Inactivation of Stat3 in tumor cells: releasing a brake on immune responses against cancer?

Cancer Cell. 2004 Feb;5(2):111-2. doi: 10.1016/s1535-6108(04)00028-5.

Abstract

A model of immune evasion mediated by tumors expressing constitutively activated Stat3 was recently proposed in Nature Medicine by Wang et al., suggesting opportunities for a new therapeutic approach for cancer.

Publication types

  • Review

MeSH terms

  • Cell Division
  • Chemokine CCL5 / immunology
  • Chemokine CCL5 / metabolism
  • DNA-Binding Proteins / metabolism*
  • Dendritic Cells / immunology*
  • Dendritic Cells / metabolism
  • Gene Expression Regulation, Neoplastic / immunology
  • Gene Expression Regulation, Neoplastic / physiology
  • Genes, MHC Class II / physiology*
  • Interleukin-10 / immunology
  • Interleukin-10 / metabolism
  • Interleukin-6 / immunology
  • Interleukin-6 / metabolism
  • Models, Molecular
  • Neoplasms / immunology
  • Neoplasms / metabolism
  • Phosphotyrosine
  • STAT3 Transcription Factor
  • Signal Transduction
  • T-Lymphocytes / immunology*
  • T-Lymphocytes / metabolism
  • Trans-Activators / metabolism*
  • Tumor Necrosis Factor-alpha / immunology
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Chemokine CCL5
  • DNA-Binding Proteins
  • Interleukin-6
  • STAT3 Transcription Factor
  • TNF protein, human
  • Trans-Activators
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Phosphotyrosine