EGFR-mediated tumor immunoescape: The imbalance between phosphorylated STAT1 and phosphorylated STAT3
Srivastava, Raghvendra M
Ferris, Robert L
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CitationConcha-Benavente, Fernando, Raghvendra M Srivastava, Soldano Ferrone, and Robert L Ferris. 2013. “EGFR-mediated tumor immunoescape: The imbalance between phosphorylated STAT1 and phosphorylated STAT3.” Oncoimmunology 2 (12): e27215. doi:10.4161/onci.27215. http://dx.doi.org/10.4161/onci.27215.
AbstractThe epidermal growth factor receptor (EGFR) supports the escape of malignant cells from immunosurveillance by inhibiting the activation of signal transducer and activator of transcription 1 (STAT1) while promoting that of STAT3. We have recently demonstrated that protein tyrosine phosphatase, non-receptor type 11 (PTNP11, best known as SHP2), a phosphatase that operates downstream of EGFR, is responsible for the dephosphorylation of active STAT1 and for the inhibition of the antigen-processing machinery (APM), hence favoring tumor immunoescape. Thus, EGFR signaling may skew the tumor microenvironment to suppress cellular immune responses.
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