Description
The changes in the cell biology of tumor cells are conditioned by epigenetic and genetic reprogramming, genomic instability being an essential feature of both oncogenesis and tumor progression despite intrinsic tumor suppressing barriers. These modifications of cancer cells can be accompanied by the emission of danger signals that can be perceived by the innate and cognate immune systems. Likewise, promoting tumor cell death or autophagy may enhance or probe the activation of the immune system. Therefore, unravelling the links between the intrinsic barriers against tumor progression and the extrinsic anticancer checkpoints may contribute to unravelling the key molecular sensors of the host-tumor equilibrium and create novel therapeutic targets. The major objectives will be as follows:
1) examine the molecular links between tumor intrinsic checkpoints (p53, NF-Kappa B, autophagy, DNA damage response ) and immunity or immunosuppression,
2) explore the indirect effects of anticancer therapies (conventional or targeted) on the immune system,
3) describe the rationale for and the potential benefit of novel strategies of cancer vaccines or immunotherapies exploiting this knowledge.
