Gene/Protein Disease Symptom Drug Enzyme Compound
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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)

HIV-1-related neurological diseases, excluding opportunistic infections and HIV encephalitis, are considered here. Most occur in severely immunosuppressed patients, with CD4 counts of under 200 x 10(6) l-1. Primary brain lymphoma and metastases from systemic non-Hodgkin's lymphoma, the second commonest cause of cerebral mass lesions in AIDS, are usually aggressive B cell tumours. Their poor median survival after treatment, compared with that of lymphomas in non-AIDS patients, seems related to systemic complications, particularly opportunistic infections. Kaposi's sarcoma produces neurological symptoms exceptionally. Cerebral infarction is often unrecognized clinically but large vessel arteritic occlusions may occur. Intracranial haemorrhages occur mostly in thrombocytopenic patients. Seizures are frequently referred to the neurologist; investigation may lead to a diagnosis of AIDS. Nearly 50% of patients with seizures have cerebral toxoplasmosis or cryptococcal meningitis; HIV-1 encephalitis is presumed to be the cause in 30%. A subacute or chronic vacuolar myelopathy with pyramidal and posterior column signs is the commonest form of spinal cord involvement in AIDS; its cause remains unknown. Peripheral nerve syndromes occur at all stages of HIV-1 infection. Distal symmetrical peripheral neuropathies are the most frequent, particularly a painful form with axonal atrophy, associated with CMV infection, and seen during ARC or AIDS. Mononeuritis multiplex due to vasculitis, CMV, or lymphoma and a serious lumbosacral polyradiculopathy due to CMV are infrequent. The commonest myopathy is due to zidovudine (AZT); it usually responds to drug withdrawal. The nature, prognosis and optimal management of most other myopathies is yet to be determined.
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PMID:Other neurological diseases in HIV-1 infection: clinical aspects. 134 49

In this series of 426 consecutively ascertained, karyotypically abnormal non-Hodgkin's lymphomas (NHLs) derived from 407 patients, a t(9;14)(p13;q32) was encountered in 7 cases; an additional case demonstrated t(9;14)(p1?3;q32). At the time of detection of t(9;14), four cases were small lymphocytic lymphomas with plasmacytoid features; in three of these the t(9;14) was the sole karyotypic abnormality. In two cases of large-cell NHL demonstrating t(9;14), retrospective review of prior lymph node biopsies showed the presence of a small lymphocytic lymphoma of the plasmacytoid subtype. The remaining two cases comprised a large-cell lymphoma of the brain and a follicular NHL. Thus, six of eight cases (75%) had an initial identical low-grade histology. Immunohistochemical analysis of six cases showed no reactivity with CD1, CD2, CD4, CD5, CD8, and CD10 and high reactivity with CD19 and CD20. All four lymphocytic lymphomas and one of the two large-cell NHLs showed cytoplasmic Ig, consistent with plasmacytoid differentiation. Of the eight cases in this series, six presented with or developed stage IV disease; all were characterized by a 6-month to 5-year clinical phase of indolent disease before treatment was instituted. All five patients with low-grade NHL at the time of cytogenetic analysis were alive with recurrent disease at 3-year median follow-up. The remaining three patients with large-cell diffuse histologies relapsed after intensive therapy and expired at a median of 3 years from diagnosis; two of these showed previous or metachronous small lymphocytic tumors. These results suggest a novel biologically distinct subset of NHL; a neoplasm of mature B lymphocytes with plasmacytoid differentiation, characterized by t(9;14); and an indolent presentation followed by gradual clinical progression of disease.
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PMID:t(9;14)(p13;q32) denotes a subset of low-grade non-Hodgkin's lymphoma with plasmacytoid differentiation. 138 92

Approximately 3% of acquired immunodeficiency syndrome cases present with non-Hodgkin's lymphoma. By 6 to 8 years after human immunodeficiency virus infection, lymphoma risk is elevated 100-fold, and the risk approaches 1% per year following acquired immunodeficiency syndrome diagnosis. The proportions presenting as lymphoma differ by age, sex, and race, with relative rates being higher in older persons, males, and whites. The differences are similar in magnitude and direction to those seen in non-human immunodeficiency virus-infected persons and account for the variation by risk group. The relative risk of high-grade lymphoma is greatest, but significant increases are also seen for some intermediate-grade tumors. At diagnosis, persons with Burkitt's lymphoma, more common in children, have significantly higher average CD4 counts than those with immunoblastic tumors. Human immunodeficiency virus-associated lymphoma risk is probably related to dysregulation of the immune system leading to uncontrolled proliferation of transformed cell clones and subsequent genetic accidents. Environmental factors are unlikely to be important. By 1994, 10% of all lymphomas will be human immunodeficiency virus related, but this proportion will increase in the future. New approaches to the therapy of lymphoma are needed for this tumor, which we can neither prevent nor adequately treat.
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PMID:The epidemiology of acquired immunodeficiency syndrome-related lymphomas. 145 3

As patients with human immunodeficiency virus infection live longer because of better antiretroviral therapy and infection prophylaxis, the incidence of non-Hodgkin's lymphoma has increased. The risk increases inversely with CD4 count--the most widely used surrogate marker for progressive immune suppression. Zidovudine itself does not appear to be a risk factor. Patients frequently present with extranodal advanced disease. The central nervous system is the primary site in 10% to 20% of cases. Important prognostic factors are performance status, a prior history of acquired immunodeficiency syndrome, and bone marrow involvement. Therapy is complicated by underlying immunosuppression, opportunistic infection, and poor bone marrow reserve. Progress has been made using colony-stimulating factors and less intensive chemotherapy regimens in systemic non-Hodgkin's lymphoma. Treatment of primary central nervous system lymphoma with radiation therapy has not improved survival.
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PMID:Clinical aspects of human immunodeficiency virus-related lymphoma. 145 4

Little is known about the role of tumor infiltrating T lymphocytes (TIL-T) in the pathogenesis of malignant diseases and collaboration between normal and malignant cells has not yet been proved. In the present work, we have investigated whether immune T lymphocytes exist in tumors invaded by B-cell non-Hodgkin's lymphoma (NHL) or Hodgkin's disease (HD). Therefore, we have studied the reactivity of the CD45RA monoclonal antibody, which discriminates between naive and memory CD4 T lymphocytes. Our results showed far lower percentages of CD4+ CD45RA+ in malignant lymphoma (30.3 +/- 15.0% in B-cell NHL, and 37.4 +/- 18.6% in HD) than in reactive hyperplasia (54.7 +/- 13.2%), leading to the conclusion of an accumulation of immune cells in tumor microenvironment. A further heterogeneity in the relative proportion of naive and memory TIL-T was also observed within lymphoma (range: 11 to 68% in B-cell NHL, 5 to 69% in HD). In B-cell NHL, it was related to histological features, as documented by the Kiel classification (P = .028), and to a stronger extent to cytological characteristics analysed with the Grenoble classification (P less than .0001): class 1 NHL, which are essentially indolent NHL displayed lower naive cells (22.2 +/- 7.4%) than class 3 NHL, which are more aggressive (40.1 +/- 16.1%). Among the monoclonal antibodies (mAb) defining the B-cell clone phenotype or activation state (CD19, CD20, CD21, CD22, CD23, CD24, CD5, CD10, CD11a, and Ki67), only CD23 (P = .0003) and Ki67 (P = .0007) revealed statistical association with the percentage of naive CD4 lymphocytes. No correlation could be demonstrated with the proportion of whole TIL-T, activated CD3 DR TIL-T, or CD4 subset.
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PMID:CD45RA expression by CD4 T lymphocytes in tumors invaded by B-cell non-Hodgkin's lymphoma (NHL) or Hodgkin's disease (HD). 153 69

A case is described of an HIV+ man who was successfully treated for Hodgkin's lymphoma, but who later developed non-Hodgkin's lymphoma 3 years later when his immune system became suppressed. The patient was 22 years old when he presented with fever, asthenia, weight loss, and cervical lymphadenopathy. With Hodgkin's lymphoma he also had positive serology for HIV and hepatitis B. He was treated with alternate courses of MOPP and ABVD chemotherapy. In 1990 he again appeared with high fever, progressive cervical, axillary and inguinal lymphadenopathy, with hilar and mediastinal lymph node enlargement on x-ray. CD4 lymphocytes were 577/cubic mm, and the CD4/CD8 ratio was 0.57 (normal 1.8). His cervical lymph node biopsy was classified as non-B non-T large-cell anaplastic lymphoma which was EBV-positive. A Western Blot was positive for small amounts of p24 and p18 antigens. The man was treated with MACOP-B chemotherapy, with some results, but died of sepsis 6 weeks later. The relationships between Hodgkins and non-Hodgkin's lymphoma, the timing of the neoplasm in the course of HIV infection, and the possible re-activation of hepatitis virus were discussed.
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PMID:Non-Hodgkin's lymphoma after prolonged remission of Hodgkin's disease in an HIV-infected patient. 166 42

The case of a 31 year old man who had been intravenous drug abuser for years is reported. He was studied because of abdominal pain, jaundice, a weight loss of 10 kg, and the presence of a subclavicular mass. Biopsy of the mass demonstrated a high-grade B-cell non-Hodgkin's lymphoma, and the patient was classified in group IV-D of the human immunodeficiency virus infection because he had HIV serum antibodies and a reduced CD4/CD8 lymphocyte ratio. Although lymphoma had a good response to chemotherapy, persistent cholestasis led to liver and biliary evaluation. Sclerosing cholangitis and papillary stenosis were found. He has been followed for two years, without evidence of any secondary infectious disease associated to the acquired immunodeficiency syndrome.
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PMID:[Sclerosing cholangitis, papillary stenosis and B-cell lymphoma in a patient with acquired immunodeficiency syndrome]. 189 85

The majority of non-Hodgkin's lymphomas (NHLs) are of B-cell lineage, with less than 20% of cases being of T-cell lineage. The B-cell NHLs phenotypically correspond to normal cells in the mid stages of normal differentiation. More specifically, by their expression of B-cell activation antigens, these tumors are the neoplastic counterparts of normal activated B cells. The follicular lymphomas--including the small cleaved, mixed small and large cell, and large cell types, as well as the small noncleaved cell (Burkitt's) lymphomas--represent malignant expansions of normal germinal center B cells by their expression of pan-B cell antigens, B-cell activation antigens, and CD10 (CALLA). The diffuse lymphomas also correspond to normal activated B cells. The small lymphocytic lymphomas express the low-affinity IL-2 receptor and CD5, both of which are induced on normal B cells following mitogen stimulation. The other diffuse B-cell NHLs similarly express activation antigens and resemble "transformed" B cells. The T-cell NHLs generally correspond to normal activated CD4+ T cells. These tumors--which include most peripheral T-cell lymphomas, cutaneous T-cell lymphomas, and HTLV-I-associated adult T-cell leukemias/lymphomas--express antigens induced on activated T cells, including IL-2 and transferrin receptors (CD25 and CD71, respectively), as well as HLA-DR. The lymphoblastic lymphomas, which are generally of T-cell lineage, phenotypically correspond to stages of intrathymic differentiation, often by their coexpression of CD4 and CD8, as well as expression of CD1. It remains controversial whether the immunophenotype of lymphoblastic lymphoma differs significantly from T-cell acute lymphoblastic leukemia. Since immunologic heterogeneity of NHL was first observed, attempts have been made to employ the data as a prognostic variable. Early studies suggested that lineage derivation or expression of markers of proliferating cells affected outcome in NHL. However, these reports were often retrospective, included various histologies, and did not treat patients uniformly. More recent prospective studies with relatively uniformly treated patients, predominantly involving DLCL, suggest that certain immunologically defined subgroups may have significantly different clinical outcomes. However, additional clinical studies will be necessary before treatment options are based upon immunologic markers.
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PMID:Immunologic markers in non-Hodgkin's lymphoma. 193 59

In this study we investigated the pattern of T lymphocyte changes in 16 adult patients with acute myeloid leukaemia (8), non-Hodgkin's lymphoma (4) and Hodgkin's disease (4) treated with continuous infusion of recombinant interleukin-2 (rIL-2). Effects indicative of lymphocyte activation occurred even prior to any rIL-2 therapy in these patients, being most prominent in patients with active diseases. Following each course of cytokine therapy, there were further changes in these parameters. Significant rebound lymphocytoses occurred with a concomitant increase in the cytotoxic functions and induction of the cytotoxicity-linked cytoplasmic serine esterase. Hence, both the natural killer and lectin-dependent cellular cytotoxicity activities were up-regulated. There were also increases in the serum sIL-2 receptor, sCD4 and sCD8 levels. More CD3+ lymphocytes, especially cells bearing CD4, were also recruited to the pool of potential effector cells, as demonstrated by the greater proportion of cells expressing the cytoplasmic serine esterase.
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PMID:Lymphocyte activation and serine-esterase induction following recombinant interleukin-2 infusion for lymphomas and acute leukaemias. 203 61

We report the characterization of a novel human T-cell line, HPB-MLp-W, which was established from blastic cells of a lymph node specimen from a patient with non-Hodgkin's lymphoma. They demonstrated the T-cell association antigens, CD2 and CD4, but no CD3, CD8, CD1, CD5, CD7 nor T-cell antigen receptor on their cell surfaces. They were also positive for Ia and Ki-1 antigen, and negative for CD25 (Tac-1). The cell line HPB-MLp-W had the same pattern of antigen expression as the patient's cells. Southern-blot analysis of DNA showed a rearrangement of the T-cell receptor-alpha and beta genes. To our knowledge, this is a novel cell line with unique T-lineage marker, to be established from a case of non-Hodgkin's lymphoma.
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PMID:Establishment of a novel cell line with T-lineage phenotype (HPB-MLp-W) from a non-Hodgkin's lymphoma patient. 204 90


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