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Similar results were also seen in prostate cancer (38) and in nonsmall cell cancer (35). Although this anergic state in solid tumors may be attributable to the ARG1- and/or NOS-dependent suppressive activity of MDSCs, MDSC-mediated immunosuppression has not been previously reported in hematological malignancies. PBMCs from MM patients were stimulated with anti-CD3/CD28 antibody-coated beads in the presence of N-(omega)-hydroxy-nor-L-arginine (NorNOHA; an ARG1-specific inhibitor), NG-monomethyl-L-arginine (L-NMMA; an NOS2 inhibitor), both inhibitors, or neither. As shown in Fig. 8 A (top), T cell expansion was considerably enhanced in the presence of both NorNOHA and L-NMMA, whereas the single inhibitors failed to increase T cell proliferation over the baseline. Interestingly, sildenafil yielded results equivalent to the combination of NorNOHA and L-NMMA. These results suggest involvement of both ARG1 and NOS2 in MDSC-mediated immunosuppression in myeloma and confirm the in vitro results demonstrating the ability of PDE5 inhibitors to affect both pathways. Recent data from our lab identified human MDSCs as ARG+, CD14+ cells (unpublished data). We therefore examined T cell expansion in CD14+-depleted PBMCs under the same conditions (Fig. 8 A, bottom). Although CD14+ depletion alone increased CD3+ T cell expansion fourfold, pharmacologic inhibitors failed to further enhance proliferation, suggesting that CD14+ cells are the mediators of ARG1- and NOS2-mediated immunosuppression in MM. As seen with purified mouse T cells (Fig. 5 B), sildenafil also failed to enhance the CD3+ T cell proliferation of CD14-depleted PBMCs from cancer patients. Furthermore, 91 percent of all prostate cancers are found while they are still within the prostate or only in nearby areas. The five-year relative survival rate for those men is almost 100 percent. 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