Cases reported "Lymphoma"

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1/8. Characterization of Epstein-Barr virus (EBV)-infected natural killer (NK) cell proliferation in patients with severe mosquito allergy; establishment of an IL-2-dependent NK-like cell line.

    The clinical evidence of a relationship between severe hypersensitivity to mosquito bite (HMB) and clonal expansion of EBV-infected NK cells has been accumulated. In order to clarify the mechanism of EBV-induced NK cell proliferation and its relationship with high incidence of leukaemias or lymphomas in HMB patients, we studied clonally expanded NK cells from three HMB patients and succeeded in establishing an EBV-infected NK-like cell line designated KAI3. immunoblotting and reverse transcriptase-polymerase chain reaction (RT-PCR) analyses revealed that KAI3 cells as well as infected NK cells exhibited an EBV latent infection type II, where EBV gene expression was limited to EBNA 1 and LMP1. As KAI3 was established by culture with IL-2, IL-2 responsiveness of peripheral blood NK cells from patients was examined. The results represented markedly augmented IL-2-induced IL-2R alpha expression in NK cells. This characteristic property may contribute to the persistent expansion of infected NK cells. However, KAI3 cells as well as the NK cells from patients were not protected from apoptosis induced by either an anti-Fas antibody or NK-sensitive k562 cells. Preserved sensitivity to apoptosis might explain the relatively regulated NK cell numbers in the peripheral blood of the patients. To our knowledge, KAI3 is the first reported NK-like cell line established from patients of severe chronic active EBV infection (SCAEBV) before the onset of leukaemias or lymphomas. KAI3 cells will contribute to the study of EBV persistency in the NK cell environment and its relationship with high incidence of leukaemias or lymphomas in HMB patients.
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2/8. Digital ulcers and necroses: novel manifestations of angiocentric lymphoma.

    We describe a patient with angiocentric lymphoma whose presenting features were multiple areas of digital ulceration and necrosis, including deep ulcers on both great toes. He lacked the lateral halves of both earlobes because of multiple ulcers. skin biopsy revealed a patchy and diffuse infiltrate of lymphoid cells with nuclear atypia in the dermis and subcutaneous tissue. Angiocentric and angiodestructive features of the lymphoid cells, a prominent histiocytic infiltrate and some epithelioid cell granulomas were found. The results of immunohistochemical staining showed a T-cell phenotype, and showed positive staining for apoptosis. He died in July 1999. Peripheral vascular disturbances including Raynaud's phenomenon, digital skin ulcers and necroses are novel clinical symptoms in patients with angiocentric lymphoma, which should be added to the differential diagnosis in patients with peripheral vascular disturbances.
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3/8. The development of lymphomas in families with autoimmune lymphoproliferative syndrome with germline Fas mutations and defective lymphocyte apoptosis.

    Lymphomas were studied in kindreds with autoimmune lymphoproliferative syndrome (ALPS; Canale-Smith syndrome), a disorder of lymphocyte homeostasis usually associated with germline Fas mutations. Fas (CD95/APO-1) is a cell surface receptor that initiates programmed cell death, or apoptosis, of activated lymphocytes. lymphoma phenotype was determined by immunohistochemistry, frequency of CD3( )CD4(-)CD8(-) T-cell-receptor alpha/beta cells by flow cytometry, nucleotide sequences of the gene encoding Fas (APT1, TNFRSF6), and the percentage of lymphocytes undergoing apoptosis in vitro. Of 223 members of 39 families, 130 individuals possessed heterozygous germline Fas mutations. Eleven B-cell and T-cell lymphomas of diverse types developed in 10 individuals with mutations in 8 families, up to 48 years after lymphoproliferation was first documented. Their risk of non-Hodgkin and Hodgkin lymphomas, respectively, was 14 and 51 times greater than expected (each P <.001). Investigation of these 10 patients and their relatives with Fas mutations revealed that all had defective lymphocyte apoptosis and most had other features of ALPS. The tumor cells retained the heterozygous Fas mutations found in the peripheral blood and manifested defective Fas-mediated killing. These data implicate a role for Fas-mediated apoptosis in preventing B-cell and T-cell lymphomas. Inherited defects in receptor-mediated lymphocyte apoptosis represent a newly appreciated risk factor for lymphomas.
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4/8. Marked elevation of soluble fas ligand and cytokine secretion after splenectomy in aggressive natural killer cell leukemia/lymphoma.

    We report a case of Epstein-Barr virus-associated aggressive natural killer cell leukemia/lymphoma with giant splenomegaly in which splenectomy resulted in progression of apoptosis and hemophagocytosis. The serum level of ferritin, triglycerides, interferon-gamma (IFN-gamma), interleukin 10 (IL-10), and soluble Fas ligand (sFasL) increased markedly, and liver damage progressed after splenectomy. The number of apoptotic cells in peripheral blood smears increased following splenectomy. In the present case, splenectomy caused disruption of the cytokine network, resulting in apoptosis of blood cells and hepatocytes, as well as phagocytosis.
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5/8. Fluorodeoxyglucose positron emission tomography (FDG-PET) for monitoring lymphadenopathy in the autoimmune lymphoproliferative syndrome (ALPS).

    autoimmune lymphoproliferative syndrome (ALPS) is associated with mutations that impair the activity of lymphocyte apoptosis proteins, leading to chronic lymphadenopathy, hepatosplenomegaly, autoimmunity, and an increased risk of lymphoma. We investigated the utility of fluorodeoxyglucose positron emission tomography (FDG-PET) in discriminating benign from malignant lymphadenopathy in ALPS. We report that FDG avidity of benign lymph nodes in ALPS can be high and, hence, by itself does not imply presence of lymphoma; but FDG-PET can help guide the decision for selecting which of many enlarged nodes in ALPS patients to biopsy when lymphoma is suspected.
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6/8. Fas ligand-mediated lethal hepatitis after rapid lysis of a localized natural killer cell lymphoma.

    Natural killer (NK) cell malignancies have been associated with neutropenia and disturbances of liver function tests, thought to be related to high levels of soluble Fas ligand (FasL) in the circulation. We report a case of fulminant hepatitis occurring 3 weeks after the initiation of salvage therapy by arginine butyrate and ganciclovir for refractory Epstein-Barr virus-positive NK cell lymphoma. Pathologic examination revealed disappearance of the NK tumor and massive liver injury caused by apoptosis of virtually all hepatocytes. immunohistochemistry revealed an intense staining for FasL. To our knowledge, this is the first description of the occurrence of FasL-mediated lethal hepatitis after lysis of a NK cell lymphoma.
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7/8. Malignant lymphoma arising from natural killer cells: report of the first case in 1970 and newer developments in the FasL-->FasR system.

    In 1970 at the University of texas MD Anderson Hospital, Houston TX, we attended a patient with malignant lymphoma and "lymphosarcoma cell leukaemia". The malignant cells were large with fine granular cytoplasm. The patient was febrile without positive cultures and exhibited wasting resembling "graft-vs-host" disease. Both his lymphoma cells collected from the blood, and his serum, exerted strong cytotoxicity toward a battery of human tumour cell lines established in culture. We reported him as the first case of a new entity; "cytotoxic lymphoma". Later, elsewhere, natural killer (NK) cells were characterized, and cases of malignant lymphomas arising from large granular lymphocytes were described, as those of NK cells. Malignant NK cells constitutively express Fas ligand (L), both membrane-bound (m) and soluble (s). Upon binding FasL Fas receptor (R)-positive hosts cells succumb to apoptotic death. patients with FasL-producer lymphoma cells suffer from anaemia, neutropenia, hepatotoxicity and autoimmunity. The FasL-->FasR system regulates normal lymphocyte homeostasis. This system is used by the placental trophoblast against maternal lymphocytes; by transplants against host lymphocytes; and by donor lymphocytes exerting graft-vs-host-reaction. In tumour immunology, FasR tumour cells can be killed by FasL lymphocytes and, vice versa, FasL tumour cells can induce apoptotic death of FasR host lymphocytes ("counterattack on lymphocytes"). Some tumour cells co-express FasL, FasR and bcl-2 and not only escape programmed cell death but also utilize the FasL-->FasR system as an autocrine growth loop ("counterattack on apoptosis").
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8/8. Expression of cytotoxic molecule TIA-1 in malignant lymphomas mimicking fulminant hepatitis.

    Involvement of malignant lymphoma in the liver inducing fulminant hepatic failure has rarely been reported. Therefore, a close association between some lymphoma types with severe liver damage and the mechanism underlying the liver damage is intriguing. Three malignant lymphoma cases, which were clinically diagnosed as fulminant hepatitis, were collected from the autopsy records of Kawasaki Medical School (Kurashiki, japan). All three cases were characterized by the presence of hepatosplenomegaly without superficial lymph node swelling, high elevation of transaminase and lactate dehydrogenase (LDH; especially LDH-2), and a quite aggressive clinical course. Immunohistochemically, the tumor cells in all three cases were positive for T cell intracellular antigen (TIA-1), which is a cytolytic protein in cytotoxic T and natural killer (NK) cells. The lymphomas were CD8 peripheral T cell lymphoma (case 1), CD56 T/NK cell lymphoma (case 2), and T cell lymphoma in a patient with mosquito hypersensitivity (case 3). Epstein-Barr virus infection was demonstrated on the tumor cells of cases 2 and 3 using an in situ hybridization method and those cases showed high titers of serum interferon-gamma and Fas. Frequent apoptosis of liver cells, where the lymphoma cells had infiltrated, was revealed by a terminal deoxyribosyl transferase-mediated deoxyuridine nick end-labeling (TUNEL) method. The findings in this study suggest that fulminant hepatic injury is closely associated with cytotoxic molecule TIA-1 expression of the lymphoma cells and that some specific mechanism may be involved in liver damage.
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