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Query: UMLS:C0079731 (
B-cell lymphoma
)
16,671
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The EFII cis element is a 38-bp sequence at the 5' end of the Rous sarcoma virus long terminal repeat, extending from nucleotides -229 to -192 (with respect to the viral transcription start site), which is recognized by sequence-specific DNA-binding proteins in avian fibroblast nuclear extracts (L. Sealy and R. Chalkley,
Mol
. Cell. Biol. 7:787-798, 1987). We demonstrate that multiple copies of the EFII cis element strongly activate transcription of a reporter gene in vivo. We correlate the region of the EFII cis element which activates transcription in vivo with the in vitro binding site for three nuclear factors, EFIIa, EFIIb, and EFIIc. The sequence motif recognized by EFIIa, -b, and -c is also found in consensus binding sites for members of a rapidly growing family of transcription factors related to the CCAAT/enhancer-binding protein (C/EBP). EFIIa, -b, and -c are present in fibroblast and epithelial cell lines from various species but are much less abundant in differentiated rat liver and kidney cells. The EFIIa binding activity is particularly abundant in an avian
B-cell lymphoma
line. As judged from molecular weight analysis, cell type distribution, and sequence recognition properties, the EFII factors under study appear to differ from most of the previously described C/EBP-related factors and thus may expand the diversity of the C/EBP family.
...
PMID:Characterization of nuclear proteins that bind the EFII enhancer sequence in the Rous sarcoma virus long terminal repeat. 132 70
Four allelic forms of the immunoglobulin lambda light chain constant region (C lambda) genes are found in the caucasoid population and are recognised by the presence of Eco RI restriction fragments of sizes 8, 13, 18, and 23 kb hybridising with a C lambda probe. The less common allelic forms of the C lambda genes are marked by the 13, 18, and 23 kb fragments, and these may be misinterpreted as rearranged fragments derived from a monoclonal population of B-cells. The 13, 18, and 23 kb alleles result from the insertion of one, two, and three copies, respectively, of a 5.2 kb repeat unit that can be demonstrated by hybridising genomic DNA digested with Hind III with a C lambda probe. Using selected histologically and immunophenotypically well-defined cases, we assessed the usefulness of the 5.2 kb Hind III/C lambda fragment in distinguishing between rearrangements indicative of a
B-cell lymphoma
and germline configurations representing uncommon allelic forms of the C lambda genes. From these studies, we conclude that Hind III digestion should routinely be performed when using the C lambda probe to assess B-cell monoclonality. Identification of the 5.2 kb Hind III fragment obviates the need to examine DNA from normal peripheral blood granulocytes to exclude allelism of the C lambda genes in cases exhibiting the uncommon restriction fragments after Eco RI digestion.
Diagn
Mol
Pathol 1992 Jun
PMID:Distinguishing between monoclonal rearrangements and allelic forms of the immunoglobulin lambda light chain constant region genes. Significance in the diagnosis of non-Hodgkin's lymphoma. 136 71
Vaccination of BALB/c mice with idiotypic (id) IgM derived from the murine
B cell lymphoma
BCL1, protects the animals from challenge with tumour cells. Escape of the tumour cells from immune control is associated with the selection of variant cells which fail to express significant levels of id IgM on their cell surface. We have previously isolated one such variant, SNAG 1, and shown that, while it expresses less than 10% of the levels of surface IgM of the parental BCL1 lymphoma, it continues to synthesise id material which can be detected within the cell. In this report we present a detailed characterisation of this variant and show that the tumour cells no longer synthesise the lambda light chain. This failure to produce the light chain causes the mu heavy chains in SNAG 1 to remain marooned in the endoplasmic reticulum. The mu heavy chains in SNAG 1 have a normal mol. wt and isoelectric point, and so appear not to be mutated. This is unlike the vast majority of light chain loss variants, in which the heavy chains have been shown to contain deletions. Investigation of the mechanisms responsible for the loss of light chain synthesis demonstrated that, while mRNA for the light chain is present, and of a normal size, there was no production of light chain protein in a cell free system. This indicates that the failure to express light chain by SNAG 1 cells is due to an inability to translate the light chain mRNA into the detectable levels of lambda light chain protein.
Mol
Immunol 1991 Jul
PMID:Characterisation of a light chain loss variant of the BCL1 lymphoma. 164 67
A newly described herpes virus, human herpes virus 6, (HHV-6), has been linked to exanthema subitum but beyond this its pathogenetic impact remains to be determined. A large body of evidence links it to various lymphoproliferative disorders and this study was conducted to identify forms of lymphoproliferation linked to HHV-6. We studied biopsy samples from 32 patients with disorders of the lymphatic system for the presence of HHV-6, both by polymerase chain reaction (PCR) and in-situ hybridization (ISH) methods, as well as Epstein-Barr virus (EBV) viral DNA, clonal rearrangements of the antigen receptor genes and bcl-2 genes. All the specimens were studied morphologically and a clinical follow-up of up to 4 years was obtained. Seven of the 32 patients were positive for HHV-6 DNA and the remainder were negative. Two of these HHV-6 positive specimens, both from elderly persons, showed a similar distinct histological pattern diagnosed as malignant
B-cell lymphoma
of high grade malignancy. Two other HHV-6-positive specimens were reactive lymphadenopathies occurring in younger adults. In addition, one further specimen with evidence of EBV-involvement was from a patient who died 3 months after biopsy with fatal infectious mononucleosis (IM). These five samples had HHV-6 DNA by PCR and ISH. Two specimens without specific histologic abnormalities showed evidence of HHV-6 only by PCR but not by ISH. Both high grade malignant lymphomas showed clonal proliferations, one of monoclonal B-cells and the other of clonal T-cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Virchows Arch B Cell Pathol Incl
Mol
Pathol 1991
PMID:Lymphadenitis and lymphoproliferative lesions associated with the human herpes virus-6 (HHV-6). 168 79
Treatment of splenic B lymphocytes and certain B-lineage cell lines with the mitogen lipopolysaccharide (LPS) and the lymphokine interleukin-4 (IL-4) induces expression of germ line immunoglobulin C epsilon transcripts and class switching to the C epsilon gene. We show that LPS-plus-IL-4 induction of germ line epsilon transcripts (termed I epsilon transcripts) occurs at the transcriptional level in an Abelson murine leukemia virus-transformed pre-B-cell line. A 1.1-kb region of DNA surrounding the I epsilon promoter endows inducible transcription to a heterologous reporter gene stably transfected into these cells; such inducible expression depends on combined treatment with LPS and IL-4. Analyses of constructs transiently introduced into a
B-cell lymphoma
line demonstrated that LPS-plus-IL-4-inducible expression can be conferred by a 179-bp segment of DNA spanning the I epsilon transcriptional initiation site. Mutational analyses demonstrated that this expression depended on DNA sequences within a conserved region directly upstream from the I epsilon transcriptional initiation region. One nuclear protein that is constitutively expressed in normal B cells binds to the downstream end of the conserved sequence; its binding specificity correlates with the functional effect of several mutations. Two additional proteins, which are induced by IL-4 treatment of splenic B cells, bind to the transcription initiation sites of I epsilon. These proteins are indistinguishable in binding assays from proteins previously shown to bind an enhancer region of the class II major histocompatibility complex gene A alpha.
Mol
Cell Biol 1991 Nov
PMID:Identification of a conserved lipopolysaccharide-plus-interleukin-4-responsive element located at the promoter of germ line epsilon transcripts. 192 63
We analyzed the overall structures of N-linked oligosaccharides on glycoproteins of various murine lymphocytic and lymphoma cells employing a newly developed method which was performed on high-performance liquid chromatography after derivatization of oligosaccharides with 2-aminopyridine. A total of 15 types of bi, tri- and tetra-antennary N-acetyllactosamine-type oligosaccharides with or without fucose and oligomannose-type oligosaccharides were identified on these cells in variable amounts depending on the type and maturation stage of the cells. It was found that all murine lymphocytic cells carry N-acetyllactosamine-type oligosaccharides with the additional alpha-linked galactose residue on the non-reducing ends. Thymocytes had exceptionally large amounts of oligosaccharides with one or even two alpha-galactose residues per molecule. In contrast, peripheral resting T cells possessed those oligosaccharides only in a small amount, although the cells produced more the oligosaccharides after stimulation with Con A. Two thymoma lines such as BW 5147 and EL-4 and one
B cell lymphoma
line WEHI231 contained relatively large amount of oligosaccharides with alpha-galactose residues. Significant change of the molar ratio of component carbohydrates by cell activation was observed also in oligommanose-type oligosaccharides which were few in resting T cells but were markedly increased in Con A activated cells. Molar ratio of triantennary oligosaccharides in total N-acetyllactosamine type oligosaccharides was high in thymocytes and low in resting T cells, but was increased in T cells after Con A activation. It was also very high in WEHI 231
B cell lymphoma
. Although BW 5147 and EL-4 thymoma did not contain tri-antennary oligosaccharides in high proportion, they carried larger tetra-antennary oligosaccharides with an N-acetyllactosamine repeating unit in definitive amounts. It is suggested from these results that overall structures of oligosaccharides on cell surface proteins of lymphocytes are finely controlled with link to cell differentiation, activation and transformation.
Mol
Immunol 1991 Oct
PMID:Cell type and maturation stage-dependent polymorphism of N-linked oligosaccharides on murine lymphocytes and lymphoma cells. 192 4
109 malignant lymphomas were surveyed by Southern blot analysis and polymerase chain reaction (PCR) for Epstein-Barr virus (EBV) DNA and compared with 16 examples of non-neoplastic lymphadenopathy and 4 normal thymuses. In specimens positive by the method of Southern and PCR, in situ hybridization studies were performed on formalin-fixed, paraffin-embedded sections. By Southern blot analysis, two of seven Hodgkin's disease samples (29%) (one of mixed cellularity and the other of lymphocyte predominance type), three of 56 B-cell lymphomas (5.6%) and five of 46 T-cell lymphomas (11%) demonstrated EBV DNA. However, the 16 examples of lymphadenitis and the 4 normal thymuses showed no EBV DNA. With PCR, EBV DNA was identified in one
B-cell lymphoma
, nine T-cell lymphomas, ten lymphadenitis specimens and two of the normal thymus, in addition to the positive specimens determined by the Southern blotting method. These results indicate that the presence of EBV DNA is not related to lymphoid malignancy, but enhancement of the DNA is demonstrated in some neoplastic conditions. By in situ hybridization, EBV genomes were not detected in all PCR-positive cases, but only in those positive by Southern blot analysis.
Virchows Arch B Cell Pathol Incl
Mol
Pathol 1990
PMID:Analysis of Epstein-Barr viral genomes in lymphoid malignancy using Southern blotting, polymerase chain reaction and in situ hybridization. 198 7
We describe the structure of the major germ line RNA transcribed from unrearranged immunoglobulin alpha heavy-chain genes in immunoglobulin M-expressing cells of the I.29 mu
B-cell lymphoma
, a cell line capable of switching to immunoglobulin A expression upon lipopolysaccharide treatment. This germ line alpha RNA has a small open reading frame that does not include the C alpha domain, and this RNA appears to be present on polysomes in I.29 mu cells.
Mol
Cell Biol 1990 Jan
PMID:Structure of germ line immunoglobulin alpha heavy-chain RNA and its location on polysomes. 215 64
Endogenous mouse mammary tumor virus (MMTV) proviral transcripts are up regulated during the normal course of B-lymphocyte differentiation. We report here that the regulatory mechanisms which lead to increased levels of MMTV transcripts in differentiating, lipopolysaccharide (LPS)-stimulated normal B cells and in the inducible
B-cell lymphoma
line CH12 are at least partially distinct from those controlling increases in immunoglobulin and J-chain gene expression. In studies designed to characterize the stimulatory pathways leading to MMTV expression in CH12 cells, we found that stimulation with either LPS or dexamethasone (Dex), a transcriptional activator of MMTV genes, induced not only MMTV expression but also differentiation to antibody secretion. Only Dex-induced and not LPS-induced MMTV expression and differentiation were inhibited by the glucocorticoid antagonist RU486, demonstrating that Dex and LPS stimulate B cells by distinct molecular pathways. Therefore, in B cells, MMTV expression can be regulated via either the conventional hormone receptor-dependent pathway or a hormone receptor-independent pathway. Furthermore, these results suggest that steroid stimulation of B cells can lead to alterations in the expression of other results suggest that steroid stimulation of B cells can lead to alterations in the expression of other steroid-responsive genes that can become involved in the process of B-cell differentiation.
Mol
Cell Biol 1990 Aug
PMID:Lipopolysaccharide and dexamethasone induce mouse mammary tumor proviral gene expression and differentiation in B lymphocytes through distinct regulatory pathways. 216 35
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.
Mol
Cell Probes 1990 Oct
PMID:Oligonucleotides for polymerase chain reaction amplification and hybridization detection of Epstein-Barr virus DNA in clinical specimens. 217 46
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