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

Splenic B cell lymphoma with circulating villous lymphocytes (SLVL) is a lymphoproliferative disorder characterized by the presence in the peripheral blood of atypical B-lymphocytes with hairy appearance. Although the clinical features with massive splenomegaly, absence of peripheral lymphadenopathy and blood cytopenia may mimic hairy cell leukemia (HCL), precise analysis of the morphologic and immunologic features allow differential diagnosis between these two entities. Bone marrow and spleen histology resemble the pattern in chronic lymphocytic leukemia (CLL). We studied 8 patients with this entity illustrating the difficulty of diagnosis between SLVL and HCL.
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PMID:Splenic B-cell lymphoma with villous lymphocytes (SLVL). A lymphocytic lymphoma simulating hairy cell leukemia. A study of 8 cases. 210 74

By in vitro transformation with Epstein-Barr virus (EBV), we have previously established EBV+ lymphoblastoid cell lines (LCL) from a patient with leukemic centrocytic B cell lymphoma. EBV-transformed LCL and EBV genome-negative leukemic B cells showed identical chromosome aberrations and IgH gene rearrangements. In the present study we have analyzed the effect of exogenous cytokines [interleukin (IL) 1, 2, 3, 4, 6, tumor necrosis factor, lymphotoxin, transforming growth factor beta, (TGF-beta)] and anti-IgM antibodies on the in vitro proliferation of EBV- leukemic B cells and EBV-converted LCL. In contrast to conventional chronic lymphocytic leukemia, B cells of the patient DUL spontaneously proliferated for up to two weeks in the absence of exogenous lymphokines. The spontaneous proliferative capacity of clonal DUL B cells was not modulated by IL 1, IL 3, IL 6, TNF or LT. In vitro growth of DUL B cells was increased, however, by exogenous recombinant (r)IL 2, and was abrogated by TGF-beta, rIL 4 and anti-IgM. rIL 4 not only inhibited spontaneous B cell proliferation but also neutralized the enhancing effect of rIL 2. In contrast, growth of the EBV-transformed DUL LCL was not affected by any of these factors. These data demonstrate that in vitro infection and transformation of a clonal B cell population by EBV induces a switch in responsiveness to rIL 4, TGF-beta and anti-IgM. In addition, this report is the first to demonstrate an inhibitory effect of rIL 4 on a spontaneously proliferating human leukemic B cell clone.
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PMID:In vitro transformation by Epstein-Barr virus induces a switch in growth factor and anti-IgM responsiveness in a human leukemic B cell clone. 215 17

Type-C virus-like particles (VLPs) were found in an Epstein-Barr (EB) virus-infected human B-cell lymphoma cell line, SP-50B, that was established from a patient with non-Hodgkin lymphoma. The cell line continuously produces a small number of type-C VLPs, 150-200 nm in diameter, over 1 year. SP-50B cells were negative for HTLV-I and HTLV-II antigens and did not contain the HTLV-I genome. In addition, two EB virus nuclear antigen (EBNA)-positive B-cell lines, SP-54-Cord and SP-57-CLL, were established from human cord blood and chronic lymphocytic leukemia (CLL), respectively, by coculture with lethally irradiated SP-50B cells. Type-C VLPs with the same morphology were also found in both cell lines.
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PMID:Type-C virus-like particles in a human B-cell lymphoma cell line. 216 9

Antiidiotype (Id) antibodies identify unique determinants within the surface immunoglobulin (Ig) that are present on B-cell tumors. Anti-Ids have been used for diagnosis and therapy of B-cell lymphoma and leukemia. A panel of 29 anti-Id monoclonal antibodies (MoAbs) that recognize shared idiotypes (SIds) on B-cell lymphomas was tested for reactivity with both B-cell leukemias and lymphomas. Ten of 40 (25%) cases of chronic lymphocytic leukemia (CLL) reacted with at least one of the 29 anti-SId MoAbs. Three cases reacted with more than one anti-SId MoAb, but there was no repetitive pattern of a single anti-SId MoAb reacting with a large proportion of CLL cases. In contrast, for B-cell lymphoma, in which 11 of 31 (36%) cases reacted, one anti-SId (B4-1) reacted with five of the positive cases; all were diffuse histology. Restricted anti-SId reactivity may lead to important insights into the etiology of certain B-cell lymphomas. In addition, these anti-SIds may obviate the need to develop "tailor-made" antibodies for individual patients.
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PMID:Shared idiotype expression by chronic lymphocytic leukemia and B-cell lymphoma. 222 30

Seventy-five peripheral T-cell lymphomas (PTLs) were classified according to the recently proposed "Updated Kiel Classification of Non-Hodgkin's Lymphomas" (mycosis fungoides and Sezary's syndrome excluded). Thirty-seven PTLs belonged to the low-grade category (T-cell chronic lymphocytic leukemia [T-CLL], 3; lymphoepithelioid, 4; angioimmunoblastic, 22; T-zone, 6; pleomorphic small cell, 2) and 38 belonged to the high-grade category (pleomorphic medium and large cell, 24; immunoblastic, 1; large-cell anaplastic Ki-1-positive, 13). Loss of pan-T antigens occurred exclusively in high-grade PTLs; on paraffin sections UCHL 1 was slightly more sensitive than MT 1. Sixty patients presented with lymphadenopathy and 15 patients (20%) presented with extranodal disease most frequently affecting the skin and upper aerodigestive tract. B-cell lymphoma symptoms were found in 43 cases (57%) and bone marrow involvement (T-CLL excluded) was found in 12 cases (17%). Staging (T-CLL excluded) revealed stage I in 13%, stage II in 15%, and stages III and IV in 72% of the cases. Among the intensively treated patients, 37% achieved complete remission and 15 are still in complete remission after 4 to 79 months (median: 24 months). The overall median survival (MS) rate was 23 months. Peripheral T-cell lymphoma of pleomorphic medium and large-cell type was the most aggressive lymphoma (MS: 8 months). B-cell lymphoma symptoms, bone marrow involvement, and Ki-67 positivity 60% or greater significantly shortened survival times, whereas age (under 60 versus over 60 years), stage (I and II versus III and IV), and grade had no significant influence. Ki-67 reactivity was found to be a prognostic factor which allows prediction of probable poor outcome, especially in cases with limited stage of disease.
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PMID:Peripheral T-cell lymphomas: a clinicopathologic study of 75 cases. 222 19

Previous studies using classical cytogenetics have demonstrated the presence of the t(11;14) (q13;q32) chromosomal translocation in some cases of lymphocytic lymphoma of intermediate differentiation (IDL), a distinct type of low grade B-cell lymphoma. This finding suggested that the bcl-1 region (located at band q13 of chromosome 11) might be involved in this neoplasm. Using a genomic probe from the major breakpoint area of the bcl-1 locus, we identified rearrangements of the bcl-1 region in 10 of 19 cases, 2 of which comigrated with a rearranged allele of the immunoglobulin heavy chain gene joining region. In contrast, bcl-1 rearrangements were not found in other types of low grade B-cell lymphoma, specifically in 36 cases of chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL) and 27 cases of follicular lymphoma (FL). To further assess the molecular pathology of IDL, we analyzed these cases for rearrangements of the bcl-2 proto-oncogene, which is associated primarily with follicular lymphomas. None of the 19 cases of IDL had rearrangements. Furthermore, none of the 36 cases of CLL/SLL showed bcl-2 rearrangements, whereas, as expected, 21 of 27 cases of FL had rearrangements of the bcl-2 locus. Our findings demonstrate an association between a rearranged bcl-1 region with approximately 50% of IDLs and suggest that abnormalities of this locus may be important in the pathogenesis of IDL.
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PMID:Association of bcl-1 rearrangements with lymphocytic lymphoma of intermediate differentiation. 224 28

A 62-year-old woman with chronic lymphatic leukemia (CLL) (RAI stage IV) with multiple organ involvement and diabetes mellitus, three months prior to death presented with a symmetrical sensory neuropathy of the upper extremities with little motor impairment and, two months later, sensory atactic neuropathy of the lower limbs. No cranial nerve or CNS impairment was noted. Clinical diagnosis was predominantly sensory neuropathy, but nerve conduction velocities were normal on upper limbs and moderately abnormal on lower limbs, the latter attributing to long lasting diabetes mellitus. The women died from acute subarachnoid hemorrhage. Autopsy revealed CLL of B-cell type with generalized organ involvement and acute craniospinal subarachnoid hemorrhage from ruptured cerebral aneurysm. There was selective neoplastic infiltration of the dorsal root ganglia and peripheral nerves, particularly the median nerve. Although selective infiltration of peripheral nerves by B-cell lymphoma cells was not associated with myelo-axonal degeneration, the relationship of this case to human neurolymphomatosis is discussed.
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PMID:Human neurolymphomatosis in a patient with chronic lymphatic leukemia. 227 42

In a series of 139 spleens involved by non-Hodgkin's lymphoma, we found that each type of lymphoma (as classified according to the Kiel classification) has a specific pattern of infiltration in the red and white pulp. Tumor infiltration in preexistent follicles was not a feature of B-cell lymphomas, but tumor nodules were found in the red pulp nonfiltering areas in cases of immunocytoma (small lymphocytic plasmacytoid) and centroblastic-centrocytic lymphoma (follicle center-cell lymphoma). B-chronic lymphocytic leukemia and centrocytic-centroblastic lymphoma were located along central arteries of T-cell areas. T-cell areas were infiltrated by B-prolymphocytic leukemia, immunocytoma, centrocytic lymphoma (lymphocytic lymphoma of intermediate differentiation), and T-cell lymphoma/leukemia. The red pulp showed diffuse involvement in leukemic cases. Additionally, there was pericapillary growth in all cases of low-grade B-cell lymphoma. The findings, which are related to the physiological counterparts of the lymphoma cells, contribute to our knowledge of the routes of circulation as well as the homing areas of lymphocytes in the human spleen.
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PMID:The distribution of non-Hodgkin's lymphoma in the lymphoid compartments of the human spleen. 250 66

To study the biology of cold agglutinin disease we previously established EBV-transformed B cell clones isolated from a patient with splenic lymphoma of an early plasmacytic cell type and immune hemolysis due to an anti-Pr2 cold agglutinin. These clones had an aberrant chromosomal marker identical to the patient's B cell lymphoma and each secreted IgMk anti-Pr2 similar to the pathologic autoantibody in the serum of the patient. In this study, we have further investigated the Pr2-specific autoimmune response through nucleotide sequencing of VH and VL region genes. We have shown that the seven clones share the same VDJ/VJ gene segments and junctional elements confirming their clonal origin. The VH sequences were 88% homologous to a VHI germline gene while the VL sequences were 97% homologous to a VkIII germline gene. Only 4 somatic mutations (3 silent and 1 conservative) were found in greater than 5,000 bp sequenced, suggesting that a low mutation rate existed. Based on a tumor mass of 10(12) cells and a minimum of 40 divisions, we estimated the somatic mutation rate to be 4.45 x 10(-5) m/bp/d. This somatic mutation rate is similar to those estimated for acute lymphocytic leukemia (pre-B cell) and chronic lymphocytic leukemia (intermediate B cell), but significantly lower than the mutation frequency in follicular lymphomas (activated B cell). We propose that the difference in somatic mutation frequency of a B cell tumor may be related to the stage of B cell differentiation. In addition, the low mutation frequency observed in the Pr2-specific B cell tumor may also reflect, in part, selection by autoantigen to conserve sIg structure and specificity.
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PMID:Relationship of variable region genes expressed by a human B cell lymphoma secreting pathologic anti-Pr2 erythrocyte autoantibodies. 254 Dec 21

Hairy cell leukemia is a preplasmacytic B cell leukemia which is not EBV associated, although elevated titers of Epstein-Barr virus (EBV) antibodies have been seen in this leukemia and chronic lymphocytic leukemia. Hairy cells are not readily susceptible to EBV infection in vitro, even though they are EBV receptor-positive B cells. We have observed a 59-year-old patient who after 9 years of hairy cell leukemia developed a well-differentiated IgG-kappa monoclonal B cell lymphoma without further evidence of hairy cell leukemia. Pathologically, the lymphoma showed plasmacytic differentiation, and in the patient's serum, a 2 g/dl monoclonal IgG-kappa component was present. DNA extracted from the lymphomatous lymph node hybridized with DNA fragments of a reiterated sequence of EBV, IR1. The transformation, with no chemotherapy involved, from a preplasmacytic leukemia into a lymphoplasmacytic lymphoma with monoclonal gammopathy may be related to the entry of EBV into these cells. Studies at the molecular level may help understand mechanisms of malignant transformation or interconversion in lymphoproliferative disorders of the B cell type.
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PMID:Transformation of hairy cell leukemia to EBV genome-containing aggressive B cell lymphoma. 282 16


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