We developed a mathematical model which includes in addition to tumor cells, MDSCs, CD8z T cells, IL-35, and VEGF, also Tregs, endothelial cells, oxygen concentration, TGF-b, and M-CSF that is produced by cancer cells. The model is described by a system of partial differential equations. The simulations of the model are in qualitative agreement with the experimental results of Wang et al.. We next extended the model to include anti-IL-35 as an anticancer drug. We compared the efficacy of the drug under two schedules: continuous versus intermittent injections of the same total amount of the drug. We found that continuous injection has better efficacy while the treatment is ongoing. Since it is well known that some cancers including lung and colorectal cancers most likely secrete large amounts of IL-35, we also investigated the efficacy of the drug for such cancers. We found that the percentage of tumor reduction under anti-IL-35 drug improves when the production of IL-35 by cancer is increased. There are currently only few experimental results by which our model can be tested. In recent experiments by Nicholl et al. it was demonstrated that IL-35 promotes pancreatic cancer cells proliferation while anti-IL-35 reduces this promotion. More specifically, in Figure three of Nicholl et al. it is shown that IL-35 increases, on the average, by 100% the proliferation of colonies of several pancreatic cancer cell lines, while in the presence of anti-IL-35 this increase is reduced to 50%. These in vitro results are in qualitative agreement with our results in Figure three. Another example is taken from colorectal cancer in patients. As reported in Zeng et al.. Foxp3zTreg increases linearly with IL-35, and this is in qualitative agreement with Figures 3D and 3E of our simulations. As more experimental and clinical data become available, we should be able to test our model in more quantitative way, so that the model can further be refined. In this paper we focused on the role of IL-35, although Treg secrete besides IL-35 also other cytokines that promote tumor, such as IL-10 and IL-9 ; these were not included directly in the Y-27632 129830-38-2 present model, since we wanted to base the model on the recent experimental data by Wang et al.. When data for other cytokines become available to the same precision as, for instance, in, our model could then be extended to include these cytokines, and to obtain a more comprehensive evaluation of antiIL-35 efficacy in combination with other drugs. MFRP mutations in humans are associated with nanophthalmia or posterior microphthalmia with autosomal recessive retinitis pigmentosa, characterized by retinal spots, foveoschisis and optic nerve head drusen. A homozygous mutation of Mfrp in mice recapitulates central features of the human disease, including retinal spots and a slowly progressing retinal degeneration.