University of Rochester scientists, while investigating the two most frequent types of mutations in cancer, discovered a possible new route to treatment that would take advantage of the mutations instead of trying to repair them. The research is reported online this week in the journal Nature Structural & Molecular Biology.
In experiments with rodent and human cells, co-authors Mingxuan Xia, Ph.D., and Hartmut Land, Ph.D., explored how the Rho family of proteins, which are involved in cell movement, and thus in the progression from benign to malignant cancer, are controlled by two well-known cancer genes, p53 and Ras. By closing in on this deadly collaboration, researchers showed for the first time why some molecules such as Rho are targeted by cancer genes - and how they might lead to a promising way to intervene against cancer.
We have very little understanding of how Ras and p53 or any other potent gene mutations cooperate to cause malignant tumors,
said Land, who is professor and chair of the Department of Biomedical Genetics and scientific director of the James P. Wilmot Cancer Center at the University of Rochester. But we have suspected for a long time that the way to develop rational searches for new drug targets is to first understand how these oncogenes cooperate. And in this study we’ve shown for the first time that this idea might work.