These authors contributed equally to this study.
Profiling Meta-Analysis Reveals Primarily Gene Coexpression Concordance between Systemic Lupus Erythematosus and Rheumatoid Arthritis
Article first published online: 27 SEP 2007
DOI: 10.1196/annals.1423.005
Issue

Annals of the New York Academy of Sciences
Volume 1110, Autoimmunity, Part B Novel Applications of Basic Research pages 33–46, September 2007
Additional Information
How to Cite
SILVA, G. L., JUNTA, C. M., MELLO, S. S., GARCIA, P. S., RASSI, D. M., SAKAMOTO-HOJO, E. T., DONADI, E. A. and PASSOS, G. A. S. (2007), Profiling Meta-Analysis Reveals Primarily Gene Coexpression Concordance between Systemic Lupus Erythematosus and Rheumatoid Arthritis. Annals of the New York Academy of Sciences, 1110: 33–46. doi: 10.1196/annals.1423.005
Publication History
- Issue published online: 27 SEP 2007
- Article first published online: 27 SEP 2007
- Abstract
- Article
- References
- Cited By
Keywords:
- systemic lupus erythematosus;
- rheumatoid arthritis;
- cDNA microarray meta-analysis
Abstract: Consensus gene expression profiling by meta-analysis of 4,500 cDNA sequence microarray data obtained from patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) was assembled and systematically analyzed. The normalized data were statistically analyzed by the significance analysis of microarray (SAM) program (false discovery rate ≤ 0.01). Patient data input was realized together, in the Cluster and Tree-View program, using the unsupervised function. Individual expression signatures permitted a hierarchical clustering of samples, separately identifying SLE and RA patients and the transcriptome profiling featured modules of the specifically induced or repressed and the comodulated genes. Gene expression profiling meta-analysis showed that patients with SLE or RA share gene modulation but also present genes whose expression patterns are exclusive (induced or repressed) in corroboration with their clinical features. Among the genes that were differentially expressed, we found those that could play specific roles in these two diseases. This approach permits a clearer understanding of the molecular basis of SLE and RA concordance/divergence.

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