ive age, and they become symptomatic in 2530% of all women and in up to 70% of African American women of reproductive age. Compared with white women, African American women are 3 times more likely to develop symptomatic leiomyoma, which also develops at earlier ages with more numerous and larger fibroids. The clinical symptoms associated with uterine leiomyoma are abZotarolimus normal uterine bleeding, which can lead to anemia, pelvic pressure and pain; reduced fertility; and frequent pregnancy loss. In the United States, 600,000 hysterectomies are performed each year; of these, approximately 40% are performed to treat uterine leiomyoma. The surgical costs alone represent an economic burden of $2 billion per year, and when taking into account the social costs and associated long-term health problems, it is clear that better prevention and treatment options for women with uterine leiomyoma are urgently needed. Understanding the molecular mechanisms underlying the pathogenesis of uterine leiomyoma will facilitate the discovery and development of new approaches to the treatment of this disease. Gene expression profile studies have demonstrated that hundreds of genes with critical functions in differentiation, apoptosis, proliferation and extracellular matrix formation are dysregulated in uterine leiomyoma. Currently, a few cytogenetic aberrations in specific genes have been discovered; however, it remains unknown whether these dysregulated genes act as effectors or growth promoters in uterine leiomyoma. Epigenetic mechanisms such as DNA methylation, histone modification, and non-coding RNAs are described as heritable changes in gene expression not associated with changes in the primary DNA sequence; rather, these changes affect secondary interactions that play a crucial role in the regulation of gene expression. In the mammalian genome, DNA methylation is the most common and well-characterized epigenetic mark, which consists of the covalent addition 23416332” of a methyl group to the 59-carbon of the cytosine ring within the context of CpG dinucleotides following replication. The methylation of this cytosine is catalyzed by specific DNA methyltransferases, which transfer a methyl group, from the donor S-adenosyl methionine to Genome-Wide DNA Methylation in Uterine Leiomyoma the 59-position of the pyrimidinic ring. Recent studies reveal that there is differential expression of DNMTs in uterine leiomyoma and that there is aberrant DNA methylation in uterine leiomyoma compared with normal myometrial tissue. One study demonstrated that hypomethylation of ESR1 in uterine leiomyoma correlates with increased mRNA expression in uterine leiomyoma. These findings suggest that, DNA methylation might play a key role in the pathogenesis of uterine leiomyoma by altering the normal myometrial mRNA expression profile. Further characterization of the role of epigenetics in the tumorigenesis of uterine leiomyoma, requires an analysis of global, genome-wide DNA methylation in disease and normal uterine tissue. The objective of this study was to determine the relationship between differential DNA methylation and mRNA expression in uterine leiomyoma by performing a genome-wide analysis. We sought to determine whether differentially regulated genes 
in uterine leiomyoma versus adjacent normal 18003836” myometrial tissue are under epigenetic control. We attempted to identify a subset of genes whose differential DNA methylation correlated with differential mRNA expression. Our findings will adva