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. Author manuscript; available in PMC: 2012 Jun 15.
Published in final edited form as: Cancer Res. 2011 Apr 20;71(12):4106–4116. doi: 10.1158/0008-5472.CAN-10-3597

Figure 6. Loss of Akt1 and Akt2 had opposing effects on latency of Pten deficient tumors.

Figure 6

Kaplan-Meier curves of mice following intracranial implantation of (A) PtenWT;p53cKO;EGFRvIII or (B) PtencKO;p53cKO;EGFRvIII PMAs that were (upper) Akt1 WT or KO, or treated with (middle) Akt2- or (lower) Akt3-shRNAs. (C) Left: IHC for Ki67 (brown) was performed on PtencKO;p53cKO;EGFRvIII tumors from (B, upper) and counterstained with hematoxylin (blue). Bar is 100 μm. Right: Quantification of Ki67 positive cells. Shown is the mean ± SEM. The significance value (p) was determined using an unpaired t test. (D) Kaplan-Meier curves of mice following intracranial implantation of (left) PtenWT;p53cKO;EGFRvIII or (right) PtencKO;p53cKO;EGFRvIII PMAs that were Akt1WT (black), Akt1KO (green) or Akt1KO expressing (blue) Akt2 or (red) Akt3 shRNAs. For A, B and D, n=number of mice per group and p values were calculated using the logrank test.

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