Anemia induced in splenectomized mice by administration of rhG-CSF.

Normal and splenectomized mice (SPLXM) were given rhG-CSF for 10 to 128 days and serial observations were made on blood counts for 128 days. After 10 days, mice were killed for histologic studies. All treatment schedules produced, in addition to elevated white blood counts, a macrocytic anemia which only partially responded to large doses of Epo.

Tumor-induced granulopoiesis unrelated to colony-stimulating factor.

A transplantable granulocytosis-inducing mammary adenocarcinoma of mice was used to provide evidence about the role of tumor-generated factors in granulopoiesis. The original tumor produced high levels of colony-stimulating factor (CSF) in culture as well as inhibitor to CSF. The tumor was passaged repeatedly, both in host mice and in culture, and eventually displayed a varying capacity to induce granulocytosis.

Forced differentiation of CFU-S by Iron-55 erythrocytocide.

Cascades of Auger electrons are emitted in the decay of 55Fe and absorbed in tissue within a 1 micrometer radius. Cytocidal amounts of 55Fe can therefore eliminate erythroid precursors with minimal damage to adjacent cells. A single intravenous injection leads to continued erythrocytocide in mice because the isotope is reutilized and has a 2.

Relevance of specific activity in experimental erythrocytocide by 55Fe.

Iron loads between 0.20 microgram and 26 microgram, added to 5 mu Ci 59Fe, were followed for up to 150 days in mice. Relative organ uptake increased as a function of iron load in liver and kidneys while it decreased in bone marrow and blood.