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Status |
Public on Jan 20, 2010 |
Title |
Expression data from Epstein-Barr virus -positive and negative Akata Burkitt's Lymphoma Clones |
Organism |
Homo sapiens |
Experiment type |
Expression profiling by array
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Summary |
Transition of Akata Burkitt lymphoma (BL) cells from a malignant to nonmalignant phenotype upon loss of Epstein-Barr virus (EBV) genomes in vitro is evidence for a viral contribution to tumor maintenance despite the tightly restricted pattern of EBV gene expression in BL. Akata cells retaining virus manifest increased resistance to apoptosis under growth limiting conditions, although ambiguity exists regarding the exact mechanisms involved. By examining global cellular gene expression differences in Akata subclones that had either retained or lost EBV, we identified spermidine/spermine N1-acetyltransferase (SSAT), an inducible acetylating enzyme whose catabolism of polyamines affects both apoptosis and cell growth, as one of a limited number of cellular genes up-regulated upon loss of EBV.
Keywords: Disease state analysis
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Overall design |
We used Affymetrix microarrays to examine variations in global gene expression between the paired EBV-positive (1B6) and EBV-negative (2A8) Akata Burkitt's lymphoma clones. EBV-negative Akata clones were generated by treatment with hydroxyurea, an inhibitor of ribonucleotide reductase that forced rapid loss of EBV episomes and compared to their EBV-positive counterparts. Logarithmically growing EBV-negative and positive Akata EBV clones were seeded at 2.5x10^5 cells/ml in RPMI1640 supplemented with 10% fetal bovine serum, 2mM glutamine, and 100units/ml penicillin/streptomycin. The next day, the cells were incubated for 4 hours in media containing 1% fetal bovine serum (low serum), 2mM glutatmine and 100units/ml penicillin/streptomycin to begin selection of the Akata tumor phenotype. The short incubation time was intended to minimize cell death and other potential downstream effects of low serum treatment, while at the same time initiating expression changes contributing to the tumorigenic phenotype.
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Contributor(s) |
Scott RS, Sixbey JW |
Citation(s) |
23891576 |
Submission date |
Jan 06, 2010 |
Last update date |
Aug 08, 2019 |
Contact name |
Rona S. Scott |
E-mail(s) |
rscott1@lsuhsc.edu
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Phone |
318-675-6263
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Organization name |
Louisiana State University Health Sciences Center-Shreveport
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Department |
Microbiology and Immunology
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Street address |
1501 Kings Highway
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City |
Shreveport |
State/province |
LA |
ZIP/Postal code |
71130 |
Country |
USA |
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Platforms (1) |
GPL8300 |
[HG_U95Av2] Affymetrix Human Genome U95 Version 2 Array |
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Samples (6)
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GSM493574 |
2A8 EBV-negative Akata BL clone,4hr starve, biological rep 1 |
GSM493575 |
2A8 EBV-negative Akata BL clone, 4hr starve, biological rep 2 |
GSM493576 |
2A8 EBV-negative Akata BL clone, 4hr starve, biological rep 3 |
GSM493577 |
1B6 EBV-positive Akata BL clone, 4hr starve, biological rep 1 |
GSM493578 |
1B6 EBV-positive Akata BL clone, 4hr starve, biological rep 2 |
GSM493579 |
1B6 EBV-positive Akata BL clone, 4hr starve, biological rep 3 |
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Relations |
BioProject |
PRJNA121843 |
Supplementary file |
Size |
Download |
File type/resource |
GSE19761_RAW.tar |
15.5 Mb |
(http)(custom) |
TAR (of CEL, CHP) |
Processed data included within Sample table |
Processed data provided as supplementary file |
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