scholarly journals Levels of Murine, but Not Human, CXCL13 Are Greatly Elevated in NOD-SCID Mice Bearing the AIDS-Associated Burkitt Lymphoma Cell Line, 2F7

PLoS ONE ◽  
2013 ◽  
Vol 8 (8) ◽  
pp. e72414 ◽  
Author(s):  
Daniel P. Widney ◽  
Tove Olafsen ◽  
Anna M. Wu ◽  
Christina M. R. Kitchen ◽  
Jonathan W. Said ◽  
...  
Keyword(s):  
Cell Line ◽  
Burkitt Lymphoma ◽  
Scid Mice ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Burkitt Lymphoma Cell ◽  
Burkitt Lymphoma Cell Line

scholarly journals Molecular cloning of complex chromosomal translocation t(8;14;12)(q24.1;q32.3;q24.1) in a Burkitt lymphoma cell line defines a new gene (BCL7A) with homology to caldesmon

Blood ◽  
1996 ◽  
Vol 87 (8) ◽  
pp. 3124-3134 ◽  
Author(s):  
VJ Zani ◽  
N Asou ◽  
D Jadayel ◽  
JM Heward ◽  
J Shipley ◽  
...  
Keyword(s):  
Cell Line ◽  
Molecular Cloning ◽  
Burkitt Lymphoma ◽  
Cpg Island ◽  
Lymphoma Cell ◽  
High Grade ◽  
Lymphoma Cell Line ◽  
First Intron ◽  
Burkitt Lymphoma Cell ◽  
Burkitt Lymphoma Cell Line

Chromosome 12q24.1 is a recurrent breakpoint in high-grade B-cell non- Hodgkin lymphoma (B-NHL). To identify the genes involved at 12q24.1, molecular cloning of a three-way translocation t(8;14;12)(q24.1;q32.3;q24.1) in a Burkitt lymphoma cell line (Wien 133) was performed; all four translocation breakpoints were cloned and sequenced. Analysis of clones encompassing the der(12)(12;14)(q24.1;q32.3) breakpoint showed a CpG island from chromosome 12q24.1 juxtaposed in a tail-to-tail configuration with a productively rearranged Ig VH4-DH-JH5 gene. A total of 4.5 kb of genomic DNA including the CpG island was sequenced and analyzed using gene-identification programs; all three programs identified a potential 92-bp exon within the centromeric boundary of the CpG island. Using this as a probe, an RNA transcript of 3.8 kb, expressed at low levels in a wide variety of normal tissues, was detected. Overlapping cDNA clones were isolated and sequenced. The longest open-reading frame predicted a serine-rich protein of 231 amino acids. This protein, termed BCL7A, exhibited no recognizable protein motifs but showed homology with the actin-binding protein, caldesmon. In Wien 133, the BCL7A breakpoint occurred within the first intron and resulted in a MYC- BCL7A fusion transcript, with exon I of BCL7A being replaced by MYC exon I. The normal, untranslocated allele of BCL7A was also expressed without mutation. One of the 11 other B-NHL cell lines examined with 12q24.1 cytogenetic abnormalities, a mediastinal B-NHL cell line (Karpas 1106), showed biallelic rearrangement within the first intron of BCL7A, which was adjacent to the breakpoint observed in Wien 133. Disruption of the amino-terminus of BCL7A defines a new mechanism in the pathogenesis of a subset of high-grade B-NHL.

scholarly journals Integration of Epstein-Barr Virus into Chromosome 6q15 of Burkitt Lymphoma Cell Line (Raji) Induces Loss of BACH2 Expression

2004 ◽  
Vol 164 (3) ◽  
pp. 967-974 ◽  
Author(s):  
Tetsuya Takakuwa ◽  
Wen-Juan Luo ◽  
Maria Francisca Ham ◽  
Femiko Sakane-Ishikawa ◽  
Naoki Wada ◽  
...  
Keyword(s):  
Cell Line ◽  
Burkitt Lymphoma ◽  
Epstein Barr Virus ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Barr Virus ◽  
Burkitt Lymphoma Cell ◽  
Burkitt Lymphoma Cell Line ◽  
Epstein Barr

scholarly journals Burkitt lymphoma cell line carrying a variant translocation creates new DNA at the breakpoint and violates the hierarchy of immunoglobulin gene rearrangement.

1985 ◽  
Vol 5 (11) ◽  
pp. 3199-3207 ◽  
Author(s):  
C T Denny ◽  
G F Hollis ◽  
I T Magrath ◽  
I R Kirsch
Keyword(s):  
Cell Line ◽  
Burkitt Lymphoma ◽  
Gene Rearrangement ◽  
Lymphoma Cell ◽  
Chromosome 8 ◽  
Immunoglobulin Gene ◽  
Lymphoma Cell Line ◽  
Immunoglobulin Gene Rearrangement ◽  
Burkitt Lymphoma Cell ◽  
Burkitt Lymphoma Cell Line

The Burkitt lymphoma cell line KK124, which contains a reciprocal t(8;22) translocation, was shown to have rearranged in a region 3' to the c-myc proto-oncogene on chromosome 8 and 5' to the lambda constant region on chromosome 22. The breakpoint was cloned and sequenced, revealing that c-myc and a portion of its 3' region abutted a complete lambda variable gene that had undergone V-J recombination. Since this cell line expresses kappa light chain, this lambda rearrangement violates the previously proposed hierarchy of immunoglobulin gene rearrangement. A novel duplication of normal chromosome 8 sequences was also found at the breakpoint. The first exon of c-myc and its flanking sequence from the translocated allele was sequenced and compared with a normal counterpart. Extensive mutation was found within the first exon in contrast to its 3' and 5' flanking regions. S1 nuclease analysis revealed that it was the translocated c-myc being expressed and that there was a promoter shift from P2 to P1. The detailed structural analysis of this cell line provides clues concerning mechanisms of chromosomal translocation and c-myc deregulation in Burkitt lymphomas.

Ability of Prenylflavanones Present in Hops to Induce Apoptosis in a Human Burkitt Lymphoma Cell Line

Planta Medica ◽  
2007 ◽  
Vol 73 (8) ◽  
pp. 755-761 ◽  
Author(s):  
Reinhard Diller ◽  
Herbert Riepl ◽  
Oliver Rose ◽  
Corazon Frias ◽  
Günter Henze ◽  
...  
Keyword(s):  
Cell Line ◽  
Burkitt Lymphoma ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Burkitt Lymphoma Cell ◽  
Burkitt Lymphoma Cell Line

Dimethyl sulfoxide (DMSO) causes a reversible inhibition of telomerase activity in a Burkitt lymphoma cell line

1998 ◽  
Vol 22 (8) ◽  
pp. 663-670 ◽  
Author(s):  
Sunil Sharma ◽  
Eric Raymond ◽  
Hiroshi Soda ◽  
Elzbieta Izbicka ◽  
Karen Davidson ◽  
...  
Keyword(s):  
Dimethyl Sulfoxide ◽  
Cell Line ◽  
Burkitt Lymphoma ◽  
Telomerase Activity ◽  
Lymphoma Cell ◽  
Lymphoma Cell Line ◽  
Reversible Inhibition ◽  
Burkitt Lymphoma Cell ◽  
Burkitt Lymphoma Cell Line

Tissue inhibitor of metalloproteinase 1 (TIMP-1) promotes plasmablastic differentiation of a Burkitt lymphoma cell line: implications in the pathogenesis of plasmacytic/plasmablastic tumors

Blood ◽  
2005 ◽  
Vol 105 (4) ◽  
pp. 1660-1668 ◽  
Author(s):  
Liliana Guedez ◽  
Antonio Martinez ◽  
Shumei Zhao ◽  
Angelica Vivero ◽  
Stefania Pittaluga ◽  
...  
Keyword(s):  
B Cell ◽  
Cell Line ◽  
Plasma Cell ◽  
Burkitt Lymphoma ◽  
Lymphoma Cell ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Lymphoma Cell Line ◽  
Tissue Inhibitor ◽  
Burkitt Lymphoma Cell ◽  
Burkitt Lymphoma Cell Line

AbstractTissue inhibitor of metalloproteinase 1 (TIMP-1) is a stromal factor with multiple functions. Overexpression of TIMP-1 correlates with aggressive clinical behavior of a spectrum of tumors. Here, for the first time, we address the role of TIMP-1 in the pathogenesis of B-cell lymphomas. An Epstein-Barr virus (EBV)-negative Burkitt lymphoma cell line with ectopic TIMP-1 expression (TIMP-1JD38) was used to identify genes induced/repressed by TIMP-1. Differentially expressed genes were analyzed by cDNA microarray, and they were validated by immunohistochemistry, flow cytometry, and Western blotting. Analysis revealed changes of genes coding for B-cell growth/differentiation, transcription, and cell cycle regulators. TIMP-1 repressed expression of germinal center (GC) markers CD10, Bcl-6, PAX-5 and up-regulated plasma cell-associated antigens CD138, MUM-1/IRF-4, XBP-1, and CD44, suggesting a plasma cell differentiation. This is accompanied by activation of signal transducer and activator of transcription 3 (STAT-3) and switch to cyclin D2 expression. However, TIMP-1JD38 cells expressed an inactive form of XBP-1, lacking antibody production/secretion. This incomplete plasmacytic differentiation occurs without altering cell proliferation, and despite c-Myc deregulation, indicating an arrested plasmacytic/plasmablastic stage of differentiation. Further validation in human lymphoma cell lines and in primary B-cell tumors demonstrated a predominant TIMP-1 expression in tumors with plasmacytic/plasmablastic phenotypes, including multiple myelomas. These findings strongly support TIMP-1 as an important factor in the pathogenesis of plasmacytic/plasmablastic tumors. (Blood. 2005;105:1660-1668)

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