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11/16. Characterization of a novel HTLV-infected cell line.

    A man from chile developed an aggressive mature T cell leukemia associated with marked eosinophilia. The neoplastic lymphocytes were of T helper surface phenotype, and they expressed the p24 and p19 antigens of human T cell leukemia virus (HTLV). A cell line (ME) was established from the patient's peripheral blood cells that was initially composed of eosinophils and T and B lymphocytes. The B lymphocytes of the cell line are polyclonal and contain Epstein-Barr virus (EBV) dna. Many of the T lymphocytes, a few of the B lymphocytes, and none of the eosinophils express HTLV p19 and p24 antigens. By 6 months of culture, the ME line no longer contained eosinophils. A variant line of ME was established; this variant (ME-2) is notable because the cells (greater than 80%) adhere tightly to the bottom of the culture flask; they do not express T lymphocyte markers, but 30% of the cells contain cytoplasmic mu heavy immunoglobulin chains. These pre-B and null lymphocytes contain p19 and p24 antigens (80% of cells), have the HTLV-I genome, and are able to transform normal T lymphocytes in vitro. We isolated a B lymphocyte clone (11A) from ME that expresses cytoplasmic immunoglobulin (70% of cells) and p19 and p24 antigens (75% of cells), contains the EBV and HTLV genomes, and can transform T lymphocytes from normal volunteers. These data show that B lymphocytes can be infected with HTLV, although no disease of HTLV-infected B lymphocytes has been reported. The T lymphocytes from normal adult peripheral blood were easily immortalized (about 70% efficiency) by cocultivation with lethally irradiated ME cells. Twenty-five of 27 of the transformant lines were composed of T lymphocytes with helper antigens, and two of the lines were of T suppressor antigen phenotype. All the cell lines that were tested constitutively produce lymphokines, including colony-stimulating factor (CSF), erythroid-potentiating activity (EPA), macrophage migration-inhibitory factory (MIF), neutrophil-inhibitory factor (NIF), and differentiation-inducing factor (DIF).
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keywords = leukemia
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12/16. Parosteal lymphoblastic lymphoma. A human counterpart of Abelson virus-induced lymphosarcoma of mice.

    A 16-year-old girl with an unusual presentation of lymphoblastic lymphoma is described. The tumor originated as a paraspinal mass accompanied by lytic bone lesions in the pelvic bones. Neither an anterior mediastinal mass nor lymphadenopathy were noted. This pattern of disease is strikingly reminiscent of lymphomas induced in mice by the Abelson leukemia virus. This patient's lymphoma cells, unlike the usual lymphoblastic lymphoma cells, did not bear classical T-lymphocyte surface markers. A permanent cell line was derived from her tumor. Sparse amounts of cytoplasmic mu-immunoglobulin heavy chains were present in most of these cells, suggesting that the tumor originated in pre-b-lymphocytes. The phenotype of the cultured tumor cells is similar to Abelson virus-transformed murine bone marrow cells. Tumor cells of this phenotype may originate in the bone marrow and spread subsequently in and around the involved bones. This pattern of disease is distinctly different from that of T-cell lymphoblastic lymphoma, which typically presents in the mediastinum and cervical lymph nodes, and involves the bone marrow only as a late manifestation of advanced disease.
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keywords = leukemia
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13/16. philadelphia chromosome as the sole abnormality and p210 bcr-abl chimeric protein expression in an Epstein-Barr virus-transformed B cell line from a patient with chronic myeloid leukemia.

    A 'B' cell line, originating from a patient with chronic myeloid leukemia and containing the philadelphia chromosome, was established after Epstein-Barr virus transformation. The philadelphia chromosome was the sole chromosomal abnormality in this line, designated as PhB1 cell line. In dna hybridization studies we detected rearrangements in the bcr gene and in the immunoglobulin heavy chain joining region. The phenotypes of the cells were typical of mature B cells expressing antigens CD19, CD20, CD22, CD23, CD39, HLADR, IgM, and kappa. The expression of the 210 bcr-abl chimeric protein was detected by means of an immunoprecipitate assay.
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ranking = 2.8013302893357
keywords = leukemia, myeloid leukemia
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14/16. Richter's transformation of chronic lymphocytic leukemia with Hodgkin's-like cells is associated with Epstein-Barr virus infection.

    The appearance of a high-grade lymphoma in the setting of B-cell chronic lymphocytic leukemia (CLL) is termed Richter's syndrome. Usually the high-grade component is a monomorphous, large cell lymphoma, but occasionally the high-grade component takes the form of Hodgkin's disease or a Hodgkin's-like lymphoma. Although Richter's syndrome is thought to represent clonal evolution of the underlying B-cell neoplasm in most cases, such a progression is difficult to explain when the high-grade component is Hodgkin's disease. We report two cases of Richter's syndrome in which the large cells had a morphology consistent with reed-sternberg cells and were found in a background of CLL. The large cells in both cases expressed the CD15 and CD30 antigens in a pattern characteristic of reed-sternberg cells, and the large cells in one case also expressed monotypic cytoplasmic immunoglobulin of the same type as that expressed by the underlying CLL. In both cases, Southern blot analysis of dna from lymph nodes that contained both CLL and the Hodgkin's-like component showed single immunoglobulin gene rearrangements. Using the polymerase chain reaction, we found Epstein-Barr virus dna in lymph nodes from both cases, and in peripheral blood lymphoid cells from one case 4 yr before the onset of Richter's syndrome. Immunoperoxidase staining showed expression of EBV latent membrane protein only in the Reed-Sternberg-like cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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ranking = 2.5
keywords = leukemia
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15/16. Simultaneous progressive multifocal leukoencephalopathy, Epstein-Barr virus (EBV) latent infection and cerebral parenchymal infiltration during chronic lymphocytic leukemia.

    We report a non-hiv patient who had B chronic lymphocytic leukemia (CLL) with progressive multifocal leukoencephalopathy (PML) and diffuse cerebral leukemic parenchymal infiltration in the presence of jc virus and Epstein-Barr virus (EBV) cerebral co-infection. Multiple subcortical hypodensities lining the cortico-subcortical junction were present within the white matter on computerized tomography (CT) scan, with large areas of high signal intensity on T2-weighted sequences on magnetic resonance imaging (MRI). JCV dna was identified in peripheral blood nuclear cells and cerebrospinal fluid polymerase chain reaction (PCR) dna/dna hybridization plus Southern blot analysis. Frontal stereotactic biopsy confirmed the diagnosis of PML by immunocytochemistry, in situ hybridization (ISH) with JC Enzo probe and electron microscopy. Leukemic B cells with the same phenotype as leukemic blood cells were disseminated in the demyelinated areas. They were labeled by anti-latent membrane protein and by BamHl W EBV probe after ISH. Adhesion and activation molecules were positive for CD23. autopsy showed diffuse visceral leukemic infiltration without acutization. EBV-transformed B lymphocytes would favour JCV penetration and/or intracerebral reactivation of previously latent JCV infection with further development of simultaneous PML and cerebral CLL infiltration in an immunosuppressed patient.
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keywords = leukemia
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16/16. Simian T cell leukemia virus type I-induced malignant adult T cell leukemia-like disease in a naturally infected African green monkey: implication of CD8 T cell leukemia.

    Spontaneous T cell leukemia was found in an African green monkey (cercopithecus aethiops, AGM) naturally infected with simian T cell leukemia virus type I (STLV-I). The hematological features and the evidence for monoclonal integration of provirus dna in the leukemic cells revealed that the leukemia was an ATL-like disease. The expression of surface markers on the leukemic cells indicated that they were defined as an activated CD8 T cell subset. Together with the finding that seven in vitro spontaneously STLV-I-transformed cell lines were CD4-CD8 , it is likely that CD8 T cells are transformed by STLV-I in AGMs, in contrast with human ATL. Finally, we assessed characteristics of the CD8 chains on these transformed cells. The result indicated that the leukemic cells expressed only the alpha chains but not the beta chains. However, in the case of in vitro-transformed cell lines the expression pattern of the CD8 chains varied in individual monkeys. Thus, STLV-I may preferentially transform CD8 (both alphaalpha and alphabeta ) T cells in AGMs.
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ranking = 7.5
keywords = leukemia
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