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[Cancer Research 63, 2742-2746, June 1, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Analysis of the Phosphatidylinositol 3'-Kinase Signaling Pathway in Glioblastoma Patients in Vivo1

Gheeyoung Choe2, Steve Horvath2, Timothy F. Cloughesy, Katherine Crosby, David Seligson, Aarno Palotie, Landon Inge, Bradley L. Smith, Charles L. Sawyers and Paul S. Mischel3

Departments of Pathology and Laboratory Medicine [G. C., D. S., A. P., L. I., P. S. M.], Human Genetics and Biostatistics [S. H.] Henry E. Singleton Brain Cancer Research Program [T. F. C., P. S. M.], and The Howard Hughes Medical Institute [C. L. S.], David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California 90095; Department of Clinical Chemistry, University of Helsinki, Helsinki, Finland FIN-00014 [A. P.]; and Cell Signaling Technologies, Beverly, Massachusetts 01915 [K. C., B. S.]

Deregulated signaling through the phosphatidylinositol 3'-kinase (PI3K) pathway is common in many types of cancer, including glioblastoma. Dissecting the molecular events associated with activation of this pathway in glioblastoma patients in vivo presents an important challenge that has implications for the development and clinical testing of PI3K pathway inhibitors. Using an immunohistochemical analysis applied to a tissue microarray, we performed hierarchical clustering and multidimensional scaling, as well as univariate and multivariate analyses, to dissect the PI3K pathway in vivo. We demonstrate that loss of the tumor suppressor protein PTEN, which antagonizes PI3K pathway activation, is highly correlated with activation of the main PI3K effector Akt in vivo. We also show that Akt activation is significantly correlated with phosphorylation of mammalian target of rapamycin (mTOR), the family of forkhead transcription factors (FOXO1, FOXO3a, and FOXO4), and S6, which are thought to promote its effects. Expression of the mutant epidermal growth factor receptor vIII is also tightly correlated with phosphorylation of these effectors, demonstrating an additional route to PI3K pathway activation in glioblastomas in vivo. These results provide the first dissection of the PI3K pathway in glioblastoma in vivo and suggest an approach to stratifying patients for targeted kinase inhibitor therapy.




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