Stéphane ANSIEAU Failsafe program escape and plasticity

Course and current status

Civil status

Stéphane Ansieau

Born the 10/28/66 (Maubeuge, France).

Researcher Inserm CR1

Location : Inserm UMR-S1052, CNRS UMR 5286, Centre de Recherche en Cancérologie de Lyon, Centre Léon Bérard, F-69008 Lyon

Degree: PhD, HDR

Professional experience:

2006 : Recruited CR1 Inserm (Inserm U 590, Lyon, France)

2002-2006 : Inserm program Avenir (Inserm U412, Lyon, France)

1994-2002 : post-doctoral internship (A. Leutz’s research unit, Max Delbrück Center, Berlin, Germany)

1993: PhD (Paris XI, Orsay, France)

Awards and prizes :

2002-2005: Laureate of the Inserm program Avenir

2000-2001: Max-Delbrück grant

1995 : Association pour la Recherche sur le Cancer  (ARC) grant.

1993: Juliana Oser prize, ARC.

1992: Fondation Schlumberger grant.

1989-1991: Scholarship from the Ministère de la Recherche et des Techniques.

Highlights

- Role of EMT-inducers in failsafe program escape and tumor initiation

- Identification of CBF1 and BS69 as novel targets shared by various viral oncoproteins.

Publications

23 international publications

7 national publications

2 chapters

Scientific support :

5 post-doctorants, 4 PHD students, 7 students

Scientific collaborations:

National

Pr U. Hibner (UMR5535, IGMM, Montpellier)

Pr P. Laurent-Puig (UMR S-775, Paris Descartes) 

Dr P. Clézardin (Inserm U664, Lyon) 

International

Dr D. Spicer (Scarborough, Main, USA)

Dr E. Tulchinsky (Leicester, UK)

Scientific summary

Premature senescence and apoptosis constitute failsafe programs that counteract the aberrant mitotic effects of activated oncoproteins. In vivo, they are induced in premalignant lesions, and malignant progression requires their inhibition. We have recently demonstrated that the reactivation of either of the TWIST embryonic transcription factors, TWIST1 or TWIST2, favours tumour progression by inhibiting these two onco-suppressive mechanisms and by inducing an epithelial-mesenchymal transition (EMT). We also demonstrated that the hijack of this embryonic transdifferentiation process is associated with the acquisition by pre-cancerous and cancer cells of cell motility but also of properties of self-renewal. Based on these observations, we proposed that (i) EMT plays a role during the growth of the primary tumour (ii) the reactivation of the TWIST genes promotes the early dissemination of pre-cancerous or cancer cells. Our objectives are to validate the whole of these data in in vivo models and to evaluate if the link established between the evasion of failsafe programs - EMT - properties of self-renewal and early metastatic dissemination can be extended to other embryonic EMT-inducing transcription factors. Beyond their cognitive interest, our work aims to identify novel markers allowing the isolation of circulating and disseminated cancer cells exhibiting mesenchymal characteristics and the evaluation of their potential interest to forecast the metastatic risk in patients with mammary carcinomas.