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Three complementary axes

Our project includes three complementary axes, based on our recent findings and technological developments :

Axe 1. Role of neurotrophins in promoting cancer cell aggressive phenotype.

    Pr. Xuefen      Pr. Robert-Alain
    Le Bourhis             Toillon
We were the first to show the implication of neurotrophins in breast cancer; our ongoing works reveal that tumorigenesis and resistance to therapeutic agents vary according to the recruitment of different signaling platforms by neurotrophins receptors. We will a) determine the signaling and the impact of neurotrophins receptors platforms in the acquisition of cancer cell aggressiveness; b) evaluate the potential of neurotrophins receptors platforms as prognostic markers and/or therapeutic targets.


Axe 2. Role of epigenetic effectors such as Polycomb group (PcG) proteins in the regulation of cancer cell plasticity.

Pr. Pierre-Olivier        Pr.Eric
      Angrand          Adriaenssens
Increasing data describe the pivotal role played by proteins of polycomb repression complexes such as Bmi1 and Ezh2 in cell proliferation and differentiation of both normal and tumor cells. We will a) characterize PcG proteins expression pattern in human cancer cells and in a mouse mammary tumorigenesis model; b) determine the involvement of PcG proteins in the control of cancer cell plasticity and resistance to conventional therapies.


Axe 3. Identification of molecular mechanisms involved in therapy-induced cancer stem cell (CSC) plasticity.

    Dr. Chann          Dr. Samuel           Dr. Pierre
      Lagadec             Meignan              Leblond
We will a) evaluate how anticancer treatments modulates the production of soluble factors (such as growth factors/cytokines/chemokines) that induce non-CSCs into CSCs reprogramming; b) assess the involvement of intrinsic factors such PcG proteins in CSCs reprogramming; c) target the identified factors to prevent treatment-induced reprogramming in an in vivo context using transgenic mice.