Fig. 8.
Fig. 8. Mutation of the binding site for PI3K abolished tumor formation induced by MIHC-D816V. / Syngeneic (CBA) mice were injected subcutaneously with 2 × 106 MIHCs expressing D816V c-Kit (n = 7), D816V/Y721F c-Kit (n = 7), wild-type c-Kit (n = 6), Y721F c-Kit, or parental MIHC (n = 6; not shown). All cells were maintained in GM-CSF before injection. The experiment was terminated after 24 weeks with no tumors identified in mice injected with MIHC parent, MIHC-Y721F, or MIHC-D816V/Y721F.

Mutation of the binding site for PI3K abolished tumor formation induced by MIHC-D816V.

Syngeneic (CBA) mice were injected subcutaneously with 2 × 106 MIHCs expressing D816V c-Kit (n = 7), D816V/Y721F c-Kit (n = 7), wild-type c-Kit (n = 6), Y721F c-Kit, or parental MIHC (n = 6; not shown). All cells were maintained in GM-CSF before injection. The experiment was terminated after 24 weeks with no tumors identified in mice injected with MIHC parent, MIHC-Y721F, or MIHC-D816V/Y721F.

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