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 language | English |
|---|---|
| Pages (from-to) | 75-79 |
| Number of pages | 5 |
| Journal | Annals of the New York Academy of Sciences |
| Volume | 1284 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 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
Cite this
Common pathways to tumor rejection. / Wang, Ena; Bedognetti, Davide; Tomei, Sara; Marincola, Francesco M.
In: Annals of the New York Academy of Sciences, Vol. 1284, No. 1, 05.2013, p. 75-79.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Common pathways to tumor rejection
AU - Wang, Ena
AU - Bedognetti, Davide
AU - Tomei, Sara
AU - Marincola, Francesco M.
PY - 2013/5
Y1 - 2013/5
N2 - 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.
AB - 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.
KW - Autoimmunity
KW - Cancer immunotherapy
KW - Melanoma
KW - Rejection
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U2 - 10.1111/nyas.12063
DO - 10.1111/nyas.12063
M3 - Article
C2 - 23651198
AN - SCOPUS:84877346511
VL - 1284
SP - 75
EP - 79
JO - Annals of The Lyceum of Natural History of New York
JF - Annals of The Lyceum of Natural History of New York
SN - 0890-6564
IS - 1
ER -