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

Patients with HIV infection are at high risk for the development of high-grade B-non-Hodgkin's lymphoma (B-NHL). The aim of this study was identification of a predictive diagnostic marker for HIV-associated B-cell lymphomas, using simian-immunodeficiency-virus (SIV)-infected Rhesus monkeys as a well-established in vivo model of HIV-associated lymphomagenesis. We infected 26 monkeys (Macaca mulatta) with SIVmax and measured serum levels of sCD23 longitudinally until necropsy. Of the 26 monkeys, 9 developed high-grade B-NHL, which was preceded by lymphadenopathy (NHL+/LA+) (group 1). Among the 17 animals that remained without clinical evidence of lymphoma during the observation period, 8 developed LA (group 2) and 9 were NHL- and LA-negative (NHL-/LA-) (group 3). Elevation of sCD23 serum levels preceded B-cell lymphoma development, with a median of 44 U/ml in group 1 vs. 7 U/ml and 8 U/ml in groups 2 and 3 respectively, 32 weeks after infection. Differences in the serum level of sCD23 between group 1 vs. groups 2 and 3 became statistically significant 32 to 56 weeks after infection. At necropsy, serum levels of sCD23 were significantly higher in group 1 than in group 2 or group 3; 6/6 samples of SIV-associated B-NHL were positive for gene transcription of CD23 and its receptor CD21 as assessed by RT-PCR. The data point to a potential role of sCD23 as a predictive marker for the development of HIV-associated B-NHL. Moreover, the in vivo model of SIV-infected monkeys suggests the possibility of exactly analyzing the pathobiological role of sCD23 in the lymphomagenesis of SIV-associated B-NHL.
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PMID:Elevated serum level of soluble CD23 precedes development of B-non-Hodgkin's lymphoma in SIV-infected Rhesus monkeys. 968 7

Many chemotherapeutic regimens will induce remission in dogs with lymphoma, but almost all dogs suffer relapse. Mitoxantrone was selected for evaluation as single-agent chemotherapy for relapsing canine lymphoma based on its use in humans undergoing salvage chemotherapy for non-Hodgkin's lymphoma and its tumoricidal effect against canine lymphoma. Dogs entered into study had multicentric lymphoma, and all had been treated solely with a standard combination chemotherapy protocol. At 1st relapse, all dogs were again staged and underwent lymph node biopsy. Mitoxantrone was administered IV at 6 mg/m2 every 21 days. Dogs were evaluated for lymphadenopathy before each dose of mitoxantrone. Fifteen dogs were entered into study. The average age (+/- SEM) of the dogs studied was 7.7 +/- 0.91 years, and most dogs were large (mean +/- SEM weight, 24.44 +/- 2.15 kg). Twelve dogs (80%) had B-cell lymphoma, and 3 had T-cell lymphoma. Dogs were staged IV (n = 12) or V (n = 3). The median duration of chemotherapy before entry into the study was 98 days. Overall median duration of response after mitoxantrone chemotherapy was 21 days. Complete responses were attained in 7 of 15 dogs (47%) with a median response duration of 84 days. Nine of 15 (60%) dogs attained a complete remission with additional chemotherapy after failing mitoxantrone chemotherapy. Mild toxicities were observed after mitoxantrone administration. No adverse reactions were observed during mitoxantrone infusions. The results of this study demonstrate that mitoxantrone, as a single agent, has limited value for dogs with lymphoma at 1st relapse after conventional multidrug chemotherapy.
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PMID:Evaluation of single-agent mitoxantrone as chemotherapy for relapsing canine lymphoma. 977 7

To analyze the value and limitations of flow cytometry (FCM) in the investigation of patients with lymphadenopathy, a retrospective study of 196 patients, referred for fine-needle aspiration (FNA) cytology, was carried out in Canberra, Australian Capital Territory, Australia, between 1992-1997. Complete cytological, flow-cytometric, and outcome (clinical and histological) data were available on all the cases. The FNA appearances were read in conjunction with FCM findings. The following cytological categories were recognized: benign, 78 cases (39.8%); indeterminate, 9 cases (4.6%); and malignant, 109 cases (55.6%). None of the 78 cytologically benign cases had malignant outcome. All 109 cytologically malignant cases had malignant histology, and 8/9 of the cytologically indeterminate FNAs had malignant histology. The cytologically malignant category contained 106 B-cell lymphomas and three T-cell lymphomas. All 65 B-cell lymphomas with K light chain predominance had K/L ratio greater than 3/1, and all 34 B-cell lymphomas with L light chain predominance had an L/K ratio greater than 2/1. Clonality was therefore established for K/L and L/K at 3/1 and 2/1, respectively. When K/L and L/K ratios were below these figures (7 cases), other parameters, including the proportion of CD20 and the dual expression of CD19/CD10 and CD20/CD5, were used to determine the nature of the aspirate. In the B-cell lymphomas without demonstrable light chain restriction, CD20 positivity in excess of 85%, CD19/CD10 positivity of more than 18%, or CD20/CD5 positivity greater than 35% were independently diagnostic of B-cell lymphoma. In the T-cell lymphomas, greater than 90% of the cells were T cells, and aberrant T-cell antigen expression with loss of at least one pan-T-cell antigen was detected. In conclusion, the sensitivity of diagnosis of malignancy, false-negative rate, and predictive value of malignant diagnosis with combined FNA cytology and FCM were 99%, 0%, and 100%, respectively.
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PMID:Flow-cytometric algorithm on fine-needle aspirates for the clinical workup of patients with lymphadenopathy. 978 91

Between June 1988 and May 1996, 428 patients underwent allogeneic BMT (288 related donor (RD) and 140 unrelated donor (UD)) at the Vancouver General Hospital. Eight patients (UD six and RD two) developed a post-transplant lymphoproliferative disorder (PTLD). Median age at BMT was 38 years (range 22-51). Five of the six UD allografts were T cell depleted. Cyclosporine+/-methotrexate was used for GVHD prophylaxis. All eight patients developed GVHD; in six this was refractory to treatment with corticosteroids. Rabbit antithymocyte globulin (ATG) or an anti-CD5-ricin A chain immunotoxin (Xomazyme) was used as second-line therapy for GVHD. Presentation with PTLD occurred at median day 90.5 (range 34-282) post BMT. Five of the eight patients had a rapidly progressive course characterized by fever, lymphadenopathy, lung and liver involvement and died within 3-8 days. PTLD was an incidental finding at post mortem examination in two patients. The remaining patient had localized disease and recovered. Pathological analysis revealed two morphological patterns; diffuse large B cell lymphoma (DLBC lymphoma, five patients) and polymorphous B cell hyperplasia (PBCH, three patients). EBV expression was positive in all eight cases and monoclonality was demonstrated in seven cases. In multivariate analysis, T cell depletion of the allograft (P=0.0001, relative risk (RR)=30.5), anti-T cell therapy for GVHD (P=0.006, RR=12.7) and acute GVHD grades 3-4 (P=0.04, RR=7.7) were the significant factors for development of PTLD. In conclusion, we have identified two forms of PTLD after BMT: one is characterized by disseminated disease with a rapidly progressive and often fulminant course and the other by localized, relatively indolent disease. Morphology, EBV positivity and clonality do not appear to correlate with the clinical course. The major risk factors for development of PTLD after BMT are ex vivo T cell depletion of the allograft and in vivo anti-T cell therapy for GVHD.
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PMID:Lymphoproliferative disorders following allogeneic bone marrow transplantation: the Vancouver experience. 984 95

Twenty-four years after apparently successful treatment for nodular lymphocyte predominant Hodgkin's disease (nLPHD), a 41-year old male developed "B" symptoms and extensive adenopathy. A right axillary lymph node biopsy showed two distinct regions including (1) histiocyte-rich B-cell lymphoma and (2) diffuse small T-cell lymphoma. A clonal rearrangement of the gene for the T-cell receptor beta chain confirmed the presence of a T-cell neoplasm, and this was further confirmed by selective polymerase chain reaction (PCR) on this morphologic zone. PCR on the morphologic B-cell lymphoma confirmed the presence of an immunoglobulin gene rearrangement. These two regions were separated by a less-defined zone containing a mixture of small CD57 positive T lymphocytes, small B lymphocytes, and rare lymphocytic and histiocytic (L&H) cells, highly suggestive of recurrent LPHD. The development of composite B-cell and T-cell lymphoma in this patient raises the speculation that nLPHD may be a neoplasm of lymphoid cells, which can differentiate in both B- and T-cell directions, with the "L&H" cells constituting their B-cell progeny.
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PMID:Composite B-cell and T-cell lymphoma arising 24 years after nodular lymphocyte predominant Hodgkin's disease. 999 Jan 10

Mantle cell lymphomas comprise 2 to 8% of non-Hodgkin's lymphoma in the United States. They occur in older adults with a distinct male predominance, who present with generalized lymphadenopathy, and often have disseminated disease at the time of diagnosis. Pathologically, mantle cell lymphomas are characterized by a proliferation of small lymphocytes, with irregular nuclei, clumped chromatin, and sparse cytoplasm that can grow in nodular or diffuse patterns in lymph nodes, that localize to the splenic white pulp and that produce interstitial, paratrabecular, and intertrabecular lymphoid aggregates in the bone marrow. Phenotypically, mantle cell lymphomas are B cell neoplasms that express pan B cell lineage antigens, CD5 and CD43, and that are negative for CD10 and CD23. On a genetic level, many cases of mantle cell lymphomas have the t(11;14)(q13;q32) that causes overexpression of cyclin-D1, a protein that can be demonstrated by immunohistochemistry in many examples of mantle cell lymphoma and that can be exploited diagnostically to distinguish mantle cell lymphomas from other low-grade B cell lymphoproliferative disorders. The differential diagnosis of mantle cell lymphoma includes small B cell lymphoma, lymphoplasmacytic lymphoma, nodal, extranodal, and splenic marginal zone lymphomas, and follicular small cleaved cell lymphoma. In most instances, these disorders can be separated from one another by morphology, distinctive immunophenotypic profiles, and genetic features.
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PMID:Mantle cell lymphoma. 1009 79

B-cell lymphoma associated with haemophagocytic syndrome (HPS) is extremely rare in Western countries but has recently been increasingly reported in Asian countries. We describe seven patients with B-cell lymphoma associated with HPS, six males and one female, age range 41-82 years (median 63 years). All patients had fever and splenomegaly, and six of the seven patients had hepatomegaly with no associated lymphadenopathy. The bone marrow showed haemophagocytosis and an infiltration of lymphoma cells. All patients showed increased levels of lactate dehydrogenase, C-reactive protein, ferritin and soluble interleukin-2 receptor. Lymphoma cells were positive for CD19. CD20 and surface immunoglobulin in all patients examined, and positive for CD5 in four of seven patients. Cytogenetic analyses of bone marrow cells showed a complex structural abnormality including chromosome 14q32 in two patients, 19q13 in three patients and deletion of the terminal part of 8p21 in six patients. The prognosis was poor; only two of the seven patients have survived in complete remission with a median survival of 11 months. These data suggested that B-cell lymphoma associated with HPS might constitute a distinct biological and clinical disease entity. Abnormality of chromosome 19q13 and loss of 8p21 might be involved in the pathogenesis of this disease.
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PMID:B-cell lymphoma associated with haemophagocytic syndrome: a clinical, immunological and cytogenetic study. 1052 18

Benign monocytoid B cells are seen in lymph nodes in different types of lymphadenitis and they occur in the form of clusters within and around sinuses and in the interfollicular areas, but rarely completely surround benign follicles to produce a marginal-zone pattern. The cytologic hallmark of these cells is the presence of abundant pale to clear cytoplasm; these cells usually are of medium size, and they have a rather bland-appearing, irregular nuclei with inconspicuous nucleoli. Malignant monocytoid B-cell proliferations in a lymph node have been classified as monocytoid B-cell lymphomas (MBCL), which are now called nodal marginal-zone B-cell lymphoma (MZL) in the World Health Organization (WHO) classification. In the recently published clinical evaluation of the International Lymphoma Study Group classification of non-Hodgkin's lymphoma, 25 of 1,378 cases (1.8%) were classified as primary MZL, whereas four times as many cases (105 or 7.6%) were classified as low-grade mucosa-associated lymphoid tissue (MALT)-type lymphoma. Transformation to large-cell lymphoma at the time of diagnosis was seen in five of 25 (20%) cases of nodal MZL and in 32 of 105 (30%) cases of MALT-type lymphoma. Comparison of the clinical findings at presentation and the survival results indicate that nodal MZL is more aggressive clinically than low-grade MALT-type lymphoma. For example, patients with nodal MZL had a significantly higher incidence of advanced-stage disease, including peripheral and paraaortic lymphadenopathy, than those with MALT-type lymphoma. Moreover, patients with nodal MZL had lower 5-year overall survival and failure-free survival than patients with MALT type lymphoma. When analysis was restricted to those patients with zero to three adverse risk factors in the International Prognostic Index, patients with nodal MZL still had a significantly lower overall and failure-free survival at 5 years than patients with MALT-type lymphoma. We conclude that nodal MZL is a distinctive disease entity and is similar to other low-grade nodal lymphomas, such as the follicular or small lymphocytic lymphomas, but different than MALT-type lymphoma.
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PMID:Nodal monocytoid B-cell lymphoma (nodal marginal-zone B-cell lymphoma). 1031 81

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

Malignant histiocytosis-like B-cell lymphoma (MH-like BCL) is characterized clinically by hemophagocytic syndrome (HPS), bone marrow involvement at presentation, and an aggressive clinical course. Yet, it remains an ill-defined disease entity. We recently described five cases of MH-like BCL and suggested that these may be regarded as a peculiar variant of intravascular lymphomatosis (IVL), based on clinical and pathological observation. Interestingly, this type of lymphoma has been reported exclusively among Asians, with few reports from Western countries, and therefore we propose that this variant be noted as an Asian variant of IVL(AIVL). To evaluate the incidence of this variant, we performed a literature search for English or Japanese studies dealing with MH-like BCL or B-cell IVL associated with HPS (IVL with HPS). We found 18 reports of MH-like BCL and 16 reports of IVL with HPS and re-evaluated the clinicopathologic aspects of each study with respect to AIVL. Although several differences were noted, such as gender, presence of respiratory changes, bone marrow invasion and disseminated intravascular coagulopathy, there were also overlapping profiles and they appeared to be consistent with the AIVL single disease entity. Of particular note was the absence of peripheral lymphadenopathy and tumor formation which posed diagnostic problems in the initial phase of the presentations. Thus, based on analysis of the clinical findings of these 34 cases, the diagnostic criteria for AIVL consists primarily of cytopenia (anemia and/or thrombocytopenia), hepatosplenomegaly, absence of peripheral lymphadenopathy and tumor formation, and erythrocyte-hemophagocytosis along with intravascular proliferation of the neoplastic B cells. The pathologic findings of the 19 autopsied cases which fulfilled the criteria are also summarized, and they reveal morphologic, immunologic, and genotypic features of typical IVL.
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PMID:An Asian variant of intravascular lymphomatosis: an updated review of malignant histiocytosis-like B-cell lymphoma. 1034 74


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