Novel inhibitor implicates the TORC2 kinase in genome stability

FMI scientists have identified a novel inhibitor, which synergizes with low-doses of other DNA damaging agents, to induce a dramatic chromosome fragmentation even in normal cells. Unexpectedly, the compound acts an as inhibitor of a large kinase complex called TORC2, which regulates actin polymerization. With this study the scientists revealed a previously unappreciated link between the cytoplasmic regulator TORC2, actin, and repair of DNA damage. Since the 1960s, combinations of chemotherapies have been used in cancer treatments, first mostly to reduce the risk of resistance, then, as cancer-driving mutations became better understood, to be able to interfere with several molecular processes in the cancer at the same time. Over the years, combination therapies have become increasingly sophisticated. Currently, scientists are searching for new combination therapies that provoke cell death in well-defined situations, such as in cells that carry cancer enhancing mutations. The group of Susan Gasser, Director and Group leader at the Friedrich Miescher Institute for Biomedical Research, in collaboration with colleagues from the Novartis Institutes for BioMedical Research, have identified a very powerful inhibitor that enhances the effects of other chemotherapeutics in cancer cells.