The dose and type of anticancer therapy that a patient receives is usually determined empirically — patients with a certain type of cancer receive a certain type of chemotherapy, usually based on the maximum dose of drug(s) that they can tolerate, and then they wait and hope that their tumour will shrink. Thankfully, the process is being refined — it is now not only possible to select the patients who are most likely to respond to a particular drug, but also to optimize its dose and to monitor its efficacy in vivo.

On page 415 of this issue, a Highlight discusses the ability to select patients with non-small-cell lung cancer who are most likely to respond to gefitinib, based on mutations in the epidermal growth factor receptor. And in many cases, the practice of giving the 'maximum tolerated dose' to patients might also be on its way out — on page 423, Robert Kerbel and Barton Kamen describe how continuous administration of comparatively low doses of drugs can improve the antitumour efficacy of both chemotherapy and targeted agents. This approach not only produces fewer side effects, but also prevents resistance by destroying both the cancer cells and the tumour vasculature.

Imaging techniques are being developed to monitor the effect of a drug on its target once administered to a patient. For instance, positron-emission tomography (PET) can be used to measure the degradation of the receptor tyrosine kinase ERBB2 after treatment with 17-AAG (page 417) and a luciferase reporter can be used to track cyclin-dependent kinase inhibitor activity (page 418). PET can also be used to image drug-resistance mechanisms (Catharine West and colleagues, on page 457).

Developments such as these will hopefully lead us to truly targeted and tailored anticancer therapies.