It was previously reported that monocytes/macrophages play an important role in mediating T-cell dysfunction in tumor-bearing hosts, in which monocytes/macrophages were found to induce the loss of T-cell functions concomitantly with induction of defects in T-cell signaling molecules. These observations encouraged us to investigate monocyte status in cancer-bearing hosts. We characterized peripheral blood monocytes in gastric cancer patients with advanced disease (n = 14), in those with early disease (n = 17) and in healthy individuals (n = 14), based on surface marker, oxygen-burst capacity, and intracellular cytokine status (IL-10 and IL-12). To clarify which mediators induced the characteristic differences of monocytes in cancer-bearing hosts, healthy donor-derived monocytes were co-incubated with the patients' plasma. Intracellular IL-10 and IL-12 status on monocytes in advanced disease was significantly increased in comparison with early disease or healthy individuals, while there were no differences in the surface marker or oxygen-burst capacity of monocytes. The plasma from the patients with advanced disease could induce increased intracellular IL-10 and IL-12 status in healthy monocytes. The phenomenon was significantly inhibited with neutralizing mAbs specific for VEGF.