MIT News
November 14, 2013
Mutation of the p53 gene occurs in about half of all cancer patients, and tumors with the mutation continue growing even after intense chemotherapy. Previously, the lab of Michael Yaffe, David H. Koch Professor of Biology and Biological Engineering, discovered that blocking a gene called MK2 can overcome the effects of the p53 mutation and make these tumors more vulnerable to chemotherapy in vitro. In a new study published in Cell Reports, Yaffe lab researchers collaborated with KI Director Tyler Jacks to create mice with MK2 genes that can be turned on and off and test the process in vivo. They found that in p53-deficient tumor-bearing mice with MK2 turned off, tumors shrank successfully upon treatment with the DNA-damaging therapeutic cisplatin, whereas tumors in mice with unblocked MK2 genes continued growing. This study suggests potential for new cancer treatments combining MK2 inhibitors with DNA-damaging drugs. Drugs that inhibit MK2 are in the works for other diseases such as arthritis, but this is the first time they are being considered for cancer therapy. The research was primarily funded by a TRANSCEND grant from Janssen Pharmaceuticals, Inc. The study was profiled in MIT Technology Review.
