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Molecular medicine: a clinician's primer on microarrays

Cancer medicine is poised on the cusp of long-awaited change. For example, cancer taxonomy remains based on histopathological and anatomical principles, originating in concepts established prior to 1900. This classification has proven useful, but imperfect. Often, two histologically identical tumours frustratingly behave quite differently. Similarly, our current treatment strategies were established in the 1950s. Although great progress has been made in optimizing the use of cytotoxic therapies, these treatments by and large are nonspecifically targeted to all dividing cells. The toxicities associated with palliative treatments conferring a routine response rate of 25% have generated understandable cynicism, even (or especially) in the medical fraternity. Novel treatment and prognostic paradigms are needed, which we assume will be based on a molecular understanding of cancer. After some years of expectancy, recent proofs-of-principle suggest that molecular biology is generating effective and specific treatments. For example, a monoclonal antibody-based treatment for breast cancer, trastuzumab, was developed because molecular studies had identified a critical oncogenic role for amplified epidermal growth factor signalling 1 . Imatinib mesylate has provided important options for the treatment of chronic myeloid leukaemia 2 and gastrointestinal stromal tumours 3 by targeting specific molecular aberrations. The remarkable aspect of these treatments is not simply that they work, but their relative lack of toxicity. The recent development of robust, affordable and high-throughput methods of molecular analysis in the past decade promise to radically accelerate the pace at which new potential targets are identified. These technical developments have been based on the following achievements (in historical order): 1 Acceptance that cancer is a genetic disease, caused by somatic or germline mutations. This was predicted in 1914 by Theodor Boveri 4 but not proven until the 1980s with cloning of the first human oncogene ( ras ) 5 and tumour suppressor gene (the retinoblastoma tumour suppressor). 6