Tumours have often been referred to as 'wounds that never heal'. A report published by Marc van de Vijver and colleagues used gene-expression-profiling analysis to make a direct comparison between wounds and tumours, and found that a wound-response gene-expression pattern can indeed predict metastasis and survival likelihoods in patients with breast cancer.

Processes involved in wound healing, such as activation of matrix remodelling, cell motility and angiogenesis, are also common features of tumour progression. By analysing the gene-expression patterns of cells that mediate the wound-healing response, researchers previously identified a 'core serum response' signature that excluded cell-cycle genes and was representative of this process. Previous studies showed that in common epithelial tumours such as breast, lung and gastric cancers, expression of this wound-response signature predicted poor overall survival and increased risk of metastasis.

Van de Vijver and colleagues set out to validate these observations in a large independent data set. Using a database of 295 patients with breast cancer, they tested the reproducibility of the association between the wound-response signature and breast cancer progression by comparing the expression of 280 of the 459 core serum-response genes. They found that tumours with the activated wound-response signature were more likely to metastasize. Furthermore, patients with these tumours had decreased survival times.

In patients diagnosed with early breast cancer, there is a 30% risk of developing distant metastases. This risk can be decreased by giving adjuvant systemic chemotherapy and/or hormonal therapy after surgical removal of the primary tumour. Using the wound-response signature, the authors were able to more accurately identify the patients who later developed metastases — after 10 years, 49% of patients with an activated wound signature developed distant metastases. Adding this signature to other prognostic tests could therefore help to determine which patients could forgo adjuvant chemotherapy, and which ones should be recommended for more intensive forms of treatment.

The authors also conclude that identifying the molecular mechanisms that activate, sustain and eventually shut down the wound response in epithelial tumours might lead to targeted therapeutics.