Fig. 6
WEE1 kinase inhibition sensitizes MOC2 tumors to control by adoptively transferred KIL cells. a KIL cells were irradiated to 18 Gy and assessed for control of MOC2 cell index via impedance analysis at E:T ratios of 12.5:1 and 3.125:1. % loss of cell index 48 h after the addition of control or irradiated KIL to MOC2 cells is quantified on the right. b KIL cells were CFSE labelled, then adoptively transferred (tail vein injection) into MOC2 tumor-bearing WT B6 mice following 2 doses of AZD1775 (120 mg/kg via oral gavage) or control. Eight hours after tail vein injection of 1 × 107 KIL or PBS, mice (n = 5/group) were euthanized and MOC2 tumors were harvested, processed into a single cell suspension, and assessed for CFSE-positive cells via flow cytometry. Quantification of CFSE-labelled cell entry into AZD treated or untreated MOC2 tumors quantified on right. c Treatment schema and in vivo treatment of MOC2 tumor-bearing WT B6 mice (n = 10 mice/group) with adoptively transferred KIL (1 × 107 cells via tail vein injection) alone or in combination with AZD1775 (120 mg/kg via oral gavage). For each of five treatments with AZD1775 and KIL, AZD1775 was administered 8 h before adoptive transfer of KIL. Control mice were treated with oral gavage of carrier only and tail vein injection of PBS only. Individual tumor growth curves shown for each cohort, with survival on the right. Experiment was repeated in two independent assays with similar results. *, p < 0.05; ***, p < 0.001