Genetic instability promotes cancer progression (by increasing the probability of cancerous mutations) as well as hinders it (by imposing a higher cell death rate for cells susceptible to cancerous mutation).

With oncogene activation or the loss of tumor suppressor gene functions known to be responsible for a high percentage of breast and colorectal cancer (and a good fraction of lung cancer and other types as well), it is important to understand how genetic instability can be orchestrated toward carcinogenesis. In this context, this research gives a complete characterization of the optimal cell mutation rate for the fastest time to a target cancerous cell population through the loss of both copies of a tumor suppressor gene or through oncogene activation.