Metastasis, also called secondary neoplastic disease, is a tumour newly formed in a site different from that of
origin, as a consequence of cancer progression and dissemination largely through blood and lymphatic vessels. The ability
to form metastases is the main property that distinguishes malignant from benign tumours. Treatments for metastatic cancer
are similar in practice to those for primary tumours, but such treatments are mostly palliative; indeed, almost all deaths
caused by solid tumours occur in the metastatic phase. Increasing evidence supports the concept that therapies for primary
tumours are inadequate to treat metastasis and can even promote formation of metastases, while exerting local growth
control. Furthermore, recurrent tumours, which are denoted by increased aggressiveness and therapy resistance in comparison
with the primary tumour, have an increased metastatic potential. Genetic modifications occurring during tumour
progression lead to substantial differences between the primary and metastatic tumours. This emphasises the importance
of designing novel therapies for metastasis. In the last decade, a number of studies have contributed to the understanding
of the genetic rearrangements underlying the conversion of cancer cells into the metastasis founder cells. The present article
aims at reviewing recent advances in metastasis research and attempts to discuss the reasons for which the therapeutic
strategies against primary tumours may not satisfactorily address their metastatic counterparts.
Keywords: Cancer therapy, CSC, EMT, genetic and epigenetic modifications, metastasis, tumour heterogeneity, Tumour progression.
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