A case of hepatoma associated with erythrocytosis and increased levels of plasma ESF is described. Normal or tumorous liver tissue from this patient possessed neither erythropoiesis-stimulating activity nor a capacity to generate the ESF when incubated with normal human serum. Homogenates of tumor tissue served effectively as substrate for hypoxic rat REF in the generation of the ESF. Homogenates of nontumorous liver exhibited no substrate activity, but inactivated human urinary ESF when incubated with it. Homogenates of tumorous liver tissue lacked the capacity to inactivate the ESF.
It is suggested that the increased production or availability of substrate for the REF by the tumor significantly contributed to the increased levels of plasma ESF in this patient.