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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immunohistochemical detection of CD1c antigen is described in mantle zone B-cells of the tonsil, lymph node, and spleen, and also in the marginal zone B-cells of the spleen. CD1c expression was observed in most cases of low-grade, but in only a single case of high-grade, B-cell non-Hodgkin's lymphoma. It was not detected in germinal centre cells, nor in Epstein-Barr virus-transformed or Burkitt's lymphoma B-cell lines. This distribution suggests that CD1c expression may occur preferentially in slowly proliferating B-cell populations and does not support previous suggestions that CD1c is a human equivalent of the mouse thymus leukaemia antigens.
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PMID:CD1c antigens are present in normal and neoplastic B-cells. 326 33

Primary lymphoma of the central nervous system (CNS), including reticulum cell sarcoma, microglioma, and histiocytic lymphoma, represents less than 1% of all primary brain tumors. In the last 10 years, this tumor has tripled in frequency in the nonimmunosuppressed population. By 1991, the tumor will be the most common neurological neoplasm by virtue of the increase in sporadic occurrence and in the acquired immunodeficiency syndrome (AIDS) population. Three percent of AIDS patients will develop this tumor either prior to AIDS diagnosis or during their subsequent course. In addition to acquired immunosuppression, patients with inherited disorders (such as Wiskott-Aldrich syndrome, severe combined immunodeficiency, and X-linked immunodeficiency) and other acquired disorders of the immune system are predisposed to the development of CNS lymphoma. Immunological studies have suggested a role for Epstein-Barr virus in the production of this tumor. Although subtypes exist, non-Hodgkin's lymphoma of the CNS most commonly consists of histiocytic cells or large immunoblastic cells bearing B cell surface markers in close proximity to the lateral and third ventricles. Sixty percent of these deposits are multiple, and subarachnoid invasion is seen in one-quarter of patients. Vitreous involvement of the eye occurring prior to and during the course of CNS lymphoma has been noted in up to 25% of patients. The involvement of multiple areas of the neuraxis, the eye, and multiple intracranial sites often occurs in the absence of obvious systemic lymphoma. Therapeutic trials of brain radiation therapy are associated with median survivals of less than 1 year. Uniform complete responses of intracranial deposits are recorded following chemotherapy with high-dose intravenous methotrexate, CHOP (cyclophosphamide, hydroxydaunomycin/doxorubicin, Oncovin (vincristine), and prednisone), high-dose cytosine arabinoside, and intra-arterial methotrexate with barrier modification.
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PMID:Primary central nervous system lymphoma. 328 32

The spectrum of neoplastic disease seen in patients with the acquired immune deficiency syndrome (AIDS) is similar to that seen in several congenital and iatrogenic immunodeficiency states and provides a human model for studying neoplastic transformation in the immune compromised host. High grade lymphoid neoplasia, particularly of the central nervous system (CNS), as well as a virulent form of Kaposi's sarcoma (KS) and several types of squamous cell carcinomas, are appearing at an alarming rate in patients with AIDS. There is substantial serologic, pathologic and molecular evidence linking cytomegalovirus (CMV) to KS and Epstein-Barr virus (EBV) to squamous cell carcinoma and high-grade B-cell non-Hodgkin's lymphoma (NHL). The human T-cell lymphotropic virus type III/lymphadenopathy associated virus (HTLV-III/LAV) may be responsible for the permissive immune deficient state allowing for opportunistic neoplasia and the aggressive biologic behavior and atypical anatomic distribution these neoplasms exhibit. The clinical features as well as potential etiopathogenetic mechanisms of these malignancies are reviewed.
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PMID:Cancers-associated with HIV infection. 332 37

Hodgkin's disease was found in five members of the same generation in a large Swiss family. At presentation, the patients were between 20 and 30 years old. The histological diagnosis was confirmed in three patients. In one woman the differential diagnosis of histiocytic non-Hodgkin's lymphoma was considered. The patient history did not provide any conclusive evidence for environmental factors shared by all patients. Three siblings had grown up in the same household. They had never been in contact with the other pair of affected sisters. No clustering of cases in time occurred, as individual cases were diagnosed at least two years apart. Antibodies against Epstein-Barr viral capsid antigen were found in four patients (IgG: 1:10 to 1:160). There was no single HLA-haplotype common to all patients. However, two affected sisters were HLA-identical (paternal haplotype: Aw24(9), Bw62(15), DRw6; and maternal haplotype: A2, B7, DR2). Their brother with Hodgkin's disease was homozygous for A-, B- and DR-antigens. He shared all these antigens with his two affected sisters (A2, Bw62(15), DR2). A genetic predisposition in combination with environmental factors, in particular subclinical Epstein-Barr virus infection, may have been responsible for the development of Hodgkin's disease in this family.
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PMID:[Hodgkin's disease in a Swiss family]. 358 32

Three sisters developed non-Hodgkin's lymphoma (NHL). Thirteen maternal relatives had adenocarcinomas of various types, predominantly breast and large bowel. Detailed laboratory assessment of this family revealed a variety of immunologic abnormalities. Two lymphoma patients had elevated anti-early antigens (EA) Epstein-Barr virus (EBV) titers. One of the two also had a markedly elevated anti-viral capsid antigen (VCA) EBV titer. The two lymphoma patients were human leukocyte antigen (HLA)-identical, but two unaffected siblings shared the same HLA haplotypes. One of the lymphoma patients and four unaffected family members were anergic; and three unaffected family members had a decreased percentage of T-cells. These data suggest that a subtle disturbance in cellular immune functions may play a causal role in some familial aggregations of malignant lymphoma.
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PMID:Clinical and laboratory observations in a lymphoma-prone family. 359 4

Lymph-node and tonsillar biopsies occasionally are obtained from patients with the infectious mononucleosis syndrome secondary to Epstein-Barr viral infection, particularly if the clinical presentation is atypical and a viral etiology is not suspected. The presence of Reed-Sternberg-like cells in infectious mononucleosis resulting in confusion with Hodgkin's disease is well-known; however, similar difficulty in excluding a non-Hodgkin's lymphoma can be encountered. Eleven cases of reactive lymphoid hyperplasia with the morphologic features of infectious mononucleosis are reported, nine of which had documented Epstein-Barr viral infection. The spectrum of morphologic changes associated with Epstein-Barr viral infection is discussed, with emphasis on the features that permit their distinction from non-Hodgkin's lymphoma. Morphologic features mimicking lymphoma included extensive immunoblastic proliferations in sheets and nodules and marked cytologic atypia. Hodgkin's disease was simulated by the tendency in some cases for the atypical Reed-Sternberg-like cells to cluster about necrotic foci and to show pronounced cytologic atypia. Features permitting the distinction from non-Hodgkin's lymphoma included persistent reactive foci with the classic features of infectious mononucleosis, a polymorphous background of transformed lymphocytes rather than irregular or twisted lymphoid cells as seen in non-Hodgkin's lymphoma, and preservation of underlying reticulin architecture rather than destruction, even in cases with extensive immunoblastic proliferation. Hodgkin's disease was excluded by requiring strict criteria for Reed-Sternberg cells and noting the reactive background as inconsistent with Hodgkin's disease. Immunoperoxidase staining of seven of the cases with anti-Leu-M1 failed to demonstrate immunoreactivity of the Reed-Sternberg-like cells with this monoclonal antibody.
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PMID:Infectious mononucleosis. The spectrum of morphologic changes simulating lymphoma in lymph nodes and tonsils. 381 72

The designation Burkitt's lymphoma (BL) has proved to be of great convenience but has left undetermined the histogenesis of the tumour and its relationship to other B-cell lymphomas. One definition proposed for BL has been based on its relationship to Epstein-Barr virus (EBV). The EBV negativity of some BLs and the association of EBV with other non-Hodgkin's lymphoma, however, makes this definition unsatisfactory. Cytogenetic changes involving the translocations of part of chromosome 8 also are not specific for BL. In the Kiel classification, BL appears as a lymphoblastic lymphoma. However, lymphoblastic lymphomas and leukaemias arise from pre-B and early T cells, whereas BL shows characteristics of a more mature B cell. Mann et al. (1976) considered BL to be related to follicle centre-cell lymphomas. The morphology and immunological phenotype of BL are consistent with this hypothesis, although it would appear that BL is more restricted in its capabilities of further differentiation than other follicle centre-cell lymphomas. This lack of differentiation may be related to EBV infection. The characteristic anatomical distribution of BL is quite unlike that of most follicle centre-cell lymphomas and should be considered in the search for its histogenesis. BL involves the jaws during the period of maximum dental development, and also the salivary glands, thyroid, abdominal viscera and abdominal lymph nodes. Massive involvement of the breasts during pregnancy and lactation is characteristic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histogenesis of Burkitt's lymphoma: a B-cell tumour of mucosa-associated lymphoid tissue. 387 85

The acquired immunodeficiency syndrome (AIDS) occurs in a subgroup of male homosexuals having sexual contact with a large number of partners. Uncommonly, AIDS has also been diagnosed in Haitians, hemophiliacs, and intravenous drug users and their infants. Manifestations include autoimmune disturbances, opportunistic infections, Kaposi's sarcoma, chronic lymphadenomegaly, non-Hodgkin's lymphoma, or squamous cell carcinoma. The hypothesis receiving most consideration is that a yet-to-be-identified virus causes AIDS. An alternative view is that repeated sexual involvement with multiple partners, in a subgroup of male homosexuals, exposes the men to the immunosuppressive impact of cytomegalovirus (CMV) and allogeneic semen. Antibody to asialo-Gm1 and other antigens on sperm react with and impair lymphoid cells. We propose a biphasic process. First, a reversible acquisition phase of impaired T-cell immunoregulation permits reactivation of Epstein-Barr virus (EBV), and autoantibodies are produced by the activated B cells. If sexual activity continues at a high level, accumulating immune defects, including destruction of thymic epithelium, lead to a second, self-sustaining phase wherein cytotoxic lymphocytes fail to eliminate herpesvirus-infected cells. Evidence is mounting that Kaposi's sarcoma is caused by CMV and that EBV is responsible for the B-cell lymphomas in these patients. Multiple factors, rather than a novel virus, probably induce AIDS in male homosexuals. If this hypothesis is correct, then rational bases for prevention and intervention can be designed.
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PMID:Acquired immunodeficiency syndrome, opportunistic infections, and malignancies in male homosexuals. A hypothesis of etiologic factors in pathogenesis. 630 Apr 80

We have studied nine Hodgkin's lymphoma (HD) and ten non-Hodgkin's lymphoma (NHL) patients with extraordinarily high anti-viral capsid antigen (VCA) titers (greater than 5120). Controls were 13 HD and 23 NHL patients with anti-VCA titers between 40 and 2560. High anti-VCA titers were present in NHL patients at the time of diagnosis or within 16 months, whereas the rise of anti-VCA titers in HD patients appeared to be a late event during the clinical course of the disease (mean time from diagnosis, 68 months). In particular, we have asked whether the exceptionally high anti-Epstein-Barr virus (EBV) titers in some HD and NHL patients can be correlated to some of the EBV-specific and -nonspecific parameters of cell-mediated immunity. The battery of non-EBV-specific immunological tests included the assessment of natural killer cell activity and the analysis of T-lymphocyte subclasses according to surface markers, together with spontaneous and mitogen-induced DNA synthesis and their helper or suppressor activity on PWM-generated immunoglobulin synthesis. Outgrowth inhibition (Ol) and leukocyte migration inhibition were used to assess EBV-specific cell-mediated immunity. The majority of the high-titer HD and NHL patients showed a drastically reduced OKT4:OKT8 ratio in their peripheral lymphocyte population. Low-titer HD and NHL patients showed no such reduction. There was no strict correlation between the number of OKT8-positive cells and suppressor activity in the functional PWM-induced immunoglobulin production test. Part of the high-titer HD patients showed defective cellular responses in the outgrowth inhibition test, directed against the proliferation of EBV-transformed (EBV-determined nuclear antigen-positive) cells. Some of them showed also a deficient leukocyte migration inhibition response to EBV-determined nuclear antigen but, interestingly, not to early antigen-VCA. In the NHL group, only one of the high-titer patients showed a similar defect. None of the low-titer HD and NHL patients showed such defects.
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PMID:Immunological characterization of Hodgkin's and non-Hodgkin's lymphoma patients with high antibody titers against Epstein-Barr virus-associated antigens. 631 84

This paper describes the course of a patient with treated non-Hodgkin's lymphoma, which originally presented as a large nasopharyngeal mass. The tumor, though irradiated, recurred on two separate occasions in the right and left inguinal regions. At the time of tumor recurrence, markers were present which have been associated with past or recurrent Epstein-Barr virus (EBV) infection, namely, antibodies to the EBV viral capsid antigen (VCA) and the Epstein-Barr nuclear antigen (EBNA). EBNA was detected in approximately 10% of the neoplastic cells. An unusual immunoglobulin heavy and light chain switch within the tumor cells of the two separate inguinal node tumor recurrences was also observed. Whether EBV plays a role in the pathogenesis of lymphomas remains unclear.
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PMID:Epstein--Barr virus nuclear antigen in a non-Hodgkin's lymphoma. 632 37


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