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. Author manuscript; available in PMC: 2012 Aug 24.
Published in final edited form as: Cancer Res. 2010 Apr 20;70(9):3526–3536. doi: 10.1158/0008-5472.CAN-09-3278

Figure 3. MDSC in 4T1 tumor bed are relatively protected from sunitinib-mediated downregulation.

Figure 3

(A) Tumor growth in Renca+, CT26+ and 4T1+mice +/−sunitinib treatment. (B) Renca, CT26, and 4T1 tumor cells were seeded and allowed to adhere overnight. Sunitinib was added to cultures at various doses the following morning for 72 hours. At the end of treatment, the recovery of adherent cells (cells counted following trypsonization of washed cells) was counted, as well as the viability of all cells (adherent and non-adherent combined) determined with Annexin V and 7AAD FACS staining. (C) MDSC were measured as a percentage of viable, scatter-gated cells in tumors digested following the various doses of sunitinib treatment in each tumor model. (D) Left- Cells from spleen and tumor-derived suspensions from untreated-or sunitinib-treated 4T1+mice were stimulated in vitro. IFNγ production in T-cells was assayed and compared to that produced by T-cells from naïve spleen suspensions. Right- MDSC from untreated-4T1+ spleens or from untreated- and sunitinib-treated 4T1+ tumors were isolated using either magnetic bead-bound antibodies to Gr1, or FACS flow sorting, and then added to naïve T-cells. Cultures were stimulated and assayed for IFNγ production.