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

Neoplastic disease, especially malignant lymphomas, are often observed in cats infected with feline immunodeficiency virus (FIV). In order to clarify the characteristics of lymphoma cells and to investigate the pathogenesis in FIV-infected cats, we examined the lymphoma tissues developed in five cats naturally infected with FIV by Southern blot analyses using feline immunoglobulin (Ig), T-cell receptors (TCR) and FIV probes. All of the five cases were serologically positive for anti-FIV antibody and negative for feline leukemia virus antigen. Of these five lymphoma samples, two displayed rearrangement of the Ig heavy chain gene and deletion of the Ig light (kappa) chain gene, indicating that the tumor cells were committed to B-cell development. One tumor sample was identified as a T-cell lymphoma because of the presence of a rearranged TCR beta-chain gene. The other two cases were considered to be non-T non-B cell lymphoma because they did not show any rearrangement of the Ig and TCR genes. Therefore, no consistent tumor type was found in lymphoma cases infected with FIV. Clonal integration of FIV provirus was not detected in any of the five lymphoma samples obtained from FIV-infected cats using Southern blot analysis, although FIV proviral genome was detected in the genomic DNA of all the lymphoma samples by using a polymerase chain reaction (PCR). These results indicated that FIV might not play a direct role in tumorigenesis of lymphoma in cats.
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PMID:Molecular characteristics of malignant lymphomas in cats naturally infected with feline immunodeficiency virus. 926 55

The MHC class II molecule I-Ad has been reported to bind peptides containing a motif of six consecutive amino acids. We demonstrate that binding of the murine IgG2ab heavy chain allopeptide gamma 2ab 435-451 (Kabat numbering) to I-Ad is strongly enhanced by a novel first primary anchor (P1) three residues N-terminal to this hexamer. This is based on flow cytometric assessment of the I-Ad binding capacity of gamma 2ab peptide analogues, their antigenicity for I-Ad-restricted T cell clones and molecular modelling. The P1 pocket is broadly specific since allphatic, aromatic, acidic, the basic histidine and small polar side chains all allowed good binding. By contrast, asparagine, arginine and glycine reduced the binding capacity 10-, 16- and > 100-fold respectively. Truncation or glycine substitution at P1 decreased antigenicity by a factor > 1000. Nevertheless, I-Ad-restricted T cells are not completely dependent on this anchor since high concentrations of a peptide with glycine-substituted P1 elicited maximal responses. Additional anchoring side chains are found at P4, P6 and P9. The autologous IgG2aa heavy chain shares prominent epitopic residues with gamma 2ab 435-451 at P3, P5 and P8. However, the lysine of gamma 2aa at P9 impairs binding to I-Ad, which may explain why the gamma 2ab allopeptide-reactive T cells escaped negative selection. The data rationalize our observation (Bartnes, K. and Hannestad, K. 1997. Eur. J. Immunol. 27:1124) that these T cells recognize a syngeneic B cell lymphoma, provided its presentation of intrinsic gamma 2aa is enhanced by surface IgG2aa ligation.
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PMID:A novel first primary anchor extends the MHC class II I-Ad binding motif to encompass nine amino acids. 926 16

Although it is possible to diagnose primary high-grade thyroid lymphoma from a fine needle aspiration (FNA) biopsy, the distinction of low-grade B-cell lymphoma of mucosa-associated lymphoid tissue (MALT) from lymphocytic thyroiditis is sometimes problematic. Definitive diagnosis of lymphoma on cytologic specimens may be facilitated by the documentation of a clonal lymphoid proliferation within the specimen by flow cytometric immunophenotyping or immunocytochemistry. Recently, molecular techniques have also been developed to detect clonal lymphoid proliferation based on immunoglobulin (Ig) or T-cell receptor gene rearrangement. We have used a polymerase chain reaction (PCR)-based assay for Ig heavy chain gene arrangement to identify a clonal population of lymphocytes within the thyroid FNA specimen from a low-grade thyroid MALT lymphoma. Using this assay, we identified no distinct clonal population in five cytologic specimens of lymphocytic thyroiditis. Therefore, this PCR-based clonality assay represents a potentially useful adjunct to the cytologic diagnosis of thyroid lymphoma.
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PMID:Polymerase chain reaction-based detection of B-cell clonality in the fine needle aspiration biopsy of a thyroid mucosa-associated lymphoid tissue (MALT) lymphoma. 926 38

The isolation of rearranged immunoglobulin (Ig) variable region (V) genes is usually performed by PCR with consensus primers binding to conserved regions within the V sequences. However, the isolation of Ig genes by this method is hampered in 15-35% by technical difficulties, mostly mismatches of oligonucleotide primers to V sequences. In order to obtain DNA sequences from V heavy chain (VH) genes which could not be amplified with consensus primers, we used a modified PCR technique, the rapid amplification of cDNA ends (RACE) PCR in combination with new heavy chain constant region primers for the isolation of human and murine VH genes. In comparison, consensus primer PCR with different sets of previously published oligonucleotide primers was used. Both methods were applied to isolate VH genes from murine B cell lymphoma (A20 and BCL1), myeloma (NS1) and hybridoma (SP6) cell lines and from freshly isolated human chronic lymphocytic leukemia and lymphoma cells. RACE PCR allowed the amplification and subsequent cloning of the complete VH gene in all cases. In contrast, consensus primer PCR failed to isolate the VH sequence of the murine A20 cell line; this was explained by a mismatch of consensus primers with VH sequences. When both PCR methods amplified VH sequences, the DNA sequences obtained were identical. Taken together, RACE PCR represents a reliable and versatile method for the isolation of VH genes from human and murine lymphoma cells, in particular if consensus primer PCR fails.
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PMID:Rapid amplification of cDNA ends (RACE) improves the PCR-based isolation of immunoglobulin variable region genes from murine and human lymphoma cells and cell lines. 932 2

This is the second report of histiocyte-rich B-cell lymphoma and the first case analyzed by flow cytometry and cytogenetic study. The immunophenotype determined by flow cytometry was that of a B-cell antigen-positive, surface immunoglobulin-negative B-cell lymphoma with 79% CD11c positive histiocytes. The lymphoid cells were composed of 76% neoplastic B-cells and 24% reactive T-cells. Immunohistochemical staining showed large numbers of histiocytes positive for CD68 and lysozyme in the lymph node and the bone marrow. Neoplastic lymphoid cells were positive for CD20, CD45, CD74 and CDw75. The monoclonality of the tumor cells was established by the evidence of rearrangements of the heavy chain and kappa light chain genes and a complex clonal cytogenetic abnormalities including t(8;14)(q11;q32). The tumor cells were large, pleomorphic lymphoid cells and showed no features resembling those of the L/H cells of Hodgkin's disease as previously reported. The rapidly progressive clinical course in the present case is consistent with the clinical features shown in the original study. The histiocytic component in this tumor is presumably recruited by a lymphokine with the nature of a growth factor from the tumor cells that may also be responsible for the rapid proliferation of the tumor cells and the aggressive clinical course. This entity merits special recognition because it leads to a predictable poor prognosis and because of its potential of being misdiagnosed as true histiocytic lymphoma.
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PMID:Histiocyte-rich B-cell lymphoma. 938 44

A case of multicentric lymphoma with a mixed cell population of large to small round cells with the same nuclear features in a pig was studied immunohistochemically. Neoplastic tissues were composed of 20-50% B-cell lymphoma cells with lambda-type light chain restriction, and 50-80% cluster of differentiation (CD)3+ T-cells. These findings were similar to those of human T-cell-rich B-cell lymphoma (TCRBCL). In addition, both immunoglobulin IgM and IgG were detected in the cytoplasm of the identical lymphoma cell. This pattern of heavy chain expression appeared to be due to maturational arrest in cellular development at the point of heavy chain class switching, as occurs in biclonal gammopathy in human lymphoid malignancy. This case as TCRBCL containing two types of heavy chains with light chain restriction (IgM-lambda and IgG-lambda) appears to be the first of its kind reported in the English literature for either pigs or domestic animals.
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PMID:T-cell-rich B-cell lymphoma in a pig. 953 70

Relationship and histogenesis of Hodgkin's disease (HD) and anaplastic large cell lymphoma (ALCL) still remain unclear. Recently, Reed-Sternberg cells or Hodgkin cells in HD with B cell phenotype (B-HD) are considered to originate from germinal center B cells, ALCLs of B cell phenotype (B-ALCL) are involved in diffuse large B cell lymphoma (DLBCL) as anaplastic variant, but an origin of tumor cells of B-ALCL has not been elucidated. We have therefore investigated somatic mutation of the lg heavy chain (IgH) genes among 17 cases of B-ALCL to clarify whether there is a difference in characteristic and origin of tumor cells between B-ALCL, B-HD and DLBCL. Amplificates of IgH variable (V) region of 10 cases by the polymerase chain reaction method were sequenced and compared with reported germ line configurations. Nine cases (90%) with heavily somatic mutations were found. A case with an out-of-frame rearrangement and a case with 9 base pairs insertion were included. The mutation pattern revealed the tumor cells were selected for antibody expression and discriminated from B-HD. These findings suggest the tumor cells of B-ALCL are derived from germinal center or postgerminal center (memory and effector) B cells and an origin of B-ALCL is not different from DLBCL.
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PMID:Most of CD30+ anaplastic large cell lymphoma of B cell type show a somatic mutation in the IgH V region genes. 959 74

Evolution of angioimmunoblastic lymphadenopathy with dysproteinemia (AILD) into aggressive B cell lymphoma is thought to be a rare event and the cause of this transformation has not been fully elucidated. We describe two patients with AILD that progressed to aggressive large-cell lymphoma with a B cell phenotype. At presentation, the lymph nodes of both patients showed the typical features of AILD by hematoxylin-eosin staining. Immunohistochemical staining with monoclonal antibodies revealed positive staining of atypical cells with UCHL-1 and negative staining with L-26. In situ hybridization of EBV RNA showed rare positive cells in one patient and was negative in the other patient. At relapse, both patients showed systemic lymph nodes swelling, which is characteristic of diffuse large immunoblastic lymphoma. Single-cell analysis with monoclonal antibodies and immunohistochemical staining showed the monoclonal proliferation of B cells. Southern blot analysis of the lymph nodes showed a rearrangement in both patients of the Ig heavy chain gene and germ line configuration of the T cell receptor beta chain gene. Southern blot analysis using the EBV terminal repeat region probe detected clonal proliferation of EBV in the lymph nodes of both patients. In situ hybridization studies identified considerable EBV mRNA in both patients. These observations suggest that EBV proliferation plays an important role in the development of B cell lymphoma that arises from AILD. We suggest that infection or reactivation of EBV may occur in some patients with AILD, probably due to their immunodeficient state, and that this infection or reactivation is directly involved in the development of B cell lymphoma.
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PMID:Development of Epstein-Barr virus-associated B cell lymphoma after intensive treatment of patients with angioimmunoblastic lymphadenopathy with dysproteinemia. 965 Apr 54

A 60-year-old woman had an abnormal shadow in the right lower lung field on chest roentgenogram. Transbronchial lung biopsy revealed findings consistent with malignant lymphoma, and a right middle lobectomy was performed. Pathological findings showed that tumor cells had infiltrated the epithelium, forming so-called lymphoepithelial lesions. Flow cytometric analysis of the resected specimen revealed that B-cell associated antigens (CD 19, 20) were expressed, and that the tumor cells were CD 5-, CD 10-. A marked increase in the number of lymphocytes with an IgM kappa component suggested monoclonal origin for the tumor cells in the resected specimen. Southern blot analysis showed clonal rearrangement of the heavy chain of the immunoglobulin gene. A diagnosis of malignant lymphoma of bronchus-associated lymphoid tissue was made. This tumor was defined according to the revised European. American classification of lymphoid neoplasms as a marginal zone B-cell lymphoma.
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PMID:[A case of marginal zone B-cell lymphoma]. 969 59

The cell of origin of parafollicular (monocytoid) B cell lymphoma (PBCL), splenic marginal zone lymphoma (SMZL), and hairy cell leukemia (HCL) is controversial. To better understand the relationship between these low-grade B-cell neoplasms, we analyzed the nucleotide sequences of the rearranged immunoglobulin heavy (IgH) chain variable (V) region of the clonal population of cells in five cases of PBCL, four cases of SMZL, and seven cases of HCL to determine whether these neoplasms could be differentiated by the degree of somatic mutation in the IgH V gene or by the IgH V gene family usage. DNA was extracted from diagnostic material and clonality confirmed by PCR. The DNA was reamplified using V heavy chain family specific primers, and the amplicons were sequenced. Sequences were compared with germline IgH V gene sequences, and base changes were determined to be silent or to represent amino acid replacements by using three different methods. Four of five (80%) cases of PBCL, three of four (75%) cases of SMZL, and three of seven (43%) cases of HCL showed evidence of antigen selection, suggesting that these neoplasms involved clonal expansions of postgerminal center memory lymphocytes. Only SMZL showed a preferential usage of V(H)1 family genes.
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PMID:Somatic mutation analysis of IgH variable regions reveals that tumor cells of most parafollicular (monocytoid) B-cell lymphoma, splenic marginal zone B-cell lymphoma, and some hairy cell leukemia are composed of memory B lymphocytes. 1008 50


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