Joint Linkage and Imprinting Analyses of Rheumatoid Arthritis Data
Author Information
Author(s): Zhou Xiaojun, Chen Wei, Swartz Michael D, Lu Yue, Yu Robert, Amos Christopher I, Wu Chih-Chieh, Shete Sanjay
Primary Institution: The University of Texas M. D. Anderson Cancer Center
Hypothesis
Are imprinted genes involved in susceptibility to rheumatoid arthritis?
Conclusion
Imprinted genes are unlikely to be involved in susceptibility to rheumatoid arthritis, although a point-wise p-value of 0.03 for the TGFBR3 gene was found for imprinting.
Supporting Evidence
- Imprinted genes have been implicated in several human disorders.
- Only 41 transcriptional units have been identified as imprinted in humans.
- The study used both model-based and model-free methods for analysis.
- Significant signals for linkage were found for gene expression data.
- Two regions showed significant imprinting in Hispanic families.
Takeaway
The study looked at whether certain genes that are inherited differently based on which parent they come from affect rheumatoid arthritis, and found that they probably don't.
Methodology
The study used genome-wide joint linkage and imprinting scans on data from high-risk rheumatoid arthritis families and gene expression data.
Limitations
The study was exploratory and did not exhaustively search for all imprinted genes.
Participant Demographics
659 Caucasian and 29 Hispanic families were included in the study.
Statistical Information
P-Value
0.03
Statistical Significance
p<0.05
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