Tumor counterattack: fact or fiction?

Cancer development relies on a variety of mechanisms that facilitate tumor growth despite the presence of a functioning immune system. Understanding these mechanisms may foster novel therapeutic approaches for oncology and organ transplantation. By expression of the apoptosis-inducing protein CD95L...

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Hauptverfasser: Igney, Frederik (VerfasserIn) , Krammer, Peter H. (VerfasserIn)
Dokumenttyp: Article (Journal) Konferenzschrift
Sprache:Englisch
Veröffentlicht: 12 May 2005
In: Cancer immunology immunotherapy
Year: 2005, Jahrgang: 54, Heft: 11, Pages: 1127-1136
ISSN:1432-0851
DOI:10.1007/s00262-005-0680-7
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s00262-005-0680-7
Verlag, lizenzpflichtig, Volltext: https://link.springer.com/article/10.1007%2Fs00262-005-0680-7
Volltext
Verfasserangaben:Frederik H. Igney, Peter H. Krammer
Beschreibung
Zusammenfassung:Cancer development relies on a variety of mechanisms that facilitate tumor growth despite the presence of a functioning immune system. Understanding these mechanisms may foster novel therapeutic approaches for oncology and organ transplantation. By expression of the apoptosis-inducing protein CD95L (FasL, APO-1L, CD178), tumors may eliminate tumor-infiltrating lymphocytes and suppress anti-tumor immune responses, a phenomenon called “tumor counterattack”. On the one hand, preliminary evidence of tumor counterattack in human tumors exists, and CD95L expression can prevent T-cell responses in vitro. On the other hand, CD95L-expressing tumors are rapidly rejected and induce inflammation in mice. Here, we summarize and discuss the consequences of CD95L expression of tumor cells and its contribution to immune escape.
Beschreibung:This article is a symposium paper from the conference ‘‘Tumor Escape and Its Determinants’’, held in Salzburg, Austria, on 10–13 October 2004
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Beschreibung:Online Resource
ISSN:1432-0851
DOI:10.1007/s00262-005-0680-7