Mechanisms of metastatic spread: invasion, angiogenesis and organ tropism
The invasion-metastasis cascade (E-cadherin loss, matrix metalloproteinases, circulation, colonisation), the routes of spread, why cancers favour particular organs (venous drainage, Batson plexus, seed and soil), lytic versus sclerotic bone metastases, and angiogenesis with the pharmacology of VEGF blockade.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Metastasis causes most cancer deaths (often quoted as up to 90%; a 2019 registry analysis found about two-thirds of solid tumour deaths). It is inefficient: a tumour sheds millions of cells a day but well under 0.01% form a deposit.
- The invasion-metastasis cascade: local invasion → intravasation → survival in the circulation → arrest and extravasation → colonisation.
- Where a cancer goes depends on anatomy (the first capillary bed downstream) and biology ("seed and soil", Paget 1889).
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Sources
- Robbins and Cotran Pathologic Basis of Disease, 10th editionElsevier (Kumar V, Abbas AK, Aster JC), 2021
- Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation. Cell 2011;144:646-74Cell, 2011
- Fidler IJ. The pathogenesis of cancer metastasis: the 'seed and soil' hypothesis revisited. Nat Rev Cancer 2003;3:453-8Nature Reviews Cancer, 2003
- Paget S. The distribution of secondary growths in cancer of the breast. Lancet 1889;133:571-3The Lancet, 1889
- Kaelin WG. The von Hippel-Lindau tumour suppressor protein: O2 sensing and cancer. Nat Rev Cancer 2008;8:865-73Nature Reviews Cancer, 2008
- Last updated
- 14 November 2026
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