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)

Two degenerate oligonucleotide primers derived from regions of pol conserved among retroviruses have been synthesized. Polymerase chain reactions utilizing these primers amplify a 135-bp pol fragment in every retrovirus DNA tested to date. The polymerase chain reaction has been linked to a reverse transcriptase step so that a pol-specific DNA fragment can be obtained from a moderate amount of a purified retrovirus or viral RNA. The identity of an unknown retrovirus can be determined by sequencing of the amplified fragment following molecular cloning. This procedure was tested on an unidentified (non-HIV) retrovirus expressed by a B-cell lymphoma line obtained from an AIDS patient. Our PCR assay identified the retrovirus as being highly similar to Mason-Pfizer monkey virus (MPMV) and simian retrovirus 1, which are closely related immunosuppressive type D viruses that cause simian AIDS.
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PMID:The use of primers from highly conserved pol regions to identify uncharacterized retroviruses by the polymerase chain reaction. 169 69

Recently G alpha 16, a new guanosine triphosphate (GTP) binding protein alpha subunit has been described to be specifically expressed in human hematopoietic cells. Expression of G alpha 16 was observed in human cell lines of myelomonocytic and T-lymphocytic origin, but not in human B-cell lines Raji and IM9. We studied the expression of G alpha 16 in human B cells corresponding to different stages of B-cell differentiation by means of reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blotting. The human Burkitt's lymphoma cell lines Raji, Ramos, BJAB, the lymphoblastoid cell line SKW6.4, and the plasmocytoma cell line U266 were devoid of G alpha 16. In contrast, G alpha 16 was detected in the human progenitor B cell lines Reh and Nalm-6. Using the mu+, k- cell line BLIN-1 (pre-B cell phenotype) and its derived subclone 1E8 (surface mu+, k+; B-cell phenotype) G alpha 16 expression was found to disappear on transition from pre-B to B-cell differentiation stage. The analysis of a broad panel of human neoplastic B lymphocytes ranging from progenitor B-acute lymphatic leukemia (pre-pre-B-ALL), common acute leukemias (cALL), pre-B-ALL, mature B-ALL to low grade B-cell lymphoma (chronic lymphocytic leukemia of B-cell type, leukemic centrocytic non-Hodgkins lymphoma [NHL], hairy cell leukemia) showed that G alpha 16 expression is limited to progenitor and pre-B-ALL cells. Therefore, we conclude that within B-cell differentiation, G alpha 16 is expressed solely during early B cell ontogeny and downregulated during differentiation. Thus, G alpha 16 might be an important regulator involved in signaling processes in progenitor B cells.
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PMID:G protein subunit G alpha 16 expression is restricted to progenitor B cells during human B-cell differentiation. 770 90

In general, the large cell lymphomas are a cytogenetically heterogeneous group of diseases, and the cytogenetic findings do not correlate with morphological findings in this group of malignant lymphomas. The CD30-positive anaplastic large cell lymphomas, however, are thought to be an exception, with the t(2;5) reported to correlate with the morphological changes of this disease entity. A subgroup of Hodgkin's disease cases have been reported by some investigators to have the t(2;5) translocation, leading to speculation that these two diseases are related. In the current study, the authors used a sensitive reverse transcriptase polymerase chain reaction (RT-PCR) methodology to evaluate the frequency of t(2;5) in 33 cases of large cell lymphoma, of B lineage, other than anaplastic large cell lymphoma. The authors detected evidence of t(2;5) in four of the cases (12%), a frequency similar to that of the authors' previous study of cases of CD30 positive anaplastic large cell lymphoma. Three of the positive large B-cell lymphoma cases were CD30 negative and were morphologically indistinguishable from the cases without evidence of t(2;5). The fourth case had a subpopulation of CD30 positive cells but also did not have morphological features of anaplastic large cell lymphoma. These results would suggest that t(2;5) is not restricted to cases of malignant lymphomas with anaplastic morphology or to CD30 expression.
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PMID:Detection of the t(2;5)(p23;q35) chromosomal translocation in large B-cell lymphomas other than anaplastic large cell lymphoma. 866 70

The present study demonstrated that a human B-cell line derived from non-Hodgkin's lymphoma. HCF-MLpN. constitutively expressed G-CSF receptor on the cell surface. G-CSF binding to the cell surface was shown by immunofluorescence staining using biotinylated G-CSF preparation and analysed by flow cytometry. Specific binding of G-CSF to the cells was shown by pretreatment with unlabelled G-CSF. In the radioreceptor assay and Scatchard plot analysis using radiolabelled ligand, MLpN cells revealed a single species of binding site with an equilibrium dissociation constant of 167 (153-182) pM and a maximal binding site per cell of 1076 (1044-1116). The G-CSF receptor mRNA transcript was exhibited in the RNA from MLpN cells by reverse transcriptase polymerase chain reaction procedure. [3H]thymidine incorporation and trypan blue exclusion showed that the G-CSF receptor was capable of transducing the growth signal to HCF-MLpN cells. A small fraction of fresh B blasts from six patients with B-cell lymphoma and leukaemia displayed G-CSF binding by two-colour immunofluorescence staining. In contrast, a panel of seven B-cell lines was negative for the binding to biotinylated G-CSF preparation. These results suggest that the phenotype of G-CSF binding may be lost during the culture. The expression of G-CSF receptor in HCF-MLpN cells appeared to be exceptional.
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PMID:Constitutive expression of granulocyte-colony stimulating factor receptor on a human B-lymphoblastoid cell line. 875 83

Seven cases of large B-cell lymphoma which define a previously unrecognized subgroup are reported. Morphologically they are comprised of monomorphic large immunoblast-like cells, containing large central nucleoli, which tend to invade lymphatic sinuses. Superficially they resemble anaplastic large cell lymphoma (ALCL) but they lack CD30. These lymphomas express epithelial membrane antigen (as do ALCL), but also contain intracytoplasmic IgA of a single light chain type (five cases) and an endoplasmic reticulum-associated marker detected by antibody VS38. They lack lineage-associated leukocyte antigens with the exception of CD4 (5 of 5 cases) and CD57 (5 of 7 cases). They are labeled by antibodies detecting both the intracytoplasmic and extracellular regions of the ALK receptor kinase, suggesting that they express the full-length form of this molecule. This was confirmed by Western blotting (in the one case tested) which showed a band of 200 kD in tumor cell lysates, and by polymerase chain reaction (PCR) amplification of mRNA encoding intracellular and extracellular ALK sequences (in the two cases tested). There was no evidence by cytogenetics (one case analyzed) or reverse transcriptase-PCR (three cases tested) of the 2; 5 translocation or the resultant NPM-ALK gene, as is commonly found in ALCL. All but one of the patients were male and all but one were adults, and in all but the latter case the disease followed an aggressive course.
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PMID:A new subtype of large B-cell lymphoma expressing the ALK kinase and lacking the 2; 5 translocation. 905 27

The natural history of follicular lymphoma is to accrue large cells and become diffuse, resulting in progression/transformation to a higher-grade lymphoma. Histologic transformation occurs in approximately 60% of patients. Most often, follicular lymphomas transform into diffuse large cell lymphoma, but transformation to lymphomas classified using the Working Formulation as diffuse mixed, large cell immunoblastic, or small noncleaved cell also have been reported. Evidence of transformation may be found over time in sequential biopsy specimens, or may coexist in the same biopsy specimen. Here, we describe six cases of follicular lymphoma, large cell in five cases and mixed in one case, that transformed into a diffuse or sinusoidal CD30 antigen-positive large cell lymphoma with anaplastic cytologic features. Both the follicular and diffuse/sinusoidal components were of B-cell lineage, positive for the CD20 antigen and negative for the CD3 and CD43 antigens. The neoplastic cells expressed monotypic immunoglobulin light chain in five cases, three kappa and two lambda. BCL-2 protein was positive in four tumors, in both the follicular and diffuse/sinusoidal components in three cases, and only in the latter component in one case. Using the polymerase chain reaction (PCR), three of six cases had monoclonal immunoglobulin heavy chain gene rearrangements. The t(14;18) was not amplified in any case. Using reverse transcriptase (RT)-PCR, the t(2;5) was amplified in one of four tumors. This report highlights the heterogeneity of B-lineage anaplastic large cell lymphomas and indicates the need to consider antecedent follicular lymphoma in any B-cell lymphoma with anaplastic cytologic features.
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PMID:Transformation of follicular lymphoma into CD30-large cell lymphoma with anaplastic cytologic features. 915 76

The PAX5 gene encodes the BSAP (B-cell-specific activator protein) which is a key regulator of B-cell development and differentiation. A recurring translocation t(9;14)(p13;q32) in non-Hodgkin's lymphoma moves the PAX5 on 9p13 within close proximity of the immunoglobulin heavy chain gene (IGH). KIS-1 cell line was established from a patient with diffuse large cell lymphoma of B-cell type carrying t(9;14). We analysed PAX5/BSAP expression by Northern and Western blotting in a panel of haematological tumour cell lines with other chromosome abnormalities in comparison with that of KIS-1. PAX5 mRNA and BSAP expression were detected in all B-cell lines tested, and the high level in KIS-1 was confirmed. However, a diffuse large B-cell lymphoma cell line and an acute B-lymphoid/myeloid leukaemia cell line expressed the PAX5/BSAP at levels comparable with KIS-1. PAX5 transcripts were readily detectable in clinical materials with a wide variety of B-cell neoplasms by reverse transcriptase-mediated polymerase chain reaction (PCR). Thus, PAX5/BSAP activation in haematological tumour cells is not necessarily associated with t(9;14). Although binding sites for BSAP have been identified in the promoters of CD19, this study failed to find clear correlation between the level of PAX5/BSAP expression and that of CD19. In contrast to KIS-1 in which the E mu enhancer of IGH was juxtaposed to PAX5, cloning of t(9; 14) from another case by long-distance PCR revealed that the PAX5 promoter was linked to a Cgamma constant region in divergent orientation, suggesting that the mechanism of PAX5 activation through recombination with IGH varies among individual cases. Breakpoints on 9p13 of the two translocations were clustered upstream of PAX5, leaving the PAX5 coding region intact.
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PMID:Expression of the PAX5/BSAP transcription factor in haematological tumour cells and further molecular characterization of the t(9;14)(p13;q32) translocation in B-cell non-Hodgkin's lymphoma. 972 95

Chronic viral infection has been implicated in the pathogenesis of B-cell lymphoma, and hepatitis C virus (HCV) infects lymphocytes. Chronic infection with HCV may result in B-cell proliferation. Individuals infected with hepatitis C are often co-infected with the RNA virus GB virus type C. Studies from Europe where hepatitis C infection is more common than in North America have shown a high prevalence of hepatitis C infection in patients with B-cell lymphoma. The aim of this study was to establish the prevalence of HCV and GBV-C infection in patients with B-cell lymphoma in an area of low HCV prevalence. One hundred patients with B-cell lymphoma (10 high grade, 46 intermediate grade, and 44 low grade) and 100 controls with nonhematological malignancies were studied. Serum was analyzed for HCV antibodies by third generation enzyme-linked immunosorbant assay, and HCV RNA and GBV-C RNA was analyzed by reverse transcriptase PCR. None of the controls or lymphoma patients had antibodies to HCV. HCV RNA was undetected in 60 out of 100 lymphoma patients tested. GBV-C RNA was detected in the serum of 5 out of 100 (5%) of lymphoma patients and in 3 out of 100 (3%) controls. Hepatitis C and GBV-C are, therefore, unlikely to play a major role in the pathogenesis of B-cell lymphoma in North America.
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PMID:No association between hepatitis C and B-cell lymphoma. 1049 Mar 76

Epidemiological and experimental data suggest that the hepatitis C virus infection might be associated with the development of distinct types of non-Hodgkin's lymphomas. Here, we report a case of a patient with chronic hepatitis C and type II mixed cryoglobulinemia, who developed a primary hepatic non-Hodgkin's B-cell lymphoma. A diffuse, large B-cell lymphoma was diagnosed based on morphological, immunophenotypical and molecular genetic findings. Hepatitis C virus replication, as evaluated by strand-specific reverse transcriptase-polymerase chain reaction, was detected in the nonneoplastic liver, but not in the lymphomatous tissue. High grade non-Hodgkin's lymphomas, although rare complications, have to be considered as part of the spectrum of hepatitis C virus-related hepatic lesions.
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PMID:Primary hepatic diffuse large B-cell lymphoma in a patient with chronic hepatitis C. 1047 74

The translocation of chromosome 11, long arm, region 2, band 1, to chromosome 18, long arm, region 2, band 1 (t(11;18)(q21;q21)) represents a recurrent chromosomal abnormality in extranodal marginal zone B-cell lymphoma (MZBCL) of mucosa-associated lymphoid tissue (MALT) type and leads to a fusion of the apoptosis inhibitor-2 (API2) gene on chromosome 11 and the MALT lymphoma-associated translocation (MLT) gene on chromosome 18. A 2-color fluorescence in situ hybridization (FISH) assay, which can be used for the detection of t(11;18) in interphase nuclei and metaphase chromosomes on fresh and archival tumor tissue, was developed. The P1 artificial chromosome (PAC) clone located immediately telomeric to the MLT gene and the PAC clone spanning the API2 gene were differentially labeled and used to visualize the derivative chromosome 11 resulting from t(11;18), as evident by the overlapping or juxtaposed red and green fluorescent signals. The assay was applied to interphase nuclei of 20 cases with nonmalignant conditions and 122 B-cell non-Hodgkin's lymphomas (NHLs). The latter group comprised 20 cases of nodal follicle center cell lymphoma and diffuse large B-cell NHL, 10 cases of gastric diffuse large B-cell lymphoma, 10 cases of hairy cell leukemia, and 82 cases of MZBCL (41 extranodal from various locations, 19 nodal, and 22 splenic MZBCL) including 35 cases with an abnormal karyotype, 2 of which revealed t(11;18). By interphase FISH, t(11;18) was detected in 8 gastrointestinal low-grade MALT-type lymphomas including the 2 cytogenetically t(11;18)(+) cases. In the 8 t(11;18)(+) cases, the FISH results were confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) using API2 and MLT specific primers. Our results indicate that t(11;18)(q21;q21) specifically characterizes a subgroup of low-grade MZBCL of the MALT-type and that the FISH assay described here is a highly specific and rapid test for the detection of this translocation.
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PMID:Detection of t(11;18)(q21;q21) by interphase fluorescence in situ hybridization using API2 and MLT specific probes. 1097 68


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