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Both the induction of  SPARC  expression and the loss of the p53 tumor suppressor gene are changes that occur early in glioma development. Both  SPARC  and p53 regulate glioma cell survival by inverse effects on apoptotic signaling. Therefore, during glioma formation, the upregulation of  SPARC  may cooperate with the loss of p53 to enhance cell survival. This study determined whether the loss of  Sparc  in astrocytes that are null for  p53  would result in reduced cell survival and tumor formation and increased tumor immunogenicity in an  in vivo  xenograft brain tumor model.   In vitro  , the loss of   S   parc  in  p53 ‐null astrocytes resulted in an increase in cell proliferation, but a loss of tumorigenicity. At 7 days after intracranial implantation,  Sparc ‐null tumors had decreased tumor cell survival, proliferation and reduced tumor size. The loss of  Sparc  promoted microglia/macrophage activation and phagocytosis of tumor cells. Our results indicate that the loss of  p53  by deletion/mutation in the early stages of glioma formation may cooperate with the induction of  SPARC  to potentiate cancer cell survival and escape from immune surveillance.

Loss of Sparc in p 53 ‐null Astrocytes Promotes Macrophage Activation and Phagocytosis Resulting in Decreased Tumor Size and Tumor Cell Survival