  We propose a mechanism for tumor growth emphasizing the role of homeostatic
regulation and tissue stability. We show that competition between surface and
bulk effects leads to the existence of a critical size that must be overcome by
metastases to reach macroscopic sizes. This property can qualitatively explain
the observed size distributions of metastases, while size-independent growth
rates cannot account for clinical and experimental data. In addition, it
potentially explains the observed preferential growth of metastases on tissue
surfaces and membranes such as the pleural and peritoneal layers, suggests a
mechanism underlying the seed and soil hypothesis introduced by Stephen Paget
in 1889 and yields realistic values for metastatic inefficiency. We propose a
number of key experiments to test these concepts. The homeostatic pressure as
introduced in this work could constitute a quantitative, experimentally
accessible measure for the metastatic potential of early malignant growths.
