blindness, recurrent erythema nodosum, and synovitis. In 1970 a poorly differentiated diffuse lymphocytic lymphoma appeared and was treated with radiotherapy. In 1976 she developed a mixed cryoglobulinemia and an immune complex mediated vasculitis manifested by purpura and neuropathy which improved on prednisone and chlorambucil therapy. The subsequent course of her lymphoproliferative disorder suggest that it was in fact benign.

Antigen-Antibody Complex↗