Anticancer drug development increasingly aims to target molecules that are specifically altered or upregulated in cancer cells, allowing us to move away from the traditional cytotoxic drugs, and instead move towards personalized treatment regimes.

So does this mean that DNA-targeting drugs — which have been the mainstay of cancer chemotherapy for the past 50 years — will increasingly be replaced by agents that act on more specific molecules or processes? Not necessarily, as discussed by Laurence Hurley (on page 188). Although DNA has long been thought of as a non-specific target, code-reading molecules such as triplex-forming oligonucleotides can be targeted to specific sites in DNA. The existence of secondary DNA structures — G-quadruplexes — in telomeres and gene promoters provides another means by which DNA can be targeted in cancer cells.

Despite the recent successes of drugs that act on specific molecular targets, such as tyrosine kinases, there have been many diasppointments, and none has been more publicized than the matrix metalloproteinase (MMP) inhibitors. As MMPs are involved in invasion and metastasis, their inhibition should have prevented these all-too-frequently lethal steps of cancer development. So why have MMP inhibitors proved so disappointing in clinical trials? Mikala Egeblad and Zena Werb (on page 161) suggest that MMPs might work better as preventive agents, rather than in patients with late-stage cancer, as MMPs are also involved in earlier steps of cancer development.

Finally, how can we assess which patients should receive these new targeted therapies? David Sidransky (on page 210) describes how molecular markers can be used to detect and monitor cancer, and assess the efficacy of different treatment regimes, which could lead to the type of tailored therapy that we aspire to.