Cdc42 confers resistance against CTL- and NK cell–mediated tumor suppression in vivo. (A) Growth of cA2K^b-control fibrosarcomas in NOD/SCID mice. The arrowhead indicates the time point of adoptive transfer of allogeneic C57BL/6-derived (■) or syngeneic HLA-A*0201–transgenic cA2K^b splenocytes (□). (B) Growth of cA2K^b-Cdc42 fibrosarcomas in NOD/SCID mice. The arrowhead indicates the time point of adoptive transfer of allogeneic C57BL/6-derived (●) or syngeneic HLA-A*0201–transgenic cA2K^b splenocytes (○). (C) Growth of cA2K^b-control fibrosarcomas in NOD/SCID mice. The arrowhead indicates the time point of adoptive transfer of allogeneic C57BL/6-derived (■), CD8-depleted (○), or NK cell–depleted (▲) splenocytes. The growth curves following undepleted and depleted splenocyte transfer differed significantly (P < .001; ANOVA). (D) Spontaneous growth of cA2K^b-control (□) and cA2K^b-Cdc42 (●) fibrosarcomas in NOD/SCID mice. Mean values plus or minus SE of bidimensional tumor sizes of 5 mice per group are shown for each experiment (*P < .001; **P = .025, Student t test).