Tumours are not merely masses of abnormally proliferating cancer cells. Today, we have a clearer view of cancer complexity in which the participation of cancer and host cells leads to a tremendous heterogeneity of neoplastic diseases concerning the genetics, epigenetics, proteomics and biochemistry of the tumour [1]. Such intra-tumour heterogeneity provides the basis for inter-metastatic heterogeneity among different metastatic lesions of the same patient, each originating from a founder cell, or small group of cells, with a very different mutation kit, and likely originating from different and distinct primary tumour areas. This situation has important implications regarding chemotherapeutic sensitivity and responses. In addition, the offspring of the founder cell(s) can generate heterogeneity among the cells of an individual metastasis, affecting the response to systemic therapies and providing the seeds for drug resistance.
