Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0079731 (B-cell lymphoma)
 16,671 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

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

The cloned breakpoint at 11q13.3 of the t(11;14)(q13.3;q32.3) in a B-cell lymphocytic leukemia (B-CLL) was used to analyze DNA from individuals with and without the rare folate-sensitive fragile site at 11q13.3. On Southern blots there were no discernible differences. Subclones of the ends of the leukemia breakpoint clone were prepared and used for in situ hybridization to chromosomes expressing fra(11)(q13.3). Both subclones hybridized distal to the fragile site. These experiments indicate that the breakpoints at 11q13.3 in B-CLL (and in a B-cell lymphoma) are not at the fragile site at 11q13.3.
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PMID:Translocation breakpoint in t(11;14) in B-cell leukemia is not at the rare fragile site at 11q13.3. 283 Sep 61

The expression of the enzyme marker terminal deoxynucleotidyl transferase (TdT) was examined by immunofluorescence assay in the cells from 333 cases with various types and subtypes of leukemia or lymphoma. More than 90% of cALL and T-ALL, 70% of Null-ALL and 80% of pre-B-ALL were TdT-positive. One case in the commonly TdT-negative group of B-ALL showed TdT-positive cells. All cases of mature B-cell malignancies (B-CLL, hairy cell leukemia, B-cell lymphoma) have been TdT-negative. In the group of mature T-cell malignancies, T-CLL and mycosis fungoides were negative and 2 out of 6 mature T-cell lymphomas were TdT-positive. 13% of acute myeloid leukemias and 36% of CML in blast crisis expressed TdT. Therefore, these TdT-positive cases of CML in blast crisis also carrying the common ALL-antigen belong to the lymphoid subtype. CML and erythroleukemia were invariably TdT-negative. TdT has become an indispensable indicator of immature lymphoid leukemia cells and is particularly valuable as part of the panel of markers used in leukemia phenotyping.
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PMID:Incidence of TdT positivity in cases of leukemia and lymphoma. 308 80

Recently, kappa-lambda analysis with the "D" value was developed by Ault to detect a minor population of malignant B cells in peripheral blood. This analysis is based on the Kolmogorov-Smirnov test, and the D value is calculated by a flowcytometer and a computer. We have recently devised a more sensitive parameter for the kappa-lambda analysis than the D value called the delta-curve (delta c); the delta c applies the same principle as that of the D value. Mixing experiments with kappa-type and lambda-type chronic lymphocytic leukemia cells revealed that the delta c could not only detect a minor population of malignant kappa-B cells, but also that of malignant lambda-B cells using more sensitivity than the D value. A total of 49 blood samples obtained from 27 patients with various B-cell malignancies were investigated. D values were abnormal in 37% of all samples, while abnormal patterns of the delta c were recognized in 71%. On the other hand, 59% of samples obtained from the patients with B-cell lymphoma in aleukemic phase showed abnormal delta c, whereas D values exceeded the upper limit of the normal value in only 15% of the samples. It was suggested that the delta c could detect 3% to 7% of malignant B cells that were mixed with a population of normal lymphocytes.
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PMID:The basic study on kappa-lambda imaging by delta-curve for the detection of a monoclonal B-cell population in the peripheral blood. 314 Sep 8

Multimarker studies were conducted on 195 lymph node, 59 bone marrow, 44 peripheral blood, eight body fluid, and eight internal organ specimens. The markers were identified by fluorochrome-labeled antibodies quantified with flow cytometry. T-cell receptor gene rearrangements were used for the determination of T-cell clonality. These studies confirmed that CD 19 (B4, Leu 12) is highly sensitive for B-lymphoblastic leukemia, CD 7 (Leu 9) is highly sensitive for T-lymphoblastic leukemia, and CD 5 (Leu 1) is highly sensitive for chronic lymphocytic leukemia. When these markers were compared to antigens of the same cell lineage (e.g., CD 19 to CD 20 [Leu 16] or to surface immunoglobulin, CD 7 to CD 3 [Leu 4], and CD 5 to CD 3), a marked discrepancy between them was diagnostic of the corresponding tumor. T-cell marker discrepancy (CD3 vs. CD 7) was demonstrated in T-cell lymphomas, but it was also shown occasionally in polyclonal T-cell populations. On the other hand, a marked discrepancy between the percentages of a B-lineage (CD 19 or CD 20)-positive and a surface-immunoglobulin-positive population is a reliable phenotype for the diagnosis of a surface-immunoglobulin-negative B-cell lymphoma.
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PMID:Marker discrepancy as a diagnostic criterion for lymphoid neoplasms. 326 62

Following the observation that mouse interleukin 5 (IL5) is active as a B cell growth factor (BCGF) as well as an eosinophil differentiation factor, this work was carried out to test recombinant human IL5 for BCGF activity. A highly active, partially purified batch of recombinant human IL5 was prepared and tested for BCGF activity in four laboratories. This batch gave a 50% endpoint of 1:77,450 in the human eosinophil differentiation assay, 1:983 in the mouse eosinophil differentiation assay and 1:42 in the mouse BCL1 assay, thus demonstrating that, like mouse IL5, human IL5 has cross-species activity. By comparison with the assays in the mouse this batch would be expected to have 50% maximal human BCGF activity of about 1:4000. In each assay a known positive factor was used as a positive control, and there was no inhibitory activity in the preparation. However, despite the activity towards the mouse B cell lymphoma, the results showed no detectable activity in a panel of assays used to identify human BCGF and B cell differentiation factors. These assays included (a) proliferation assays with tonsillar or splenic B cells in the presence of the co-stimulators anti-mu or phorbol myristate acetate; (b) a restimulation assay in which tonsillar B cells are first activated with either Staphylococcus aureus Cowan 1 or a mixture of phorbol dibutyrate and ionomycin, or splenic B cells are first activated with anti-mu; (c) production of immunoglobulin by B cells in a restimulation assay with Staphylococcus aureus Cowan 1; (d) production of immunoglobulin by the Epstein-Barr virus-transformed B lymphoblastoid CESS cell line; (e) the ability to stimulate proliferation of chronic lymphocytic leukemia (B-CLL) cells freshly explanted from three different patients; (f) the ability to stimulate the B lymphoma (L4) cell line and the mature B cell (HBF1) line, and (g) the ability to replace T cells in specific antibody responses. It therefore seems unlikely that recombinant human IL5 is either a growth or a differentiation factor for human B cells, and raises the interesting question of the biological significance of the BCGF activity of this factor in the mouse.
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PMID:Recombinant human interleukin 5 is an eosinophil differentiation factor but has no activity in standard human B cell growth factor assays. 350 Aug 61


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