To make a compound work better
against a specific disease target, medicinal chemists optimize the drug, tweaking its structure or physical properties to make it more effective and safer.
The Cancer Gene Census (CGC) database contains 547 such gene across various cancer types.5 Remarkably, few driver genes having
specific point mutations appear to be sufficient to rewire signalling networks in cancer, 1 which at the same time shows that — at least from the mutational side — cancer does not consist of an «infinite» number of different
diseases, and in many cases treatment options
targeted against driver genes might be transferred from one case to the next.