 Hi there, my name is Frank Sack, I'm a professor in the Department of Pathology at Beth Israel Deaconess Medical Center at Harvard Medical School, and I'm the director of the Neutiform Institute for Irony Medicine here at Harvard Medical School. For the last 15 years or so, we've been extremely interested in studying the roles of microRNAs, these small known coding RNAs, and the control of key oncogenes in cancer. And one of the oncogenes that we've spent a lot of time studying over the past 10 years or so is the oncogene K-RAS. A few years back we showed that it looked like K-RAS had an extremely long 3-prime UTR relative to the rest of the coding sequence of the messenger RNA, suggesting that it was subjected to a lot of microRNA control, and we were able to show that certain microRNAs do indeed regulate the expression of K-RAS. In this new work, we took a reductionist approach and we deleted portions of the K-RAS 3-prime UTR and identified the key, or we thought are key negative and positive regulatory elements within the K-RAS 3-prime UTR. One of the major findings of this paper is that one of these regions that we deleted that looked like it was required for negative regulation of the K-RAS expression looks like it falls within a microRNA binding site to the microRNA MiR-185, and when we deliver MiR-185 to cells, we can repress the levels of K-RAS, we can also show that we can repress the levels of a reporter gene that's under the control of the K-RAS 3-prime UTR. So MiR-185 has emerged for us as an important new regulator of this extremely important oncogene. And that's our hope that we can take these basic science discoveries and translate them into potentially new methods for regulating K-RAS in cancer. So many people know that K-RAS is mutated in about a quarter of all lung cancers and many other types of cancer, including about 95% of pancreatic cancers. And we hope then that MiR-185 might emerge as a new potential therapeutic option when delivered into lung or pancreatic cancer patients that could suppress the levels of activated K-RAS and therefore be therapeutic in that disease.