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Oncoimmunology. 2013 Dec 1;2(12):e27215. Epub 2013 Dec 5.

EGFR-mediated tumor immunoescape: The imbalance between phosphorylated STAT1 and phosphorylated STAT3.

Author information

1
Department of Immunology; University of Pittsburgh; Pittsburgh, PA USA.
2
Department of Otolaryngology; University of Pittsburgh; Pittsburgh, PA USA.
3
Department of Surgery; Massachusetts General Hospital; Harvard Medical School; Boston, MA USA.
4
Department of Immunology; University of Pittsburgh; Pittsburgh, PA USA ; Department of Otolaryngology; University of Pittsburgh; Pittsburgh, PA USA ; Cancer Immunology Program; University of Pittsburgh Cancer Institute; Pittsburgh, PA USA.

Abstract

The 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.

KEYWORDS:

APM; EGFR; SHP2; immunoescape; immunotherapy; pSTAT1; pSTAT3

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