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

We determined the configuration of the genes for the beta (T beta) and gamma (T gamma) chains of the T cell receptor in DNA from 100 consecutive cases of B cell lymphoma and B cell chronic lymphocytic leukemia (B-CLL), and compared the findings with those in 18 T cell neoplasms. In 7 of the 100 B cell specimens, a single nongermline band was detected after digestion with the restriction enzyme BamHI, but the rearrangement could be confirmed with a second restriction enzyme in only two. The B cell fragments were small in size and of limited size diversity when compared with the T cell cases, and germline bands of equal intensity were present. A rearrangement of the T gamma gene was never seen in a B cell sample. In contrast, T cell specimens usually rearranged both alleles of T beta (15 of 18), the rearrangement could be confirmed with a second restriction enzyme (17 of 18), both alleles of the first constant region gene segment of T beta always underwent either rearrangement or deletion, and the T gamma gene was also rearranged or deleted (17 of 18). We conclude that ordered rearrangement of the T cell receptor is a rare event in B cell lymphoma and B-CLL. T cell receptor gene studies allow B and T cell lymphomas to be distinguished from each other and from common acute lymphoblastic leukemia antigen-positive non-T, non-B acute lymphoblastic leukemia.
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PMID:Rearrangement of the genes for the beta and gamma chains of the T cell receptor is rarely observed in adult B cell lymphoma and chronic lymphocytic leukemia. 282 Oct 76

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

Patients with congenital and acquired immunodeficiencies are at increased risk for the development of B-cell lymphoproliferative disorders. When the appropriate tests have been performed, the Epstein-Barr virus (EBV) nuclear antigen (EBNA) or EBV DNA has been found in tissues from these tumors. These data have provided support for the idea that these tumors are associated with EBV. In this article we report about a child with severe combined immunodeficiency (SCID) who developed a malignant B-cell lymphoma that was not associated with EBV. The B-cell lymphoma in the patient proved to be, by hybridization analysis of immunoglobulin (Ig) heavy chain gene rearrangements of tumor-cell DNA, of clonal origin. However, neither EBNA nor EBV DNA could be detected in tumor tissue by anticomplement immunofluorescence or in situ cytohybridization with an EBV DNA probe. Furthermore, EBV DNA could not be detected by Southern blot hybridization using two EBV DNA hybridization probes on the same DNA blots that clearly contained the clonal Ig gene rearrangement. This case represents a clonal B-cell lymphoma occurring in a severely immunodeficient patient that was not associated with EBV. Antiviral chemoprophylaxis has been recommended for the prevention of EBV-related B-cell lymphoproliferations in transplant patients. Such prophylaxis may be ineffective in patients with B-cell lymphoproliferative disorders not associated with EBV.
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PMID:B-cell lymphoma in severe combined immunodeficiency not associated with the Epstein-Barr virus. 282 20

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

Twenty cases of Epstein-Barr virus (EBV)-associated lymphoproliferative syndrome (LPS), defined by the presence of EBV nuclear antigen and/or EBV DNA in tissues, were diagnosed in 1467 transplant recipients in Pittsburgh from 1981-1985. The frequency of occurrence in pediatric transplant recipients was 4% (10/253), while in adults it was 0.8% (10/1214) (P less than .0005). The frequency of LPS in adults declined after 1983 coincidental with the introduction of cyclosporine monitoring. However there was no apparent decline of LPS in children. We describe these ten pediatric cases and one additional case of LPS in a child who received her transplant before 1981. The frequency of EBV infection in 92 pediatric liver recipients was 63%. Of these subjects, 49% were seronegative and 77% of those acquired primary infection. Of 11 cases of pediatric EBV-associated LPS, 10 were in children who had primary infection shortly before or after transplantation. These results reinforce the importance of primary EBV infection in producing LPS, which was previously shown in adults. Children are at greater risk because they are more likely to be seronegative for EBV and to acquire primary infection. Three clinical types of LPS were recognized in children. The first (5 cases) was a self-limited mononucleosislike syndrome. The second syndrome (4 cases) began similarly, but then progressed over the next two months to widespread lymphoproliferation in internal organs and death. The third type (2 cases) was an extranodal intestinal monoclonal B cell lymphoma, occurring late after primary infection.
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PMID:The frequency of Epstein-Barr virus infection and associated lymphoproliferative syndrome after transplantation and its manifestations in children. 283 28

The development of B cell lymphoma, predominantly of the large-cell type, in patients with autoimmune diseases such as Hashimoto's thyroiditis or Sjogren's syndrome is well known. In Sjogren's syndrome, it has been recently shown that the benign-appearing lymphocytic infiltrates of the lymphoepithelial lesions in the salivary glands have clonal rearrangements of immunoglobulin genes in their DNA, even in the absence of malignant lymphoma. To investigate whether a similar situation occurs in Hashimoto's thyroiditis, we studied the thyroid glands from four patients with this disease. In all four cases, there was a benign-appearing lymphocytic infiltrate in the thyroid, with eosinophilic changes in the Hurthle cells. In immunologic studies, we determined that the lymphocytes were polyclonal in each case. We extracted DNA from the frozen tissue blocks of these four patients and analyzed it by molecular hybridization for the presence of clonal immunoglobulin (IgH, kappa, and lambda) and T cell receptor beta chain gene rearrangements, and detected none in any case. Therefore, we conclude that the lymphocytes in Hashimoto's thyroiditis are immunologically and immunogenetically polyclonal proliferations of cells, and that the initial lesion of Hashimoto's thyroiditis does not contain a detectable clone of cells that may eventually develop into malignant lymphoma.
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PMID:Hashimoto's thyroiditis lacks detectable clonal immunoglobulin and T cell receptor gene rearrangements. 284 72

Six cases of diffuse large cell lymphoma (DLCL) of the liver were studied with immunohistochemistry for common leukocyte antigen (CLA), lysozyme, alpha-1-antitrypsin (AAT), and kappa and lambda light chains on paraffin-embedded tissues. All six cases were positive for CLA. Four of the six cases showed staining for lysozyme and AAT (three focal and one diffuse staining). In three cases, frozen tissue for monoclonal antibodies and glutaraldehyde-fixed tissue for electron microscopic examination were available. Two of these showed B-cell phenotypes with monoclonal antibody studies. Electron microscopic examination on these two B-cell lymphomas showed scant cytoplasm and a paucity of cytoplasmic organelles. The third case did not show definite B- or T-cell surface markers but did show strong Leu-M1 and OKM1 staining. Electron microscopic examination of the tumor cells showed a prominent Golgi apparatus, abundant cytoplasm with numerous cytoplasmic organelles and phagolysosomes. However, DNA hybridization studies on this tumor showed immunoglobulin heavy and kappa light chain gene rearrangements typical of a B-cell lymphoma. All six lymphomas were solitary liver masses without evidence of disease elsewhere. The mean age for the six patients was 56.2 years (four males, two females).
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PMID:Primary lymphomas of the liver. Report of six cases and review of the literature. 295 12

Configurations of Ig gene DNA were examined in multiple biopsy specimens from seven cases of human B cell lymphoma that showed histologic differences among the specimens within each case. Analysis by Southern blot hybridizations with DNA probes for each of the three Ig loci revealed that the configurations of DNA within these loci were identical among the specimens in two of the cases. This result indicated the monoclonality of these lymphomas, despite differences in histology between biopsy specimens. In contrast, no common nongermline configurations of Ig gene DNA were detected among multiple biopsies in each of three other cases. Therefore, different histologies correlated with separate clones of proliferating B cells in these cases. In the last two cases, the configurations of light chain gene DNA were the same among biopsies in each case, consistent with a monoclonal origin in both lymphomas. However, differences were detected in the configuration of the heavy chain gene DNA. Analysis with a series of DNA probes of the mu heavy chain region indicated that the differences in the DNA configurations of the heavy chain genes from the biopsies probably arose from postrearrangement deletions of either the switch or constant regions of the mu gene. These studies indicate that, contrary to the conventional belief, individual tumors that contain different histologic types of lymphoma within the same patient frequently arise from separate clones of neoplastic cells. Furthermore, the heavy chain genes of monoclonal tumors may show postrearrangement deletions, often resulting from instability of DNA sequences within or around the mu switch region.
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PMID:Frequent biclonality and Ig gene alterations among B cell lymphomas that show multiple histologic forms. 298 7

A 12-year-old boy with severe combined immunodeficiency who had been kept in a gnotobiotic environment since birth received bone marrow from a histoincompatible sibling in an attempt to reconstitute immunologic function. To prevent graft versus host disease, the donor's marrow was treated in vitro with monoclonal antibody and complement to remove alloreactive T cells. Eighty days after transplantation, the patient had a systemic illness characterized by fever, thrombocytopenia, gastrointestinal pain, and bleeding; he died on the 124th post-transplantation day. Postmortem examination revealed multiple tumor-like B-cell proliferations, recipient in origin, in numerous organs. Epstein-Barr virus (EBV) was isolated from the patient's pharyngeal secretions; EBV nuclear antigen was found in spontaneously transformed peripheral-blood lymphocytes, inflammatory cells from peritoneal fluid, and bone marrow cells; and EBV genomes were discovered in all tumor tissues. The donor's serum showed evidence of past EBV infection. Analysis of cellular immunoglobulin and immunoglobulin gene DNA from the tumors indicated both monoclonal and oligoclonal B-cell proliferations. These findings provide evidence for the evolution of EBV-induced polyclonal activation of B cells to oligoclonal B-cell proliferation and finally to monoclonal B-cell lymphoma.
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PMID:Epstein-Barr virus-associated B-cell proliferations of diverse clonal origins after bone marrow transplantation in a 12-year-old patient with severe combined immunodeficiency. 298 67

Recombinant avian leukosis viruses have been constructed from the molecularly cloned DNAs of Rous-associated virus type 1 (RAV-1) and Rous-associated virus type 0(RAV-0). Virus encoded by the cloned RAV-1 DNA induced a high incidence of B-cell lymphoma and a moderate incidence of a variety of other neoplasms. Virus encoded by the cloned RAV-0 DNA did not cause disease. Virus recovered from DNA constructions that encoded the gag, pol, and 5' env sequences of RAV-0 and the 3' env and long terminal repeat sequences of RAV-1 did not cause a high incidence of lymphoma. Rather, these constructed viruses induced a low incidence of a variety of neoplasms. Virus recovered from reconstructed pRAV-1 DNA had the same disease potential as did virus recovered from the parental pRAV-1 DNA. These results indicate that the long terminal repeat sequences of RAV-1 do not confer the potential to induce a high incidence of B-cell lymphoma.
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PMID:Sequences outside of the long terminal repeat determine the lymphomogenic potential of Rous-associated virus type 1. 299 94


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