Jeremie Roux PhD in Life Sciences, HDR

Course and current status

• Habilitation à Diriger des Recherches (HDR) - September 2019

• CNRS Researcher in the Non coding genome & lung disorders, Mari lab at IPMC, Valbonne Sophia Antipolis - since December 2022  
• INRIA Associate member of the BioCore team at INRIA, Sophia Antipolis - since May 2014  

Past Positions

• CNRS Researcher in the Carcinogenesis-related chronic active inflammation, Hofman lab at IRCAN, Nice - since October 2016
  
• Principal Investigator of SysBioDRez (EC funded project, Marie Curie Actions, FP7, 2013-IIF) in the laboratory of Pr. Paul Hofman. IRCAN, Nice - 2014 - 2016
• Roche Sponsored Research fellow in the laboratory of Pr. Peter Sorger, Department of Systems Biology. Harvard Medical School, Boston - 2010-2014

• Core member and consultant at A-Cube, Inc.  Belmont, CA, USA - 2005 - 2013
• NIH T32 Research trainee in the Department of Anesthesia and Perioperative Care. University of California San Francisco (UCSF), San Francisco - 2007-2010
• American Lung Association fellow in the Departments of Anesthesia and Surgery. UCSF, San Francisco - 2005-2007
• PhD candidate in the laboratory of J.-F. Pittet  M.D. Department of Anesthesia. UCSF, San Francisco. Thesis co-mentored by Pr. Pascal Barbry (IPMC, CNRS) - 2001-2005

Scientific summary

Research effort

The overall objective of my research effort is to determine the origins of tumor cell heterogeneity in response to anti-cancer drugs, by coupling high-content analyses (dynamic live cell imaging, high-throughput assays) with theoretical and computational methods.
This is an attempt to address a deficiency in large-scale studies focusing on multiple genetic biomarkers that may be partially inadequate given the observed fractional killing of genetically-identical tumor cell populations after chemotherapeutic treatment. Ultimately this approach should serve to identify, on a tumor cell type basis, the most predictive set of biomarkers and design optimal therapeutic combinations.

Past Research summary

1. PhD research, 2001-2005 (University of California San Francisco, San Francisco USA): The main objective of my PhD work was to investigate the role of alveolar epithelial ion channel function in the pathogenesis of acute lung injury. My work showed that impaired fluid transport was due to a negative regulation of the epithelial sodium channel (ENaC) expression, trafficking and function. The studies demonstrated the role of several inflammatory factors on ENaC biosynthesis and their respective impact on the whole epithelial fluid transport.


2. Postdoctoral research 1, 2005-2010 (University of California San Francisco, San Francisco USA): The objective of my postdoctoral fellowship was to determine, in rat and human primary alveolar epithelial cells, the effect of inflammatory mediators present during the therapeutic rescue of acute lung injury (ALI). I demonstrated a novel role for TGF-β1 and IL-8 in ALI, as inhibitors of the β2-adrenergic response, correlated with lower alveolar fluid clearance in humans. These effects could be corrected by different PI3K inhibitors (isoform specific) - safe to use in humans. I then directed a study demonstrating that HMGB1, released by wounded epithelial cell monolayers, accelerates the distal lung epithelium repair via the secretion of IL-1β, playing a critical role in the resolution of ALI.


3. Postdoctoral research 2, 2010-2014 (Harvard Medical School, Boston USA): My objective was to establish a proof-of-concept work to understand the dynamics of a key molecular pathway and use advanced analytic tools to extrapolate important kinetic features that we could manipulate pharmacologically.  I developed a workflow that enables high-throughput analyses of living single cells, to specifically study drug resistance in cancer cells by probing the dynamics of tumor cells responses to anti-cancer agents.  Upon treatment with targeted chemotherapy, I have found that death receptor dynamics are extremely variable from one cell to the next, in the same genetically homogenous population of tumor cells and showed that these dynamics control cell fate (i.e. drug sensitivity).