Metastatic seeding and dormancy models
From Paget's seed-and-soil idea to models that estimate when metastases were seeded from a primary and how long they lay dormant, these frameworks explain late relapse and argue for treating micrometastases early.
Overview
Stephen Paget observed in 1889 that breast cancer metastasised to particular organs and proposed that seeds grow only in congenial soil; Fidler's experiments in the 1970s confirmed organ tropism. Mathematical models of the metastatic cascade estimate seeding rates and growth of secondary tumours from primary size and time, and sequencing-based timing suggests metastases in colorectal and other cancers are often seeded years before diagnosis, when the primary is small. Dormancy models describe cells arrested or balanced by immunity for years before relapse, explaining late recurrences in breast cancer and melanoma and the rationale for extended adjuvant endocrine therapy.
How it works
Metastatic burden follows from a seeding rate proportional to primary size and the growth law of secondaries, with dormancy as a quiescent or immune-controlled state that can be released.
- Explains late relapse and organ tropism
- Times metastasis from sequencing data
- Supports adjuvant treatment logic
- Dormancy mechanisms remain unclear
- Hard to test directly in patients
- Parameters inferred, not measured
Latest papers
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