Peliosis hepatis, characterized by the presence of blood-filled spaces within hepatic parenchyma, developed in C57Bl mice implanted subcutaneously with melanoma cells 23 days previously. The peliosis was associated with dilated hepatic sinusoids that were lined by prominent, proliferating endothelial cells. The development of peliosis hepatis was completely abrogated when melanoma growth was inhibited by administration of dexamethasone. These features support the concept that peliosis hepatis can be induced by a circulating tumor-derived endothelial growth factor such as vascular endothelial growth factor.