Sophie TARTARE DECKERT
  • E-mail :[email]
  • Phone : +33 4 89 06 43 33
  • Location : Nice, France
Last update 2011-05-27 16:10:08.896

Sophie TARTARE DECKERT PhD in Health Sciences, INSERM Research Director

Course and current status

Professional experience:

  • 1989-1993: Graduate Student (University of Nice Sophia-Antipolis). Thesis advisor: Pr E. Van Obberghen
  • 1995: Position INSERM CR2 INSERM Unit 145
  • 1996-1998: Research Associate at The Salk Institute for Biological Studies, La Jolla, USA.  Pr M. Montminy (1996) and Pr T. Hunter (1997-1998)
  • 1999-2002:  INSERM Staff Scientist at Unit 145
  • 2002-2004:  INSERM Staff Scientist at Unit 385
  • 2004-2007:  Co-leader of the team “Microenvironment and Melanocyte Tansformation” INSERM Unit 597, Head: Dr R Ballotti
  • 2006:  Visiting Scientist at Ontario Cancer Institute, Toronto, Canada.
  • 2008: Research Director (DR2 level) and group leader at INSERM Unit 895 (C3M) (http://webs.unice.fr/c3m/)
  • Present: Head of the team "Microenvironment, Signaling and Cancer" at INSERM Unit 895 (C3M)

Scientific summary

My main research area of expertise is in how tumor cells communicate with their microenvironment and in melanoma, the most aggressive and serious form of skin cancer.

I obtained my PhD from the University of Nice Sophia-Antipolis, School of Medicine, France for my work on the cross-talk between tyrosine kinase receptors and the molecular dissection of insulin signaling. I became interested in cell cycle control and cancer during my post-doctoral research at the Salk Institute, La Jolla, USA. Since 2003, I have developped my independent research program and established my own lab this year at INSERM Unit 895, C3M Institute. We are interested in the molecular and cellular mechanisms governing melanoma development with a particular focus on SPARC, a matricellular protein that modulates the dialogue between tumor cells and their stroma. My lab achieved important discoveries such as: (i) the role of SPARC as a matricellular regulator of Epithelial Mesenchymal Transition (EMT) and p53-dependent cell survival; and (ii) the epigenetic silencing of the tyrosine kinase Syk and its contribution in melanoma senescence bypass, Kit signaling and metastasis. Ongoing projects in the lab are pursuing our initial results on SPARC and Syk using different mouse melanoma models and the study of the role of the lymphatic microenvironment in melanoma metastasis and chemoresistance. Our aim is to translate our results on melanoma to the clinic. 

Image d’exemple