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

To determine whether a nonisotopic procedure is suitable for analyzing clinical specimens for gene rearrangements, the authors hybridized DNA from 15 specimens of lymphoid tissue with biotinylated DNA probes directed to J beta I + J beta II (T-cell receptor beta chain gene), JH (immunoglobulin gene heavy chain J region), and J kappa (immunoglobulin gene kappa light chain J region). Five cases of benign lymphoid hyperplasia, one case of dermatopathic lymphadenopathy, and one case of small noncleaved follicular center cell lymphoma had germline hybridization patterns when digested with Bam HI, Eco RI, and Hind III restriction endonucleases. Four cases of B-cell lymphoma and three cases of T-cell lymphoma had clearly detectable rearrangements of the genes for immunoglobulin or the T-cell receptor or both. One case of dermatopathic lymphadenopathy had a faint, clonal rearrangement of the T-cell receptor after digestion with Eco RI and Bam III. The authors conclude that biotinylated DNA probes can be useful for analyzing gene rearrangements in clinical specimens.
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PMID:Evaluation of biotinylated DNA probes for the detection of gene rearrangements in clinical specimens. 217 86

We designed synthetic oligonucleotide primers and hybridization probe for use in polymerase chain reaction (PCR) amplification and hybridization detection of Epstein-Barr virus (EBV) nucleic acid sequences. Primer sequences were chosen from the coding region for the Epstein-Barr virus nuclear antigen-1 (EBNA-1). PCR amplification and hybridization with these oligonucleotides was carried out on standard laboratory cell lines including African Burkitt's lymphoma and infectious mononucleosis derived cell lines, as well as cell lines recently established from clinical EBV isolates from bone marrow transplant recipients. All EBV cell lines tested were positive. No false-positives were detected with uninfected cell lines, human placental DNA or with other viruses. The sensitivity of the detection procedure was such that four copies of the EBV genome could consistently be detected in a background of 1 microgram of placental DNA. EBV was detected in DNA extracts from the peripheral blood mononuclear cells of two patients with infectious mononucleosis and one patient with viral-associated hemophagocytic syndrome. Three of 18 EBV seropositive patients without known ongoing EBV-associated illness undergoing ambulatory surgery also had EBV detected in DNA extracts from their peripheral blood mononuclear cells. EBV was detected in DNA extracts from lymphoma tissue from two patients with post-transplant lymphomas and two AIDS patients with primary CNS lymphomas. EBV was not detected in 12 B-cell lymphoma specimens from patients without history of immunocompromise. DNA extracts from formalin-fixed paraffin-embedded Hodgkin's tissues previously shown to be EBV positive by Southern blot were also demonstrated to be EBV positive by PCR. Thus, with the oligonucleotides described, PCR is applicable to the detection of EBV in a spectrum of clinical isolates. The broad specificity of these oligonucleotides for all strains of EBV tested is probably a function of the highly conserved sequence of the EBNA-1 DNA binding domain.
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PMID:Oligonucleotides for polymerase chain reaction amplification and hybridization detection of Epstein-Barr virus DNA in clinical specimens. 217 46

The t(14; 18) chromosomal translocation of human follicular lymphoma recombines the bcl-2 gene from chromosome 18 with the immunoglobulin heavy chain joining region. In the t(14; 18) translocation bearing cell line SU-DHL-6, this results not only in an inappropriately high rate of bcl-2 transcription for a mature B cell, but also in two potentially critical point mutations. To determine the relative importance of these mutations, we searched for their presence in DNA from the involved lymph nodes of 12 patients with t(14; 18) follicular lymphoma. bcl-2 genomic sequences were specifically amplified by the polymerase chain reaction technique and then directly sequenced. None of the 12 samples analysed revealed the codon 7 or codon 129 mutation detected in SU-DHL-6. We conclude that abnormal expression of bcl-2 rather than structural alterations at codon 7 or 129 play an important role in the disordered growth and differentiation of follicular B-cell lymphoma.
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PMID:Mechanism of bcl-2 activation in human follicular lymphoma. 218 81

A major obstacle to investigations of Hodgkin's disease is the paucity of malignant cells, i.e., Reed-Sternberg cells and their variants, in tissues of patients with this disease. Consequently, the pathogenesis, cell of origin, and clonality of this relatively frequent lymphoma have remained unresolved. Results of recent studies suggest that in some instances Reed-Sternberg cells carry rearranged immunoglobulin heavy-chain joining region (JH) loci as well as chromosomal translocations involving band 14q32. Prompted by these findings, we sought to determine if the t(14;18) (q32;q21) translocation of follicular, non-Hodgkin's B-cell lymphoma was associated with Hodgkin's disease. To detect the possible t(14;18) (q32;q21) translocation within the rare malignant cells of Hodgkin's disease, we amplified sequences created by the t(14;18) translocation using the polymerase chain reaction (PCR). With this approach, DNA sequences carrying the direct fusion of the major breakpoint region of the candidate oncogene, bcl-2, derived from chromosome 18q21, with JH on chromosome 14q32 can be detected in as few as one in 10(5)-10(6) cells. In the present study, joined bcl-2/JH sequences were detected in tissues involved by Hodgkin's disease in 17 of 53 (32%) patients. The frequent association of bcl-2 translocation with Hodgkin's disease suggests that this oncogene has a role in the pathogenesis of Hodgkin's disease. That bcl-2 is involved in a major class of lymphoma in addition to follicular lymphoma implies a role for additional factors responsible for generating the two distinctive clinical and pathologic disease states.
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PMID:Involvement of the bcl-2 gene in Hodgkin's disease. 233 93

Most composite lymphomas which are composed morphologically of two different tumor cell types are considered to represent different morphological expressions of a single clone. However, in recent years, composite B- and T-cell lymphomas and biclonality of B-cell lymphoma have been reported. We experienced a case of composite lymphoma which initially developed as cutaneous lymphoma composed of lymphoplasmacytes associated with large clear cells. It was confirmed that the tumor cells of these two systems were biclonal on the basis of surface markers and DNA rearrangements, i.e. B cells of the IgG kappa type, showing IgH and kappa chain DNA rearrangement, and T-cells with CD4 surface marker, showing rearrangement of the T-cell receptor beta chain gene. This case showed a predominant B-cell pattern at the initial stage, and terminated in T-cell lymphoma, as revealed at autopsy. Therefore we considered this case to be a unique composite lymphoma showing biclonality of both B- and T-cell systems, providing a number of suggestions for future study of malignant lymphoma.
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PMID:Biclonality of composite B- and T-cell lymphomas. A case report. 222 Mar 99

Genotypic analysis has led to the implication of certain oncogenes in the pathogenesis of specific groups of non-Hodgkin's lymphoma. Rearrangements of c-myc are associated with Burkitt's lymphoma and of bcl-2 with centroblastic/centrocytic lymphoma. Rearrangement of bcl-1 has yet to be associated with a specific group of lymphoma. In this study DNA from 62 cases of low grade B-cell lymphoma, classified using the Kiel classification, were analysed by Southern blotting and hybridization with probes to bcl-1, bcl-2, and c-myc. Rearrangements of bcl-2 were found in a proportion of centroblastic/centrocytic lymphoma comparable to other published studies. Rearrangement of c-myc was not found in any case studied. Bcl-1 rearrangement was found in 2/9 cases of B-CLL, and 3/6 cases of centrocytic lymphoma. This incidence of bcl-1 rearrangement in centrocytic lymphoma suggests that it is a characteristic change. No rearrangement of bcl-1, bcl-2 or c-myc was found in any case of lymphoma of mucosa associated lymphoid tissue (MALT), providing further evidence that, in spite of having a similar morphology to some other groups of low grade B-cell lymphoma, lymphomas of MALT comprise a distinct entity.
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PMID:A genotypic study of low grade B-cell lymphomas, including lymphomas of mucosa associated lymphoid tissue (MALT). 225 Jan 91

There is a significantly increased incidence of malignant lymphoma in patients with acquired immunodeficiency syndrome (AIDS). The lymphomas are usually of a high grade and of B-cell phenotype. While the frequent presence of reactive monocytoid B lymphocytes in patients with AIDS-related lymphadenopathy has recently been documented in several studies, to our knowledge, there are no reported cases of monocytoid B-cell lymphoma, the neoplastic counterpart of monocytoid B lymphocytes, in patients with AIDS. We now describe a human immunodeficiency virus (HIV)-positive patient with HIV-related lymphadenopathy in whom monocytoid B-cell lymphoma developed during the course of his disease. The morphologic and immunologic features of the lymphoma were characteristic of monocytoid B-cell lymphoma, and the involved lymph node exhibited a reversed CD4/CD8 ratio. Moreover, using the polymerase chain reaction, we were able to demonstrate HIV genome in DNA extracted from the lymph node tissue. To our knowledge, this is the first report of a case of monocytoid B-cell lymphoma occurring in an HIV-positive patient and in which we were able, by using a sensitive molecular biologic technique, to demonstrate HIV sequence in paraffin-embedded, fixed lymph node sections.
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PMID:Monocytoid B-cell lymphoma in a patient with human immunodeficiency virus infection. Demonstration of human immunodeficiency virus sequences in paraffin-embedded lymph node sections by polymerase chain reaction amplification. 225 23

Six unusual cases diagnosed by various scientific methods are described to highlight the role of the histopathologist in clinical ophthalmology. The first case shows the importance of fast tissue diagnosis to prevent possible radical treatment in a limbal pseudotumour. The second presentation is of a small conjunctival mass with orbital involvement, immunohistochemically a B-cell lymphoma and occurring after a recent testicular tumour. The third patient presented with the rarely described nodular hypersensitivity conjunctivitis (Splendore-Hoeppli reaction) and it is suggested that these ophthalmologically observed asymptomatic lesions are apparently clinically transient so reports may be few because of infrequent biopsy. Pan-uveal melanocytic tumours concurrent with thoracic or abdominal carcinoma are reviewed. DNA flow cytometry could, perhaps, assess those ocular lesions for malignancy. The fourteenth case in the literature of lacrimal sac melanoma and possibly the first by tear seedling is illustrated. Lastly, a paediatric orbital fibrous histiocytoma is a cautionary anecdote with successful outcome.
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PMID:Peculiar ophthalmic proliferations. 232 82

A case of malignant lymphoma showing in a lymph node the characteristic morphologic features of the so-called monocytoid B-cell lymphoma (MBCL) is described. This case differs from the reported cases in the literature because atypical cells were observed in the bone marrow biopsy and marrow and peripheral blood smears that were obtained from the patient, a 61-year-old man, during the staging procedures. Lymphocyte surface marker studies on peripheral blood by flow cytometry and DNA analysis revealed a monoclonal population of lambda-positive lymphocytes. The immunophenotype of MBCL cells was studied both in paraffin-embedded lymph node sections by immunoperoxidase method and in peripheral blood by flow cytometric analysis; the cells expressed the SIg with lambda light chain restriction and the HLA-DR antigen; they also had positive results for B-cell-associated antigens, including LN1, LN2, CD 20, CD 22, CD 19, CD 9 but not CD 21, CD 24, and CD 10, T-cell-associated antigens and monocytic markers. In addition, they had negative results for CD 25, CD 38, PCA-1. This report emphasizes that in MBCL, peripheral and marrow involvement may occur at presentation analogous to other low-grade B-cell lymphomas. The immunophenotypic characteristics of MBCL cells, though not pathognomonic, are considered to be helpful in differentiating them from circulating cells of other B-cell lymphomas.
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PMID:Monocytoid B-cell lymphoma with bone marrow and peripheral blood involvement at presentation. 236 May 58

Infection of young chickens with RAV-1, a subgroup A isolate of avian leukosis virus, results in the development of lymphoid leukosis, a B-cell lymphoma characterized by provirus insertion into the c-myc locus. We report here that when 12- to 13-day-old embryos rather than 1-day-old chickens were infected with RAV-1, a novel B-cell lymphoma developed in which proviral insertions had activated expression of the c-myb gene. These tumors expressed elevated levels of a 4.5-kilobase myb-containing mRNA transcript that contained c-myb sequences not found in v-myb. The c-myc locus in these tumors appeared normal. The biological properties of the activated myb lymphoma were distinct from those of lymphoid leukosis. Metastatic disease developed within 7 weeks of infection. Distinct intermediate pathogenic stages with preneoplastic and primary neoplastic lesions were not detected. Although bursal tissues appeared to be nonmalignant on gross examination, Southern analyses of bursal DNA revealed the presence of tumor with the same clonal origin as abdominal lymphoma masses. The dependence on embryonic infection for development of activated myb lymphoma suggests that the target cells in which c-myb is activated are found only in embryos and are distinct from those cells that give rise to lymphoid leukosis.
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PMID:RAV-1 insertional mutagenesis: disruption of the c-myb locus and development of avian B-cell lymphomas. 253 46


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