摘要
A very recent study by Russo et al.published in Science demonstrates that colorectal cancer(CRC)cells adapt to targeted therapies by downregulating DNA repair at the expense of an increased mutation frequency and microsatellite instability(MSI).1 The authors intriguingly showed that CRC cells are capable of activating stress-induced mutagenesis similar to unicellular organisms in a transient and controlled manner,allowing them to survive under targeted therapies(Fig.1).
