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. 2021 Mar 17;124(9):1491–1502. doi: 10.1038/s41416-021-01309-w

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Many mechanisms underlying inflammatory signalling, regeneration and unchecked proliferation can function in cancer progression, including during dissemination from the primary tumour, establishment of a micro-metastases, and finally overt macro-metastatic outgrowth. Chromosomal instability leads to the formation of rupture-prone micronuclei - a source of chronic inflammatory signalling in tumour cells themselves. At the invasive front of a primary tumour (a), chronic inflammatory signalling driven by sensing of cytosolic nucleic acids can trigger epithelial–mesenchymal transition (insert) and a more regenerative stem-like phenotype. Breakdown of the extracellular matrix (ECM) allows mesenchymal stem-like cells to escape the tumour microenvironment and seed micro-metastases (b). The innate immune system, especially natural killer (NK) cells, can restrict the expansion of latent, metastasis-initiating cells that have not yet adapted to evade the deleterious, immune-mediated consequences of chronic inflammatory signalling. Cells that enter an immune-evasive, quiescent state might eventually form overt macro-metastases under growth-permissive conditions (c), which can lead to re-engagement with pro-regenerative immune cells in the new tumour microenvironment.