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Cancers 2014, 6(1), 376-395; doi:10.3390/cancers6010376

STAT3 Activation in Glioblastoma: Biochemical and Therapeutic Implications

Department of Neurosurgery, The Johns Hopkins University School of Medicine, 600 N. Wolfe St., Phipps Building Rm 123, Baltimore, MD 21287, USA These authors contributed equally to this work.
* Author to whom correspondence should be addressed.
Received: 16 December 2013 / Revised: 19 January 2014 / Accepted: 29 January 2014 / Published: 10 February 2014
(This article belongs to the Special Issue STAT3 Signalling in Cancer: Friend or Foe)
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Signal transducer and activator of transcription 3 (STAT3) is a potent regulator of gliomagenesis through its induction of angiogenesis, host immunosuppression, and tumor invasion. Gain of function mutations result in constitutive activation of STAT3 in glioma cells, making STAT3 an attractive target for inhibition in cancer therapy. Nevertheless, some studies show that STAT3 also participates in terminal differentiation and apoptosis of various cell lines and in glioma with phosphatase and tensin homolog (PTEN)-deficient genetic backgrounds. In light of these findings, the utility of STAT3 as a prognostic indicator and as a target of drug therapies will be contingent on a more nuanced understanding of its pro- and anti-tumorigenic effects.
Keywords: glioblastoma; STAT3; immunotherapy glioblastoma; STAT3; immunotherapy
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.

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Kim, J.E.; Patel, M.; Ruzevick, J.; Jackson, C.M.; Lim, M. STAT3 Activation in Glioblastoma: Biochemical and Therapeutic Implications. Cancers 2014, 6, 376-395.

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