Scientists at the Duke Cancer Institute have found evidence of epigenetics at work on a genome-wide scale in cases of ovarian cancer. One major biological signaling pathway in particular was found to contain many genes influenced by DNA methylation, a mechanism for turning off genes, in tumor cells.The study showed for the first time that TGF-beta pathway function is regulated through methylation. This is only one piece of a larger puzzle about the biology of ovarian cancer, but we can say that DNA methylation does have an influence on suppressing TGF-beta pathway signaling, which contributes to ovarian cancer. The Scientists conducted a series of studies on cancer cell lines and primary tumor specimens from ovarian cancer patients by comparing the genome-wide gene expression profiles of cells that were treated or mock-treated with drugs that inhibit DNA methylation. They identified 378 candidate methylated genes, and from these all 43 of the predicted genes the researchers analyzed showed methylation in ovarian cancers. Scientists treated tumor cells with methylation inhibitors, the TGF-beta pathway showed increased activity. This is an important signaling pathway that directs many processes in cells. A perfectly functioning TGF-beta pathway ensures proper cell growth, cell differentiation, and apoptosis (programmed cell death), and helps prevent tumor formation. When this pathway isn’t regulated, it can instead help tumors grow and metastasize.In addition, the genes they studied included a cluster of genes that strongly correlated with TGF-beta pathway activity in specimens from older women, which suggested that age-related epigenetic changes can accumulate and may contribute to cancer.