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Cancer-associated fibroblasts/myofibroblasts and inflammatory cells produce a vast array of growth factors, chemokines and extracellular matrix (ECM) components that facilitate cancer progression, invasion/metastasis and neovascularization. This review highlights some surprisingly novel mechanisms of this paracrine relationship.Mesenchymal stem/stromal cells (MSCs) are known for their tropism towards certain tumours, but now we find that cross-talk between tumours and MSCs leads to greater tumour motility and metastasis. Two closely related populations of immature myeloid cells, so-called ‘cap cells’ and myeloid-derived suppressor cells (MDSCs) also cross-talk with tumour cells, promoting invasion and metastasis through matrix metalloproteinase (MMP) secretion, as well as contributing to neovascularization and T-cell tolerance. The contribution of bone marrow-derived cells (BMDCs) to tumour neovascularization is controversial, but BMD – endothelial progenitor cells (EPCs) – are strongly implicated in the angiogenic switch in a mouse model. BMDCs are also credited with the creation of premetastatic niches to which metastatic cells adhere via integrins.There is no doubt that BMDCs are not simply bystanders in the tumour battleground. The mechanisms through which they aid tumour progression are numerous; effective treatments that combat BMDC–tumour cross-talk are surely on the way.