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Functional genomics and rheumatoid arthritis: where have we been and where should we go?

James N Jarvis1* and Mark Barton Frank2

Author Affiliations

1 Department of Pediatrics, Pediatric Rheumatology Research, Basic Science Education Building #235A, University of Oklahoma College of Medicine, Oklahoma City, Oklahoma 73104, USA

2 Microarray Research Facility, Arthritis and Immunology Program, Oklahoma Medical Research Foundation, 840 NE 13th Street, Oklahoma City, Oklahoma 73104, USA

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Genome Medicine 2010, 2:44  doi:10.1186/gm165

Published: 28 July 2010


Studies in model organisms and humans have begun to reveal the complexity of the transcriptome. In addition to serving as passive templates from which genes are translated, RNA molecules are active, functional elements of the cell whose products can detect, interact with, and modify other transcripts. Gene expression profiling is the method most commonly used thus far to enrich our understanding of the molecular basis of rheumatoid arthritis in adults and juvenile idiopathic arthritis in children. The feasibility of this approach for patient classification (for example, active versus inactive disease, disease subsets) and improving prognosis (for example, response to therapy) has been demonstrated over the past 7 years. Mechanistic understanding of disease-related differences in gene expression must be interpreted in the context of interactions with transcriptional regulatory molecules and epigenetic alterations of the genome. Ongoing work regarding such functional complexities in the human genome will likely bring both insight and surprise to our understanding of rheumatoid arthritis.