Analysis of the NIH SEER database suggests that the volume-dependence of the rate of metastasis formation is slight.  One possible explanation is that metastases arise only from a slowly-proliferating sub-population of tumor cells.  However, a large part of the volume of many solid tumors consists of stromal cells, including immune cells, among which macrophages are often the most populous, as well as fibroblasts and myofibroblasts.  Experimental evidence points to a cooperative role of tumor-associated macrophages and myofibroblasts in tumor cell migration into the circulation; tumor stroma may therefore also significantly affect the metastatic rate.  The effect of factors secreted by these cells, as well as cooperativity, appears in many cases to be quite local; hence spatial distribution of the cell populations has an effect on the interactions.  A spatially-distributed model is developed for rate of metastatic formation from a solid tumor mass, including macrophages, myofibroblasts, and cell-derived factors involved in recruitment of these cell populations to the tumor, as well as migration and intravasation.  Matrix metalloproteinases and the biphasic effect of nitric oxide are considered.  The role of TGF-beta , both in promoting EMT (epithelial-to-mesenchymal transition) at the tumor site and inhibiting MET (mesenchymal-to-epithelial transition) at the metastatic site is included.  The model is used to predict rate of metastasis formation as a function of growing tumor volume.  While a few damping effects exist in the system, overall it is difficult to explain a weak dependence on volume.  The model provides insight into the important role of stroma in metastasis.