Endometrial cancer is the most common gynecological cancer among women in the United States. Large-scale epidemiological studies have demonstrated that obesity increases the risk of developing cancers in several different tissues, including endometrium. However, the molecular mechanisms of obesity in tumor development are needed to further elucidate.
DNA methylation, a common epigenetic alteration in solid tumors, includes endometrial cancer. This aberrant event frequently occurs in the promoter CpG islands of a gene and is associated with transcriptional silencing. In normal cells, the majority of CpG islands are generally refractory to chemical modification and remain unmethylated. In contrast, de novo DNA methylation (or DNA hypermethylation) has so far been observed in >200 loci with CpG islands in many different types of cancers.
Currently, Dr. Yi-Wen Huang’s laboratory is investigating how obesity can access endometrial tumorigenesis in a mouse model and how natural occurring chemopreventive agents can modular tumor development by influencing DNA methylation.