(A and B) Respective isotype controls. (C–I) Flow cytometric analysis of CEPCs in tumor-bearing, tumor-bearing plus DA-treated, and tumor-bearing plus eticlopride (Eti) plus DA-treated mice. CEPCs were detectable in tumor-bearing mice, but were undetectable in the blood of tumor-bearing DA-treated animals. DA had no effect on EPC frequency in tumor-bearing animals treated with the D₂ receptor antagonist eticlopride prior to DA administration, indicating that this inhibition was D₂ receptor mediated. Figures represent EPC frequency on posttransplantation day 6 in both tumor-bearing and DA-treated, tumor-bearing animals after completion of DA treatment schedule. (I) Absolute number of EPCs. (J and K) Late outgrowth colonies from PBMCs of tumor-bearing normal mice. The endothelial nature of the late outgrowth colony-forming cells was confirmed by the uptake of Dil–Ac-LDL. (L and M) Absent late outgrowth colonies from PBMCs of DA-treated, tumor-bearing normal mice. PBMCs isolated from circulation were plated onto fibronectin-coated dishes, and thereafter, late outgrowth colonies were scored. (N–T) Flow cytometric analysis of circulating EPCs in tumor-bearing D₂^(–/–) mice showed significantly higher CEPCs when compared with tumor-bearing wild-type mice (P < 0.05). (T) Absolute number of EPCs. DA treatment caused no change in EPC frequency in peripheral blood of tumor-bearing D₂^(–/–) mice. Scale bars: 50 μm. D₂^(–/–), D₂ receptor–knockout mice. Figures are representative of 4 separate experiments in each group. N, wild type.