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

There is a strong association (approximately 95%) of endemic Burkitt's lymphoma with Epstein-Barr virus (EBV), whereas the association is weak for the sporadic form occurring in Western countries (approximately 15%). In the Middle East, North Africa and South America, 60-80% of Burkitt's lymphomas harbour EBV. These epidemiological differences suggest that either the endemicity of EBV or socio-economic conditions, or both, may influence the pathogenetic role of EBV in Burkitt's lymphoma. Since only meagre data are available on Asians, this study was performed to address this issue by studying cases from Hong Kong, where EBV seroconversion occurs in the first few years of life but the socio-economic conditions approach those of Western countries. In situ hybridization for EBV encoded RNAs (EBERs) was performed on paraffin sections of 18 cases of Burkitt's lymphoma. Labelling of the neoplastic cells was detected in five cases (27.7%). In contrast, among 54 cases of B-cell lymphomas of various subtypes studied for comparison, signals for EBER were detected in only one case each of T-cell-rich large B-cell lymphoma, anaplastic large cell lymphoma and Reed-Sternberg-like cells occurring in B-cell chronic lymphocytic leukaemia/small lymphocytic lymphoma. The strong labelling with oligo-dT probe (which hybridized with the polyadenylated ends of mRNA) in all cases suggested that the negative results were genuine and not due to poor preservation of RNA in the tissues. Thus, among B-cell neoplasms occurring in Chinese, Burkitt's lymphoma shows a statistically stronger association (P < 0.01) with EBV than with other types of B-cell lymphoma.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A study of the association of Epstein-Barr virus with Burkitt's lymphoma occurring in a Chinese population. 779 1

Employing Northern blot analysis and the polymerase chain reaction, we investigated PRAD1 gene overexpression in the tumour tissues of 58 patients with B-cell lymphoma. These findings were then examined in relation to the patients' clinical and immunohistological characteristics. The over-expression of this gene was detected in 6/8 patients with mantle cell lymphoma (MCL) and in only 1/50 other lymphomas, indicating its close association with MCL. The patients with MCL had common clinical findings of advanced disease with generalized lymphadenopathy on admission, and they had a CD5+CD10-IgD+ phenotype. The patients with chronic lymphocytic leukaemia (CLL) also showed findings indicating a distinctive disease entity: a CD5+CD10-IgD+ phenotype and lack of PRAD1 over-expression. In contrast, most patients with diffuse low-grade lymphoma other than MCL and CLL had localized extranodal disease, expressed a CD5-CD10-IgD- phenotype, and lacked PRAD1 over-expression. These findings suggest that extranodal low-grade lymphomas differ from nodal MCL and are not part of the spectrum of CLL.
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PMID:PRAD1 gene over-expression in mantle-cell lymphoma but not in other low-grade B-cell lymphomas, including extranodal lymphoma. 791 73

The recently described monocytoid B-cell lymphoma is a low-grade lymphoma presenting most frequently in elderly women and commonly associated with autoimmune diseases. Leukaemic expression of this disease has been reported in advanced stages. A case of monocytoid lymphocytosis without lymph node enlargement is presented herein. A 60-year old woman complaining of easy bruises was found to have a 2-cm splenomegaly. Her laboratory data included the following: haemoglobin, 125 g/L; haematocrit, 0.35 L/L; white cell count, 29 x 10(9)/L with 32% PMN, 3% stabs, 2% myelocytes, 1% metamyelocytes, 30% lymphocytes and 32% atypical mononucleated cells showing wide, pale cytoplasm neatly contoured and oval nucleus with monocytoid features. The basal coagulation study showed prothrombin 50%, APTT 40 seconds, fibrinogen 68 mg/dL and FDP between 80 and 160 ng/dL. Splenomegaly without lymph-node enlargement was found on CT scan. The bone-marrow biopsy showed a 68% monocytoid lymphocytic infiltration, acid-phosphatase positive and tartrate-sensitive, without fibrosis. Bone-marrow and peripheral immunophenotype showed those cells to be CD22, CD 19 and CD11 positive, while T and CD25 markers were absent. The patient was treated with alpha-2b interferon at a dose of 3MU three times a week for 6 months, with general improvement and regression of the leukaemic expression. Eleven months after diagnosis she died of a central nervous system haemorrhage. The morphological, immunological and cytochemical features of the monocytoid lymphocytes in this case are commented, along with their variable behaviour. A review of the literature is also carried out, attention being laid on the onset and the response to therapy of B-cell monocytoid lymphomas as the singularity of this case lies on its exclusively leukaemic onset. It is concluded that an interrelationship between monocytoid B-lymphocytic leukaemia and B-cell monocytoid lymphoma might possibly exist, such as that between chronic lymphocytic leukaemia and diffuse lymphocytic lymphoma.
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PMID:[Monocytoid B-lymphocytic leukemia]. 805 92

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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PMID:Malignant lymphomas of B-cell lineage with marked tissue eosinophilia. A report of five cases. 814 29

An 80-year-old white female developed clinical signs of a large choroidal malignant melanoma in her left eye. There were no signs of metastatic disease, but an asymptomatic chronic lymphatic leukemia was discovered. Histopathologic examination of the enucleated left eye showed a mostly necrotic malignant melanoma of the choroid with areas of spindle B cell differentiation, episcleral extension and secondary angle-closure glaucoma with necrosis of the anterior segment of the eye. On the basis of immunocytochemical studies of the lymphocytic infiltrates in the iridal blood vessels, retinal blood vessels and the choroid, the leukemic disease was classified as B cell lymphoma of low malignancy (lymphoplasmacytoid immunocytoma). A reactive T lymphocytic infiltration of the conjunctival stroma was also noted. Patients with malignant melanomas of the uvea require exclusion of a second malignancy.
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PMID:Necrotic malignant melanoma of the choroid and concurrent intraocular manifestation of malignant non-Hodgkin's B cell lymphoma. 818 27

The authors studied 56 cases of diffuse low-grade B-cell lymphoma using frozen tissue sections and a large panel of monoclonal antibodies that distinguish subsets of normal B cells. They compared the immunophenotypes with the histologic subtypes defined by the Rappaport classification, Working Formulation, and Kiel classification to correlate antigen expression with the morphologic subtypes defined in these classification schemes and to define the contribution of immunophenotype to clinically relevant subclassification. All categories in all classifications showed some heterogeneity of antigen expression; however, antigen expression correlated better with four major subgroups defined by the Kiel classification: (1) CD5+ CD10- CD23+ CD43+: chronic lymphocytic leukemia (CLL); (2) CD5+ CD10-/+CD23- CD43+: centrocytic (mantle cell) lymphoma; (3) CD5- CD10+/- CD23-/+ CD43-: centroblastic/centrocytic (CB/CC) lymphoma; and (4) CD5- CD10- CD23-/+CD43-/+: immunocytoma, mucosa-associated lymphoid tissue (MALT)-type, and monocytoid B-cell lymphoma. These subgroups had distinctive clinical features. Patients with centrocytic lymphoma were predominantly male (5.5:1) and had a significantly worse probability of survival than those with either CLL or MALT-type lymphoma (P = 0.001). The group with CB/CC lymphoma had an equal male-female ratio and an intermediate prognosis. Most patients with MALT-type and nodal monocytoid B-cell lymphomas were female (2:1); the disease-free survival for patients with extranodal MALT-type lymphoma was significantly better than that for all patients with other lymphoma subtypes except CB/CC (P < 0.01). The group with non-MALT immunocytoma had a slight male predominance, a high frequency of monoclonal gammopathy, and an intermediate prognosis. In differential diagnosis, CD23 was useful in distinguishing B-cell CLL from centrocytic lymphoma (P < 0.0001); CD5 (P < 0.0001), CD6 (P < 0.005), and CD43 (P < 0.0001) distinguish centrocytic lymphoma from CB/CC lymphoma; and CD10 (P < 0.005), CD43 (P = 0.06), Leu-8 (P = 0.08), and Ig heavy chain (P = 0.01) may help distinguish CB/CC lymphoma from immunocytoma, monocytoid B-cell lymphoma, and MALT-type lymphoma. Differences in antigen expression and clinical features among these Kiel classification subgroups suggest that they represent distinct biologic entities. The Working Formulation categories do not delineate these diseases clearly.
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PMID:Diffuse low-grade B-cell lymphomas. Four clinically distinct subtypes defined by a combination of morphologic and immunophenotypic features. 821 30

Twenty-six patients, whose B-cell lymphoma had relapsed after conventional therapies, were treated in a phase I dose escalation study with an immunotoxin consisting of a mouse CD22 monoclonal antibody (RFB4:IgG1K) coupled to chemically deglycosylated ricin A chain (dgA). Two to 12 doses of the immunotoxin were infused intravenously at 48-hour intervals. The peak serum concentration and half-life (T1/2) did not correlate directly with the dose and averaged 3.8 micrograms/mL and 7.8 hours, respectively. The main dose-limiting toxicity was caused by the vascular leak syndrome (VLS) consisting of weight gain, edema, serum albumin decrease, and critically by pulmonary edema. Myalgia occurred frequently and was only dose limiting in one patient who developed rhabdomyolysis. The presence of lymphoma cells in the blood (> or = 10(10)/L) and clinically detectable splenomegaly were associated with reduced toxicity and a shorter T1/2. Nine of 24 evaluable patients (37.5%) made antibody to either mouse Ig or dgA. There were five partial responses (PR) and one complete response (CR) lasting 30 to 78 days. High peak concentrations of immunotoxin in the serum, a long T1/2, and large areas under the curve (AUC) correlated with both clinical response and toxicity. None of three patients with CD5+ lymphomas (including two CLL patients) had more than mild toxicity or responded to the immunotoxin.
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PMID:A phase I study of an anti-CD22-deglycosylated ricin A chain immunotoxin in the treatment of B-cell lymphomas resistant to conventional therapy. 821 17

Mutations of p53 gene have been recognized to be the most common genetic changes in human cancers. Recently, p53 gene mutations have been found in some patients with common subtypes of B-cell lymphoma (9/48:18.8%), Burkitt lymphoma (9/27:33.3%) and chronic lymphocytic leukemia (6/40:15%). Evidences to suggest that p53 gene mutations are associated with the disease progression in B-cell lymphoma have emerged. Functions of wild-type p53 and its mutant's probable role in B-cell lymphomagenesis are described in this review.
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PMID:Mutations of the p53 gene in B-cell lymphoma. 822 Jan 52

Biopsy specimens obtained from 2 patients with monocytoid B cell lymphoma, 7 with mantle zone lymphoma, 7 with small lymphocytic lymphoma or B chronic lymphocytic leukemia, and 6 with hairy cell leukemia were investigated using an immunohistochemical method to detect their immunophenotypic characteristics. Periodate-lysine-paraformaldehyde-fixed frozen biopsies from the lymph node, peripheral blood, bone marrow, spleen, tonsil, lung, and stomach were studied. Monocytoid B cell lymphoma exhibited the immunophenotype of surface(s) IgD-/DRC-1-/Leu-1(CD5)-/Leu-M5(CD11c)-, +/- on the neoplastic cells or neoplastic lesions, mantle zone lymphoma exhibited that of sIgD+/DRC-1++/Leu-1-,+/Leu-M5-, small lymphocytic lymphoma or B chronic lymphocytic leukemia that of Leu-1+/sIgD-,+sIgD-,+/DRC-1- > +Leu-M5-, and hairy cell leukemia that of Leu-M5++/sIgD- >> +/Leu-1- >> +/DRC-1-. We therefore suggest that these four types of lymphomas can be differentiated by a combination of anti-sIgD, DRC-1, Leu-1, and Leu-M5 monoclonal antibodies based on their immunophenotypic characteristics.
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PMID:Immunohistochemical characteristics of monocytoid B cell lymphoma, mantle zone lymphoma, small lymphocytic lymphoma (or B chronic lymphocytic leukemia), and hairy cell leukemia. 806 18

Interleukin (IL)-1 alpha, IL-1 beta, tumor necrosis factor (TNF) alpha, and IL-6 are the most important triggers in the response of the immune system to infection and neoplasia. We examined the histochemical distribution of cytokine-possessing cells in neoplastic lymph nodes of 68 malignant lymphomas. The HLA-DR positive interdigitating reticulum cells (IRCs), histiocytes/macrophages (H/Ms) and epithelioid histiocytes with these cytokines were frequently encountered in Hodgkin's disease, B cell lymphoma of lymphoplasmacytic/cytoid, centroblastic and immunoblastic types, and T cell lymphoma of Lennert's and anaplastic large cell types. In almost all cases of B cell lymphoma of chronic lymphocytic leukemia, centrocytic, follicular centroblastic/centrocytic, Burkitt's types and T cell lymphoma of lymphoblastic, angioimmunoblastic lymphadenopathy and pleomorphic types, the cytokine-possessing cells were rarely or occasionally present. These lymphomas with less cytokines had also few or occasionally encountered IRCs, while H/Ms were frequently or occasionally present. Well-developed dendritic reticulum cells in some types of lymphoma had few cytokines. The population of cytokine-possessing cells was related with histologic type of lymphoma and the volume of IRCs. The IRCs might act as an important initiator of reactive cells against tumor cells. In addition, neoplastic T cells influenced the cytokines' possession of IRCs and H/Ms. Although lacunar, Hodgkin's and Reed-Sternberg cells in Hodgkin's disease and the neoplastic cells in peripheral T cell lymphoma showed weak positive reaction of TNF alpha in one third of the cases, lymphoma cells in the majority might have few cytokines, especially IL-1s and IL-6.
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PMID:Cytokine (interleukin-1 alpha, interleukin-1 beta, tumor necrosis factor alpha, and interleukin-6)-possessing cells in lymph nodes of malignant lymphoma. 851 12


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