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1/5. Epstein-Barr virus-associated peripheral T-cell lymphoma of activated CD8 phenotype.

    Two childhood cases are reported of peripheral T-cell lymphoma; the neoplastic cells expressed activated CD8 (T8) phenotype and contained Epstein-Barr viral (EBV) dna. Both patients had an aggressive and rapid clinical course despite chemotherapy. Elevated titers of antibodies to EBV-viral capsid antigen (greater than 640) and early antigen (greater than 10) were found in both patients. histology revealed pleomorphic immunoblastic lymphoma with extensive necrosis in one case and an angioimmunoblastic lymphadenopathy-like pattern containing Reed-Sternberg-like giant cells in the other. Southern blot hybridization studies showed clonal rearrangement of the T-cell-receptor beta gene in both cases, and a cytogenetic study on one case revealed clonal structure abnormality involving chromosomes 1, 6, 7, 10, and 19. Analysis of the tumor dna showed a high copy number of EBV genome per cell compared with that of Raji and Marmoset B 95.8 lines; the study for human T-cell leukemia virus type I was negative. The EBV genome was found by in situ hybridization in the tumor nuclei in both cases. In addition to Burkitt's lymphoma, t-cell lymphoma of the helper phenotype, and Hodgkin's disease, EBV can contribute to the development of CD8-positive aggressive T-cell lymphoma.
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2/5. Malignant lymphomas of B-cell lineage with marked tissue eosinophilia. A report of five cases.

    Tissue eosinophilia is commonly seen in Hodgkin's disease and non-Hodgkin's lymphomas of T-cell lineage. In contrast, eosinophilia is infrequent in non-Hodgkin's lymphomas of B-cell origin. We describe five-B-cell lymphomas with exuberant tissue eosinophils. According to the Working Formulation, three were classified as large-cell immunoblastic, one as small lymphocytic lymphoma/chronic lymphocytic leukemia, and one as low-grade, not further subclassified, with features of monocytoid B-cell lymphoma. Immunophenotypic studies in each case revealed B-cell lineage; neoplastic cells expressed monotypic immunoglobulin light chain (four of five cases) or pan-B-cell antigens (five of five cases) and were negative for T-cell antigens. Southern blot hybridization in one case revealed immunoglobulin gene rearrangements, further confirming B-cell lineage. Eosinophilopoiesis is stimulated by interleukin 5 (IL-5), and Epstein-Barr virus (EBV) has been shown to upregulate IL-5 production. Therefore, both EBV infection and IL-5 expression were investigated as possibly pathogenetic mechanisms for the eosinophilia. However, both in situ hybridization studies for EBV mRNA and IL-5 mRNA were negative in the neoplastic cells. In one tumor, IL-5 was abundant in the cytoplasm of the eosinophils, a pattern similar to that seen in five cases of Hodgkin's disease studied with the same technique. Although rare, marked tissue eosinophilia may be associated with B-cell non-Hodgkin's lymphomas. Immunophenotypic or molecular genetic analyses are needed to make the correct diagnosis.
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3/5. Primary Epstein-Barr virus-related non-Hodgkin's lymphoma of the pleural cavity following long-standing tuberculous empyema.

    Primary non-Hodgkin's lymphomas of the pleural cavity have been described mostly in japan. We report a case of high-grade non-Hodgkin's lymphoma (immunoblastic type) of the pleural cavity occurring in a nonimmunocompromised patient 55 years after an artificial pneumothorax was performed for the treatment of pulmonary tuberculosis. Immunohistochemical study revealed a B phenotype (CD20), and an in situ hybridization detected small nuclear RNAs encoded by Epstein-Barr virus in most lymphomatous cells. A link between primary pleural lymphoma and the local long-standing chronic inflammation, inducing a clonal transformation of Epstein-Barr virus-infected immortalized B lymphocytes, is suspected.
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4/5. Non-Hodgkin lymphoma and Kaposi sarcoma in an eyelid of a patient with acquired immunodeficiency syndrome. Multiple viruses in pathogenesis.

    A 36-year-old patient with acquired immunodeficiency syndrome sought care because of an upper eyelid lesion that dramatically increased in size. The histopathologic examination revealed a high-grade diffuse large cell non-Hodgkin lymphoma in continuity with a Kaposi sarcoma. in situ hybridization revealed Epstein-Barr virus in the large cell lymphoma and Kaposi sarcoma-associated herpesvirus in the Kaposi sarcoma lesion. This collision tumor is an unusual presentation of 2 malignant neoplasms in a patient with acquired immunodeficiency syndrome, with in situ hybridization evidence of Epstein-Barr virus and Kaposi sarcoma-associated herpesvirus in the lesion.
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5/5. Follicular large cell lymphoma with immunoblastic features in a child with wiskott-aldrich syndrome: an unusual immunodeficiency-related neoplasm not associated with Epstein-Barr virus.

    patients with wiskott-aldrich syndrome, a severe inherited immunodeficiency disorder, have a markedly increased risk of developing non-Hodgkin's lymphoma compared with the general population. These are uniformly diffuse aggressive B-cell neoplasms that resemble those seen in AIDS and the posttransplantation setting and also may be associated with Epstein-Barr virus. We report what to our knowledge is the first case of follicular lymphoma in a 14-year-old child with wiskott-aldrich syndrome. The neoplasm was composed predominantly of large cells with immunoblastic features, and it possessed light chain-restricted surface immunoglobulin, clonal immunoglobulin gene rearrangements, and a t(14;18). The tumor lacked Epstein-Barr virus sequences by in situ hybridization and Southern blot terminal repeat analysis. Interestingly, however, the tumor contained c-myc gene rearrangement.
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