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Journal of Oncology
Volume 2008, Article ID 219241, 9 pages
Research Article

Stat3 Expression and Its Correlation with Proliferation and Apoptosis/Autophagy in Gliomas

1Neuro-bio-oncology Center, Policlinico di Monza Foundation, University of Turin, Via Pietro Micca, 29, 13100 Vercelli, Italy
2Clinical and Experimental Medical Department, University of East Piedmont, 28100 Novara, Italy
3Department of Chemical, Food, Pharmaceutical and Pharmacological Sciences (DISCAFF), University of East Piedmont, 28100 Novara, Italy

Received 2 July 2008; Accepted 24 November 2008

Academic Editor: Massimo Aglietta

Copyright © 2008 Valentina Caldera et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Signal transducer and activator of transcription-3 (Stat3) was studied along with several steps of the PI3/Akt pathway in a series of 64 gliomas that included both malignant and low-grade tumors, using quantitative immunohistochemistry, Western blotting, and molecular biology techniques. The goal of the study was to investigate whether activated Stat3 (phospho-Stat3) levels correlated with cell proliferation, apoptosis, and autophagy. Stat3 and activated Akt (phospho-Akt) expression increased with malignancy grade, but did not correlate with proliferation and survival within the category of glioblastomas. A correlation of Stat3 with Akt was found, indicating a regulation of the former by the PI3/Akt pathway, which, in turn, was in relation with EGFR amplification. Stat3 and Akt did not show any correlation with apoptosis, whereas they showed an inverse correlation with Beclin 1, a stimulator of autophagy, which was rarely positive in glioblastomas. Autophagy seems then to be inactivated in malignant gliomas.