Breast cancer is now the most common form of cancer in the United Kingdom, and its incidence is rising steadily elsewhere. At least some of the rise is due to the fact that therapy for breast cancer has improved enormously over the past 20 years.

As discussed by Simak Ali and Charles Coombes on p. 101, much of this improvement has its roots in George Beatson's realization — over 100 years ago — that many breast cancers rely on oestrogen for growth and survival. This discovery laid the foundation for the development of oestrogen-receptor antagonists and, later on, the selective oestrogen-receptor modulators such as tamoxifen, which antagonizes the effects of oestrogen in breast while preserving the positive effects of oestrogen in most other tissues. Another way of preventing breast cancer cells from getting this crucial growth and survival signal is by reducing circulating levels of oestrogen; as reported in Trial Watch, Arimadex, a drug that blocks oestrogen synthesis, has recently performed better than tamoxifen in a large trial.

Although endocrine therapies for breast cancer are constantly improving, many breast cancers do eventually develop resistance to all available endocrine therapies. Ali and Coombes explore the potential mechanisms behind this failure; although it's early days, there are striking parallels between the resistance tactics used by breast cancer cells and those used by androgen-independent prostate cancer, which were discussed by Brian Feldman and David Feldman in our launch issue (October 2001). One tactic is mutation of the steroid-hormone receptor, altering its interaction with ligands. Another is upregulation of crosstalk between growth-factor-signalling pathways and steroid-hormone receptors, allowing the latter to become hormone independent. Crosstalk between the researchers working on these two types of cancer would almost certainly benefit both fields.