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How cancer spreads: cells leave the tumour, squeeze into blood or lymph vessels, survive the journey, exit into a new organ, often sleep there for years, and finally grow. Metastasis causes about 90% of cancer deaths.
Invasion (EMT, matrix proteases), intravasation, survival in circulation as CTCs or clusters (platelet cloaking, anoikis resistance), arrest and extravasation, then colonisation, which is the rate-limiting step: most disseminated tumour cells (DTCs) die or stay dormant. Organ tropism follows Paget's seed-and-soil: pre-metastatic niches are prepared by tumour-derived exosomes and myeloid cells. Clinically, ctDNA and MRD assays detect the cascade before imaging; adjuvant therapy targets it blind; no drug specifically blocks colonisation yet.
A seed leaving a plant: it must detach, ride the wind, land somewhere with the right soil, survive the winter, and only then sprout. Almost every seed fails; the few that grow are the metastases.
One pathway page on OnCo cites this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing page listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
It is the clearest mechanistic answer to why microsatellite-stable colorectal cancer resists immunotherapy, and the rationale for every TGF-beta plus checkpoint combination now in trials in this disease.
Two pathway pages and one idea page on OnCo cite this paper by its DOI; this record gives the citation a page of its own so a reader can follow it without leaving OnCo. Read the abstract above alongside the citing pages listed under Related; the record was created automatically from the Europe PMC entry and its figures have not been checked by hand.
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.
It is the quantitative case for early detection: the biology allows a fifteen-year window, and the disease is lethal because we look too late, not because it moves fast.
SMAD4 status is the clearest published molecular marker of how pancreatic cancer will behave: intact argues for local control, lost argues for systemic therapy.
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 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 Invasion: proteases, adhesion & the invasive front, Epithelial-mesenchymal transition & drug efflux, Tumour microenvironment (TME), Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares The Francis Crick Institute, Epithelial-mesenchymal transition & drug efflux, Clonal evolution & minimal residual disease, Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares Clonal evolution & minimal residual disease, Memorial Sloan Kettering Cancer Center, Circulating tumour DNA (ctDNA), MRD / molecular residual disease testing and the tag mechanism.
Shares The Francis Crick Institute, Clonal evolution & minimal residual disease, Single-cell & spatial profiling, Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares Cold Spring Harbor Laboratory, Tumour microenvironment (TME), Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares Epithelial-mesenchymal transition & drug efflux, Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares German Cancer Research Center (DKFZ), Tumour microenvironment (TME), Memorial Sloan Kettering Cancer Center and the tag mechanism.
Shares The Francis Crick Institute, Memorial Sloan Kettering Cancer Center and the tag mechanism.