The effect of
hydrocortisone on blood-borne
tumor metastasis was studied in an i.v. inoculation experiment with Ehrlich hypotetraploid clone 1, Ehrlich hypotetraploid stock, and Ehrlich hyperdiploid stock
tumors. The administration of
hydrocortisone before
tumor inoculation resulted in increased
tumor take, reduced mean survival time of mice, and concentration of
tumor metastasis in a specific organ (i.e., lung
metastasis for Ehrlich hypotetraploid clone 1
tumor, and liver
metastasis for Ehrlich hypotetraploid stock and Ehrlich hyperdiploid stock
tumors). Enhancement of
tumor metastasis, as induced by
hydrocortisone pretreatment, was not reproduced by the administration of
6-mercaptopurine,
testosterone, or
estradiol. The progress of
tumor death in
hydrocortisone-conditioned mice was not affected by either
heparin or
dextran sulfate. This indicated that the effect of
hydrocortisone on
tumor metastasis was independent of the effect of these agents on immune reaction or blood coagulation. In the tracer experiment with 125-I-labeled
tumor cells,
hydrocortisone pretreatment significantly increased over the control the intrapulmonary retention of Ehrlich hypotetraploid clone 1
tumor cells from 1 through 72 hr after
tumor inoculation, the time lag required for the establishment of metastatic foci in the lung. The arrest of Ehrlich hypotetraploid stock and Ehrlich hyperdiploid stock
tumors in the liver was also temporarily increased by
hydrocortisone pretreatment. No correlation was found between
tumor cell size and differential distribution of metastatic
tumors with 3 Ehrlich
tumors. An attempt was made to use this blood-borne
metastasis system for chemotherapeutic study. Administration of
cyclophosphamide gave rise to a significant prolongation of survival time and often to complete prevention of
tumor metastasis in
hydrocortisone-conditioned mice.