Loading
Cancer that has spread from where it started to distant parts of the body, travelling through the blood or lymph. Metastasis is why staging scans look at the whole body, and the setting in which most new cancer drugs are approved first.
To metastasise, a cell must break away from the primary, invade through tissue into a blood or lymph vessel, survive the journey, exit at a distant organ, and grow there; each step is inefficient, yet enough cells succeed that around ninety percent of cancer deaths are due to metastases rather than the primary. Common destinations depend on the cancer (bone for prostate and breast, liver for colorectal, brain for lung and melanoma). Metastatic cancer is stage IV and is usually treated with systemic therapy rather than surgery, aiming at long control rather than cure, though a few sites (limited liver metastases in colorectal cancer, oligometastatic disease) can still be treated with curative intent.
This is the reference for the mechanics behind invasion and metastasis and for why partial EMT states, rather than a full switch, are now thought to matter most in cancer. It also explains the appeal and the difficulty of drugging EMT, since its drivers are transcription factors.
This review is the standard map of the tumour microenvironment and the reason microenvironment-directed drugs, from anti-angiogenics to macrophage and fibroblast targeting agents, are developed alongside tumour-cell-directed ones.
EMT is the most cited explanation for how carcinomas invade and spread and for part of their drug resistance. This primer is the entry point for the field, and its framework informs current work on partial EMT states, circulating tumour cells and therapies aimed at the transition.
This paper is why metastasis, stemness and therapy resistance are now studied as one problem. It suggests that the cells most able to spread are also the ones most able to regrow, and it motivates therapies that target the mesenchymal or stem-like state.
This is the paper that made EMT a cancer concept, cited by almost every metastasis study since. It set the research agenda that later produced the EMT stem cell link and current work on partial EMT states.
Shares Lamouille 2014: molecular mechanisms of epithelial-mesenchymal transition, Thiery 2002: epithelial-mesenchymal transitions in tumour progression, Invasive, Kalluri and Weinberg 2009: the basics of epithelial-mesenchymal transition.
Shares Benign versus malignant, Invasive, Stage.
Shares Disseminated tumour cells (DTCs), Quail and Joyce 2013: microenvironmental regulation of tumour progression and metastasis, Seed and soil hypothesis of metastasis (Paget), Tumour dormancy.
Shares Lamouille 2014: molecular mechanisms of epithelial-mesenchymal transition, Kalluri and Weinberg 2009: the basics of epithelial-mesenchymal transition, Mani 2008: the epithelial-mesenchymal transition generates cells with properties of stem cells, Hallmark: activating invasion and metastasis.
Shares Seed and soil hypothesis of metastasis (Paget), Tumour dormancy, The metastatic cascade, Oligometastatic disease.
Shares Cancer metastasis reviews, Seed and soil hypothesis of metastasis (Paget).
Shares Disseminated tumour cells (DTCs), Tumour dormancy, The metastatic cascade.
Shares Disseminated tumour cells (DTCs), Hallmark: activating invasion and metastasis, Seed and soil hypothesis of metastasis (Paget), The metastatic cascade.