Common pathways to tumor rejection

Ena Wang, Davide Bedognetti, Sara Tomei, Francesco M. Marincola

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

The control of tumor growth by the host's immunosurveillance is centered on the activation of interferon (IFN) pathways. In particular, direct study of tumors by various groups has uncovered an IFN-γ-related signature whose presence is consistently associated with better prognosis, predisposition to respond to immunotherapy, and, in its extreme manifestation, the acute phases of tumor rejection. Together, and related to the IFN-γ-associated signature, a cluster of genes are coordinately expressed that we refer to as the immunologic constant of rejection (ICR). Activation of ICR components is observed in all forms of immune-mediated, tissue-specific destruction, including autoimmunity, allograft rejection, graft-versus-host disease, and killing of affected cells during the acute phases of infection that leads to clearance of pathogens. Thus, tumor rejection is a facet of a general and conserved mechanism that favors (tumor rejection, clearance of pathogen) or encumbers (graft rejection, autoimmunity) the organism. Here, we summarize progress in the understanding of its genesis, outline the difficulties, and propose a strategy for understanding the causes of tumor rejection.

Original languageEnglish
Pages (from-to)75-79
Number of pages5
JournalAnnals of the New York Academy of Sciences
Volume1284
Issue number1
DOIs
Publication statusPublished - May 2013

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Keywords

  • Autoimmunity
  • Cancer immunotherapy
  • Melanoma
  • Rejection

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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