title: EGFR-mediated tumor immunoescape: The imbalance between phosphorylated STAT1 and phosphorylated STAT3.
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.
authors: Department of Immunology; University of Pittsburgh; Pittsburgh, PA USA.
authors: Fernando
authors: F
authors: Concha-Benavente
authors: Department of Otolaryngology; University of Pittsburgh; Pittsburgh, PA USA.
authors: Raghvendra M
authors: RM
authors: Srivastava
authors: Department of Surgery; Massachusetts General Hospital; Harvard Medical School; Boston, MA USA.
authors: Soldano
authors: S
authors: Ferrone
authors: 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.
authors: Robert L
authors: RL
authors: Ferris
keywords: APM; EGFR; SHP2; immunoescape; immunotherapy; pSTAT1; pSTAT3