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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The clinical and pathological features of acquired immune deficiency syndrome (AIDS)-related lymphomas, including their relationship with other viruses, such as Epstein-Barr virus (EBV) and human herpes virus-8 (HHV8), have been the subject of several studies from North America and Europe. No consistent data have been reported in Africa, where AIDS runs an epidemiological and clinical course different from that observed in Western countries. We retrospectively evaluated the presence of human immunodeficiency virus (HIV), HHV8, and EBV in 146 cases of malignant lymphomas collected in Kenya (Equatorial Africa), with the use of polymerase chain reaction (PCR) and in situ hybridization (ISH). The PCR technique confirmed HIV infection in 16 HIV-seropositive subjects (11%) and showed the presence of HIV sequences in five additional cases (3%) in which the occurrence of lymphoma was the only clinical manifestation. Our findings suggest that AIDS-related lymphomas are not pathogenetically homogenous, and different mechanisms may contribute to lymphomagenesis in these severely immunocompromised patients. In our series, no association of Hodgkin's disease (HD) with HIV infection could be shown. Among non-HIV-related lymphomas, EBV was present in 94% of Burkitt lymphoma (BL) occurring in patients younger than 15 years of age, in 87% of HD independently of age, sex, and histological types, in 60% of anaplastic large cell lymphoma (ALCL), and to a lesser extent (13%) in large B-cell lymphoma (LBCL) cases. Only one tumor, a case of HD, showed HHV8 by PCR.
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PMID:HIV-associated malignant lymphomas in Kenya (Equatorial Africa) 1053 80

Non-Hodgkin's lymphomas (NHL) represent a major health problem worldwide, and incidence has been on the rise continuously for the last few decades. It is estimated that approximately 55,000 new cases of NHL will be diagnosed in the United States in 1998 and that slightly fewer than 25,000 patients will die of treatment failure or recurrent disease. The rising incidence of NHL is related not only to the acquired immunodeficiency syndrome epidemic but to also a steady increase in the number of cases diagnosed in older patients without immunosuppression. The new pathologic classification of NHL (revised European-American lymphoma classification, REAL) developed by the International Lymphoma Study Group (ILSG) is already resulting in more accurate disease-specific epidemiologic and clinical investigations. These studies have brought a new awareness of the existence and the relative prevalence of discrete NHL subtypes that appear to predominate among patients in different populations according to age, sex, geographic distribution, and predisposing conditions. This developing database has also the potential to result in the discovery of specific environmental causes, predisposing genetic factors, and therapeutic approaches. Some of the entities defined in the REAL classification, such as follicular lymphomas, diffuse B large-cell lymphomas, and T-cell lymphoblastic lymphomas, were already well described in the older classification systems (Kiel and Working Formulation). Others, such as mantle cell lymphoma, (MCL) anaplastic large-cell lymphoma (ALCL), lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), and primary mediastinal B-cell lymphoma (PMBCL) are relatively new members of the family, and accurate data on their clinicopathologic features and natural histories have only recently begun to emerge. This review presents in detail the most recent data on the clinical presentation of, diagnostic evaluation of, and treatment options for the most common of the new NHL entities: MCL, MALT lymphoma, CD30+ (Ki-1+) ALCL, and PMBCL. These four entities combined represent approximately 20% of all cases of NHL and exemplify well the broad clinicopathologic spectrum of NHL and the diagnostic and therapeutic challenges facing those who care for patients affected by these conditions.
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PMID:Evaluation and management of the "new" lymphoma entities: mantle cell lymphoma, lymphoma of mucosa-associated lymphoid tissue, anaplastic large-cell lymphoma, and primary mediastinal B-cell lymphoma. 986 20

The pathogenicities of the murine AIDS (MAIDS) virus complex (LP-BM5) and ecotropic helper virus (BM5eco) isolated from the complex to BALB/c nude mice were studied to elucidate the possible role of replication-competent helper virus in inducing the monoclonal outgrowth of lymphoid cells. Neither LP-BM5 nor BM5eco was pathogenic in adult BALB/c nude mice. However, B-cell lymphoma developed with a very high frequency when either virus was inoculated into newborn BALB/c nude (nu/nu) mice. The cells from the B-cell lymphoma were easily transplanted into nude mice. These results suggested that ecotropic helper virus in the MAIDS virus complex plays an important role in inducing the monoclonal outgrowth of lymphoid cells under immunodeficient conditions caused by defective virus.
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PMID:Induction of B-cell lymphoma in BALB/c nude mice with an ecotropic, B-tropic helper virus present in the murine AIDS virus stock. 988 72

Hepatitis C virus (HCV) has been associated with various lymphoproliferative disorders, and a high prevalence (9%-32%) of chronic HCV infection has been demonstrated among patients with lymphoma. Dual coinfection by HIV and HCV has been demonstrated in approximately 40% of certain populations of HIV-infected individuals. Because of this high prevalence of coinfection by HIV and HCV, the known relations between HCV and lymphoproliferative disorders, and the association of HIV and B cell lymphoma, the potential association between chronic HCV and the development of AIDS-related lymphoma was examined. The prevalence of HCV infection in HIV-infected patients with lymphoma was compared with that in patients with AIDS, diagnosed on the basis of an illness other than lymphoma. Risk factors for HCV infection, overall, were also evaluated. Evidence of HCV infection was ascertained by assessing anti-HCV antibodies, and HCV RNA in serum. The study consisted of 99 homosexual/bisexual men with AIDS-related lymphoma, and 43 other AIDS patients. HCV infection was detected in 11 of 99 (11.1 %) men with lymphoma, and in 5 of 43 (11.6%) other AIDS patients. Further, in patients with AIDS-related lymphoma, no relation was found between HCV infection and lymphoma histology or site. History of use of injected illicit drugs was associated with a significantly elevated risk of HCV infection in the combined group of lymphoma and other AIDS patients. The current study demonstrates no relation between dual infection by HIV and HCV and subsequent increased risk of lymphoma.
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PMID:Lack of association between hepatitis C infection and development of AIDS-related lymphoma. 1007 73

Patients infected with HIV experience a spectrum of lymphoproliferative disorders, including generalized reactive lymphadenopathy to atypical lymphoproliferative lesions and lymphomas. Polymorphic B-cell lymphoproliferative disorders are rare and not well documented. We studied lung lesions from two children infected with HIV: an atypical polymorphic B-cell hyperplasia in a 14-year-old boy and a malignant polymorphic B-cell lymphoma in a 21-month-old girl. Morphologically, both lung lesions revealed similar polymorphic lymphoid infiltrations with numerous mitoses in case 1 and extensive necrosis and architectural distortion in case 2. Immunophenotypic examination showed no predominance of kappa or lambda light chain in case 1 and a predominance of kappa light chain in case 2. Genotypic analysis demonstrated an absence of immunoglobulin and T-cell receptor gene rearrangements in case 1 and the presence of biallelic immunoglobulin heavy chain rearrangement and a single clonal Epstein-Barr virus (EBV) in case 2. The clinical course was indolent in case 1 and aggressive in case 2. The clinicopathologic features were similar to those of posttransplantation lymphoproliferative disorders suggesting that these lung lesions might represent an immunosuppression-related spectrum of benign to malignant diseases. EBV infection may play a role in the pathogenesis of these lesions. This study highlights the importance of the molecular characterization of AIDS-associated lymphoproliferative disorders in children in establishing a definitive diagnosis.
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PMID:Epstein-Barr virus-associated polymorphic B-cell lymphoproliferative disorders in the lungs of children with AIDS: a report of two cases. 1032 88

A 46-year-old male presented with a rare primary non-Hodgkin's lymphoma of the central nervous system of T-cell lineage, localized primarily in the right parietal region. There was no evidence of acquired immunodeficiency syndrome. Biopsy of the tumor allowed immunohistochemical confirmation of the diagnosis. Irradiation and chemotherapy were given, and the patient has remained well for 24 months. The clinical manifestations, management, and outcome of T-cell lymphoma are very similar to those of B-cell lymphoma.
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PMID:Primary central nervous system T-cell lymphoma. Case report. 1039 21

When Epstein-Barr virus (EBV) infects B cells in vitro, the result is a proliferating lymphoblast that expresses at least nine latent proteins. It is generally believed that these cells are rigorously controlled in vivo by cytotoxic T cells. Consistent with this, the latently infected cells in the peripheral blood of healthy carriers are not lymphoblasts. Rather, they are resting memory B cells that are probably not subject to direct immunosurveillance by cytotoxic T lymphocytes (CTLs). When patients become immunosuppressed, the viral load increases in the peripheral blood. The expansion of proliferating lymphoblasts due to the suppressed CTL response is believed to account for this increase and is considered to be a major risk factor for posttransplant lymphoproliferative disease (PTLD) and AIDS-associated B cell lymphoma. Here we show that there is an increase in the numbers of latently infected cells in the peripheral blood of immunosuppressed patients. However, the cells are not proliferating lymphoblasts. They are all latently infected, resting, memory B cells-the same population of infected cells found in the blood of healthy carriers. These results are discussed in the context of a model for EBV persistence that explains why PTLD is usually limited to the lymph nodes.
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PMID:Epstein-barr virus-infected resting memory B cells, not proliferating lymphoblasts, accumulate in the peripheral blood of immunosuppressed patients. 1044 27

B cell hyperactivation accompanies HIV infection and is believed to contribute to the increased incidence of B cell lymphoma in persons with AIDS. To examine B cell activation which precedes the development of AIDS-associated lymphoma, we measured levels of two B cell stimulatory molecules, soluble CD23 (sCD23) and interleukin 6 (IL6), in the serum of HIV-infected individuals prior to the diagnosis of lymphoma. Serum sCD23 was elevated in those subjects who developed lymphoma, compared to AIDS, HIV+, and HIV- controls (P = 0.001). Serum IL6 was significantly elevated in subjects who developed Burkitt's/small noncleaved cell lymphoma (BL/SNC, P = 0.01), but not in those subjects who developed large cell, immunoblastic, or central nervous system lymphomas, compared to CD4-matched AIDS controls who did not have lymphoma. These results suggest that lymphomagenesis of the BL/SNC subtype of AIDS lymphoma reflects B cell hyperactivation of a different nature from that which precedes other subtypes of AIDS-associated B cell lymphoma.
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PMID:The development of AIDS-associated Burkitt's/small noncleaved cell lymphoma is preceded by elevated serum levels of interleukin 6. 1047 34

Cytokine dysregulation is accepted as one of the pivotal factors in the pathogenesis of B cell lymphomas in HIV-positive patients. So far no data exist on inhibitory cytokines in the regulatory network of HIV-associated B-NHL. Simian immunodeficiency virus (SIV)-infected macaques are a well-established in vivo model of HIV infection in humans. We used this model for the identification of TGF-beta as a growth-inhibitory cytokine of SIV-associated B cell lymphomas. Fifty-seven rhesus macaques were infected with SIVmac. Nine animals developed B cell lymphomas: eight with high-grade lymphomas of the immunoblastic, centroblastic, and "Burkitt-like" type, and one with the centroblastic/centrocytic type according to the Kiel classification. Six of seven analyzed lymphomas were infected with the macaque EBV, herpes virus macaca mulatta (HVMM). The lymphomas and the SIV-associated B cell lymphoma cell line H50 were positive for transcription of the TGF-beta gene. Protein expression and secretion of the active cytokine were proved by immunohistochemistry and ELISA. H50 transcribed the TGF-beta type I and type II receptor (R I/II), betaglycan, and endoglin. Furthermore, all primary lymphoma samples tested were positive for receptor type I/II transcription and protein expression. TGF-beta induced reduction of cell viability by 67% (range, 50-84% and enhanced apoptosis by 69% (range, 33-111%) compared with the control. TGF-beta activity was blocked by a specific anti-TGF-beta antibody. Thus, TGF-beta fulfilled the criteria of a negative autocrine inhibitor in H50. These data identify TGF-beta as a promising candidate as an inhibitory factor in the regulatory network of HIV-associated lymphomagenesis.
AIDS Res Hum Retroviruses 1999 Nov 01
PMID:Transforming growth factor beta is a growth-inhibitory cytokine of B cell lymphoma in SIV-infected macaques. 1055 11

Primary central nervous system lymphoma (PCNSL) is a rare disease that has been increasing in frequency. Clinical, histologic, and immunohistochemical data from 64 cases of PCNSL seen at Duke University Medical Center since 1968 were reviewed and tumors were classified using the REAL classification system. Thirty-two patients were male and 32 were female, with a mean age of 57.1 years, ranging from 16 to 82 years. Large B-cell lymphoma represented overwhelming the majority of PCNSL, accounting for 81% of all cases. Phenotypic T-cell lymphomas were rare with only two cases over the course of the study. Epstein-Barr virus was detected only in the immunocompromised patients and was identified in 75% of those immunocompromised patients who were tested. Overall survival was poor with a mean survival of 357 days and median survival of 158 days. One- and three-year survival rates were 29.6% and 7.8%, respectively. Type of treatment, duration of symptoms, site of lesion, and histologic subtype were not significant prognostic indicators, whereas concurrent immunosuppression was the strongest predictor of poor outcome. In AIDS patients (which accounted for 21.9% of the study group), the median survival was 65 days, which was significantly different than that seen in the immunocompetent group of 217 days (P = .001).
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PMID:Primary central nervous system lymphomas: a 30-year experience at a single institution. 1061 71


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