Oct 1995 to May 1999: PhD Molecular and Cellular Biology, Inserm, Montpellier, France.
Jun 1999 to Dec 2002: Post doctoral fellow, NIH, Bethesda, USA.
Jan 2003 to Sep 2007: Post doctoral fellow, IGH, Montpellier, France.
Since Oct 2007: Research scientist CR1 Inserm, IGH, Montpellier, France.
The two isoforms of the Akt kinase, Akt1 and Akt2, are differentially implicated in the proliferation-differentiation transition in muscle. This transition is defective in tumor cells derived from rhabdomyosarcomes (RMS). Embryonic RMS (ERMS) and alveolar RMS (ARMS) behave differently in case of anti-cancer treatments; ERMS can be treated with high efficiency whereas ARMS are resistant to treatment and are more invasive. The aim of my research project is to determine the different actors of the Akt signalling which are specifically implicated in ERMS and ARMS. Indeed, we have proven that Akt1, Akt2 and p21 are playing essential roles in signalling pathways leading to proliferation, cell cycle arrest before differentiation as well as tumor cell resistance to apoptosis, especially tumor cells derived from ARMS. This project should help identifying the implication of Akt1 and Akt2 both in RMS biology and in the resistance to anti-cancer treatments commonly used. I will also try to characterize the molecular components, their interactions and the specific alterations implicated in ARMS, the child solid tumor the most difficult to treat.