Project SFB 685 "Immunotherapy: Molecular basis and clinical application" - Teilprojekt TP C01 "Induktion eines…

Basic data

Title:
SFB 685 "Immunotherapy: Molecular basis and clinical application" - Teilprojekt TP C01 "Induktion eines dauerhaften Wachstumsarrests in Tumoren mittels CD4 T Helfer-Zellen"
Duration:
01/07/2013 to 30/06/2017
Abstract / short description:
Gene mutations leading to accelerated cell cycle are frequent cancer driver mutations and normally targeted by small molecules. We found that, surprisingly, Th1 cell cytokines can induce senescence-like cell cycle arrest directly, even in T antigen (Tag) expressing cancers.
Tag-specific Th1 cells arrest cancers, through IFN-γ and TNFR1 driven activation of the p16INK4a/Rb senescence pathway, and obviously preserve genomic stability. As Rb is non-redundant for cell cycle control we will now study a) the exact signaling pathways by which TNFR1-signaling activates p16INK4a/Rb in concert with IFN-γ and b) the genetic effects of Rb-mediated E2F2 suppression and gene silencing.
Keywords:
Tumor dormancy
p16INK4a/Rb senescence pathway
Th1 cells
IFN-γ
TNFR1

Involved staff

Managers

Department of Dermatology
Hospitals and clinical institutes, Faculty of Medicine

Contact persons

Department of Dermatology
Hospitals and clinical institutes, Faculty of Medicine

Local organizational units

Department of Dermatology
Hospitals and clinical institutes
Faculty of Medicine

Funders

Bonn, Nordrhein-Westfalen, Germany
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