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Metastatic dissemination and growth at distant sites are influenced by cells of the tumour microenvironment. What roles do these cells have in the underlying processes that determine metastatic growth?
Metastasis suppressors inhibit metastasis but not the development of a primary tumour. Many of these genes have now been identified, and the therapeutic potential of restoring metastasis suppressor function is beginning to be examined.
Transitions between epithelial and mesenchymal states seem to promote tumour heterogeneity and metastasis. This Review discusses the connections between epithelial and mesenchymal transitions and the acquisition of stem cell-like phenotypes.
The natural history of metastasis — which appears to be cancer-type specific — varies by target organ, latency and severity. This Review discusses how organ speciation and the competence to colonize might develop.
How are sites of metastases chosen? Accumulating evidence suggests that primary tumour cells and circulating tumour cells might facilitate changes to the microenvironment in target organs so that a pre-metastatic niche, ideal for engraftment, forms.
microRNAs have recently been shown to affect diverse processes involved in metastasis. How do microRNAs interfere with or promote metastasis, could they be used as predictive markers, and are they possible therapeutic targets?
When, in tumour progression, might metastasis be initiated? This Perspective argues that tumour cells disseminate early in malignant progression of the primary tumour so that disseminated tumour cells evolve the traits to allow growth within the metastatic site independently from the primary tumour.
The resurgence of interest in the underlying processes of metastasis has led to significant new insights and translational developments. The specially commissioned articles in this Focus on Migration and metastasis discuss the new and re-emerging models and pathways that have been redefined with regard to their role in metastasis and metastasis suppression.